37 results on '"Ryo, Oikawa"'
Search Results
2. Arterial communication around the pancreatic tail enabled division of the gastroduodenal artery during pancreaticoduodenectomy in patient with complete celiac artery occlusion: a case report
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Ryo Oikawa, Kyoji Ito, Nobuyuki Takemura, Fuminori Mihara, and Norihiro Kokudo
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Celiac artery stenosis ,Pancreaticoduodenectomy ,Three-dimensional imaging ,Gastroduodenal artery clamping test ,Peri-pancreatic arterial communication ,Surgery ,RD1-811 - Abstract
Abstract Background Stenosis or obstruction of the celiac artery (CA) is known as celiac artery stenosis (CAS) and is usually accompanied by the formation of arterial anastomosis between the superior mesenteric artery (SMA) system and the CA system. Arterial bypass is mainly achieved through the gastroduodenal artery (GDA); therefore, the division of the GDA during pancreaticoduodenectomy (PD) could pose a problem in patients with CAS. Case presentation We reported a case of PD presenting complete occlusion of the CA, in which perfusion to organs in the CA system was maintained via peri-pancreatic arterial communication. There were complicated arterial anastomoses around the pancreas, which were clearly visualized on a three-dimensional reconstruction of the arterial system using multi-detector computed tomography. Among these complicated anastomoses, one well-developed anastomosis between the SMA and the splenic artery through the dorsal pancreatic artery (DPA) was identified. The DPA was considered to work as a potential collateral pathway from the SMA to organs in the CA system after division of the GDA. During surgery, Doppler ultrasonography detected hepatopetal arterial flow even after the GDA clamping; therefore, we performed typical PD with division of the GDA. The postoperative course of the patient was uneventful, and there was no sign of ischemic complications in the CA system organs including the liver, stomach or spleen. Conclusions Three-dimensional reconstruction of the arterial system using multi-detector computed tomography and the intraoperative GDA clamping test were useful to determine whether it was possible to divide the GDA in PD, in the case of CAS.
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- 2020
- Full Text
- View/download PDF
3. Comparison of the Susceptibility to Implant Failure in the Lateral, Posterior, and Transforaminal Lumbar Interbody Fusion: A Finite Element Analysis
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Ryo Oikawa, Hideki Murakami, Hirooki Endo, Hirotaka Yan, Daisuke Yamabe, Yusuke Chiba, Ryosuke Oikawa, Norihiro Nishida, Xian Chen, Takashi Sakai, and Minoru Doita
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Lumbar Vertebrae ,Spinal Fusion ,Bone Screws ,Finite Element Analysis ,Humans ,Surgery ,Neurology (clinical) ,Range of Motion, Articular ,Biomechanical Phenomena - Abstract
There are several techniques for lumbar interbody fusion, and implant failure following lumbar interbody fusion can be troublesome. This study aimed to compare the stress in posterior implant and peri-screw vertebral bodies among lateral lumbar interbody fusion (LLIF), posterior lumbar interbody fusion (PLIF), and transforaminal lumbar interbody fusion (TLIF) and to select the technique that is least likely to cause implant failure.We created an intact L3-L5 model and simulated the LLIF, PLIF, and TLIF techniques at L4-L5 using finite element methods. All models at the lower portion of L5 were fixed and imposed a preload of 400 N and a moment of 7.5 Nm on the upper portion of L3 to simulate flexion, extension, lateral bending, and axial rotation. We investigated the peak stresses and stress concentration in the posterior implant and peri-screw vertebral bodies for the LLIF, PLIF, and TLIF techniques.The extension, flexion, bending, and rotation peak stresses and stress concentration in the posterior implant, as well as the peri-screw vertebral bodies, were the lowest in LLIF, followed by PLIF and TLIF.It was found that implant failure was least likely to occur in LLIF, followed by PLIF and TLIF. Hence, surgeons should be aware of these factors when selecting an appropriate surgical technique and be careful for implant failure during postoperative follow-up.
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- 2022
4. Bowel perfusion demonstrated using indocyanine green fluorescence imaging in two cases of strangulated ileus
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Kyoko Nohara, Nobuyuki Takemura, Kyoji Ito, Ryo Oikawa, Syusuke Yagi, Hitomi Wake, Naoki Enomoto, Kazuhiko Yamada, and Norihiro Kokudo
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Indocyanine Green ,Intestines ,Perfusion ,Ileus ,Optical Imaging ,Gastroenterology ,Humans ,General Medicine ,Intestinal Obstruction - Abstract
We report the use of indocyanine green (ICG) fluorescence for intraoperative diagnosis in two cases of strangulated ileus. We successfully preserved the bowel and avoided postoperative complications by detecting adequate perfusion and no necrosis in the intestine's strangulated regions. In the first case, enhanced computed tomography (CT) revealed a closed loop intestine, which showed poor contrast, and we performed laparotomy with ICG fluorescence. In the second case, the CT scan revealed bowel obstruction without ascites. We conservatively treated the patient with the insertion of a long tube. The patient's condition did not improve, and we performed laparotomy using ICG fluorescence. In both of these cases, the visual observation during laparotomy showed that the ileum had dark-red discoloration. We demonstrated perfusion and preserved the ileum by injecting 2.5 mg of ICG intravenously; fluorescence was observed in the dark-red ileum using the PINPOINT system (Novadaq, Kalamazoo, MI, US). Both patients recovered successfully after the surgery with no adverse events. Our data suggest that ICG fluorescence imaging can be one of the decision-making modalities in patients with strangulated ileus.
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- 2022
5. Laparoscopic hemostasis for abdominal brunt massive hemorrhage due to endometriosis
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Junko Yagi, Shiori Seki, Norihiro Kokudo, Nobuyuki Takemura, Kensuke Tomio, Hajime Oishi, Hikaru Koutake, Kyoji Ito, Fuminori Mihara, Ryo Oikawa, and Misao Nakanishi
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medicine.medical_specialty ,Abdominal pain ,medicine.diagnostic_test ,business.industry ,Uterine fibroids ,Endometriosis ,Adhesion (medicine) ,General Medicine ,medicine.disease ,Surgery ,Blunt trauma ,medicine.artery ,medicine ,Hemoperitoneum ,medicine.symptom ,business ,Uterine artery ,Laparoscopy - Abstract
In the gynecological literature, a limited number of studies have reported intraperitoneal bleeding due to abdominal blunt trauma. In this report, we describe a rare case of massive intraabdominal hemorrhage from the uterine artery triggered by a fall injury without apparent abdominal bruising in the presence of severe endometriosis and a uterine fibroid. A 28-year-old woman who fell from a railway platform was transported to an emergency hospital. Although she did not sustain abdominal bruising and initially had no abdominal symptoms, she complained of gradually worsening abdominal pain. Abdominal CT identified intraabdominal massive hematoma, and emergency exploratory laparoscopy revealed active bleeding from the right uterine artery eroded by endometriosis, which was treated with laparoscopic electrocoagulation. The cause of the intraabdominal bleeding was associated with avulsion of the endometriosis adhesion between the right perimetrium and the right uterine artery due to inertial forces of the uterus during the fall injury. A uterine fibroid discovered during laparoscopy was suspected to strengthen the inertial forces of the uterus. In the case of hemoperitoneum after trauma, gynecological sources of bleeding must be kept in mind, especially for patients with a known history of fibroids or endometriosis.
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- 2021
6. Risk Factors of Atherosclerotic Celiac Artery Stenosis Among Patients Undergoing Pancreaticoduodenectomy
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Ryo, Oikawa, Kyoji, Ito, Nobuyuki, Takemura, Fuminori, Mihara, Yoshitaka, Shida, Tsuyoshi, Tajima, and Norihiro, Kokudo
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Pancreatectomy ,Endocrinology ,Hepatology ,Celiac Artery ,Risk Factors ,Endocrinology, Diabetes and Metabolism ,Internal Medicine ,Humans ,Constriction, Pathologic ,Pancreaticoduodenectomy - Published
- 2022
7. Using Indocyanine Green Fluorescence Imaging to Identify an Anomalous Cystohepatic Duct During Laparoscopic Cholecystectomy
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Ryo Oikawa, Kyoji Ito, Nobuyuki Takemura, Mikiya Fujii, Mai Nakamura, Fuminori Mihara, Fuyuki Inagaki, and Norihiro Kokudo
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General Medicine - Published
- 2023
8. Classification of Prehospital-Electrocardiograms taken in Ambulance According to Severity using Deep Learning Neural Network
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Ryo Oikawa, Akio Doi, Basabi Chakraborty, Tomonori Itoh, and Osamu Nishiyama
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- 2022
9. [A patient with autoimmune pancreatitis complicated by pancreatic pseudocyst that caused colonic perforation-induced gastrointestinal bleeding]
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Teruaki, Inoue, Ryo, Oikawa, Eri, Shimura, Tatsuhiro, Ito, Naoya, Kaneko, and Masashi, Mori
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Cholangiopancreatography, Endoscopic Retrograde ,Male ,Pancreatitis ,Autoimmune Pancreatitis ,Pancreatic Pseudocyst ,Humans ,Middle Aged ,Gastrointestinal Hemorrhage - Abstract
A 62-year-old male patient was referred to our hospital for jaundice and bloody feces. He had hyper-IgG4-emia. Computed tomography (CT) showed diffuse pancreatic enlargement, pancreatic pseudocyst, and hematoma of the splenic flexure of the colon. Magnetic resonance imaging (MRI) showed a fistula in the pancreatic pseudocyst and splenic flexure of the colon. Moreover, lower gastrointestinal endoscopy showed a fistula in the same region. Endoscopic retrograde cholangiopancreatography (ERCP) showed narrowing of the main pancreatic duct and stenosis of the lower bile duct. Following this, the patient was diagnosed with autoimmune pancreatitis-induced pancreatic pseudocyst and colonic perforation-induced gastrointestinal bleeding. The pancreatic pseudocyst and fistula were resolved through steroid treatment.
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- 2022
10. A Power Balance Simulator to Examine Business Continuity in Hospital Facilities Due to Power Outages in a Disaster
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Akane Uemichi, Ryo Oikawa, Yudai Yamasaki, and Shigehiko Kaneko
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Fuel Technology ,Geochemistry and Petrology ,Renewable Energy, Sustainability and the Environment ,Mechanical Engineering ,Energy Engineering and Power Technology - Abstract
In hospitals, the energy supply is the key to ensuring modern medical care even during power outages due to a disaster. This study qualitatively examined whether the supply–demand balance can be stabilized by the private generator prepared by the hospital building during stand-alone operations under disaster conditions. In the nanogrid of the hospital building, the power quality was examined based on the AC frequency, which characterizes the supply–demand balance. Gas engine generators, emergency diesel generators, photovoltaic panels, and storage batteries were presumed to be the private generators in the hospital building. The output reference values for the emergency diesel and gas engine generators were set using droop control, and the C/D controller-enabled synchronized operation. In addition, to keep the AC frequency fluctuation minor, the photovoltaic panels were designed to suppress the output fluctuation using storage batteries. As a result of case studies, the simulator predicts that the frequency fluctuation varies greatly depending on the weather conditions and the fluctuation suppression parameters, even for the same configuration with the same power generation capacity. Therefore, it is preferable to increase the moving average time of the output and reduce the feedback gain of the storage battery to suppress the output fluctuation from the photovoltaics. However, there is a trade-off between suppressing the output fluctuation and the minimum required storage capacity. Furthermore, since the photovoltaics’ output varies with the weather, other private generators’ capacity and control parameters significantly impact power quality. The simulator proposed in this study makes it possible to study each hospital's desirable private generator configuration.
- Published
- 2022
11. Preferable Anesthetic Conditions for Echocardiographic Determination of Murine Cardiac Function
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Yuji Kawahara, Kouichi Tanonaka, Takuya Daicho, Mikio Nawa, Ryo Oikawa, Yoshihisa Nasa, and Satoshi Takeo
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Therapeutics. Pharmacology ,RM1-950 - Abstract
Ketamine and xylazine are routinely used for measurement of hemodynamics of mice and rats by echocardiography. The anesthetic agents produce low heart rate (HR) in the animals, which may result in misleading data in the hemodynamic profiles of the small animals. The purpose of the present study was to select an appropriate anesthetic condition in the evaluation of mouse and rat cardiac function by echocardiography. Echocardiographic measurement was performed in male C57BL6 mice anesthetized with an intraperitoneal injection of 30 or 40 mg/kg pentobarbital (P30 or P40) or a combination of 60 mg/kg ketamine and 6 mg/kg xylazine (KX) and in male Wistar rats with an intraperitoneal injection of 40 or 50 mg/kg pentobarbital (P40 or P50) or a combination of 100 mg/kg ketamine and 10 mg/kg xylazine (KX). Basal HR of P30-anesthetized mice and P40-anesthetized were comparable to those in the conscious state, whereas KX-anesthetized mice and rats were 38% and 74% of those of the conscious animals, respectively. Fractional shortening (FS) and cardiac output index (COI) of the P30-anesthetized mice or the P40-anesthetized rats were greater than those of KX-anesthetized animals. Intraperitoneal injection of dobutamine at 0.3 and 1 mg/kg increased HR, FS, and COI of the P30-anesthetized mice and the P40-anesthetized rats, respectively, whereas the percent responses of these parameters in KX animals were greater than those in pentobarbital-anesthetized ones due to the lower basal values for the cardiac functional parameters. Anesthesia with P30 for the mouse and P40 for the rat rather than ketamine/xylazine may be relevant to the evaluation of cardiac function using echocardiography. Keywords:: anesthesia, blood flow, cardiac function, echocardiography, heart rate
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- 2005
- Full Text
- View/download PDF
12. Multi-objective optimization to determine installation capacity of distributed power generation equipment considering energy-resilience against disasters
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Ryo Oikawa, Yudai Yamasaki, Akane Uemichi, Masaaki Yagi, and Shigehiko Kaneko
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Electricity generation ,Business continuity ,Operations research ,business.industry ,Total cost ,Computer science ,Distributed generation ,Photovoltaic system ,Gas engine ,business ,Resilience (network) ,Multi-objective optimization - Abstract
In 2017, the Mistry of Health, Labor, and Welfare in Japan added a requirement for domestic disaster base hospitals to install electric power generation equipment with a generation capacity at least 60% of usual demand for securing business continuity. In this study, we developed a multi-objective optimization tool for assisting the determination of the capacity of distributed generation equipment and contract plans considering energy-resiliency after a disaster. The selected objective functions are a total cost representing economy and environment, and an expected value of power shortage ratio after the catastrophe representing energy-resiliency. As a result, our developed tool could obtain the Pareto-optimal solutions for various size hospitals on the parameter plane of the two objective functions. As well as total costs, for all optimal solutions, the expected value of power shortage ratio under disaster situation resulted in less than 40% suggesting that the national requirement standard is satisfied. Then, the cluster analysis was carried out to grasp the tendency of optimal solutions. From the analysis of average value for each cluster, it is shown that the optimal introductory capacities of gas engine generators and storage batteries couple through the outage probabilities of gas supply. Furthermore, the optimal capacity of photovoltaic is much larger than the one assumed to install on the estimated rooftop area of the hospital building, which suggests that hospital can take an option to introduce more photovoltaics to an adjacent area if possible.
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- 2019
13. Detailed anatomy and procedure of celiac artery decompression in median arcuate ligament syndrome
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Fuminori Mihara, Ryo Oikawa, Norihiro Kokudo, Nobuyuki Takemura, Kyoji Ito, and Fuyuki Inagaki
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musculoskeletal diseases ,Duplex ultrasonography ,Aorta ,Left gastric artery ,Decompression ,business.industry ,Median arcuate ligament ,Anatomy ,medicine.disease ,Decompression, Surgical ,Stenosis ,medicine.anatomical_structure ,Median Arcuate Ligament Syndrome ,Celiac artery ,Celiac Artery ,medicine.artery ,parasitic diseases ,medicine ,Humans ,lipids (amino acids, peptides, and proteins) ,Surgery ,business ,Median arcuate ligament syndrome - Abstract
Median arcuate ligament (MAL) syndrome is a clinical syndrome caused by the compression of the celiac artery (CA) by the MAL. This study aimed to present the detailed anatomy and a step-by-step procedure of CA decompression for MAL syndrome. The CA decompression procedure involves exposing the diaphragmatic crura and aorta, taping the left gastric artery, and dividing the compressive tissues. The MAL and ganglionic tissue, which form a broad band with multiple layers overlying the CA, comprise the compressive tissues. Therefore, the compressive tissues overlying the CA are encircled and divided one by one until the CA stenosis is released. CA decompression is confirmed with intraoperative duplex ultrasonography of the CA, with a return to normal peak systolic velocities without variation between deep inspiration and expiration. This report presents the detailed anatomy and procedural steps for CA decompression in MAL syndrome.
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- 2021
14. System design to reduce disaster risks by installing distributed power resources
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Ryo Oikawa, Yudai Yamasaki, Akane Uemichi, Shigehiko Kaneko, and Masaaki Yagi
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Decision support system ,Operations research ,Present value ,Mechanics of Materials ,Total cost ,Computer science ,Applied Mathematics ,Return on investment ,Economic cost ,Systems design ,General Materials Science ,Subsidy ,Profit (economics) - Abstract
Subsidy and social systems should be designed to effectively promote, for example, the introduction of a mechanical system. For an effective subsidy distribution, developing evidence-based decision-making methodologies is essential. We developed a tool that minimizes an objective function includes economic costs, environmental cost, and disaster risk to determine the amount of energy distributed by the equipment when installing in hospitals against disasters. Open data available on the Internet are used as simulation values herein. This simulation model optimizes six design values using a genetic algorithm based on the values (business site area, demand for heat and electricity, and maximum allowable loss) input by customers for their construction and visualizes the total cost. The tool allows to quantitatively assess the changes in the initial and running costs owing to equipment installation and the avoidable losses related to $$\hbox {CO}_{2}$$ emission reductions and disaster risks. In addition, the net present value (NPV) can be calculated using the obtained values for initial and running costs, thereby allowing to clearly estimate the return on investments after equipment installation. The opportunity profit can be calculated based on the difference between the NPV after 15 years assuming no risk and with disaster risks. A method to set this opportunity profit as a calculated subsidy amount is proposed herein. Decision support can be provided via these simulations to the customers and government subsidy system design engineers.
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- 2018
15. Energy demand and supply simulation to examine business continuity in case of disaster in hospitals
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Naoki Kaito, Shigehiko Kaneko, Akane Uemichi, Ryo Oikawa, and Yudai Yamasaki
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Energy demand ,Development (topology) ,Business continuity ,Operations research ,business.industry ,Computer science ,Distributed generation ,business - Published
- 2019
16. Olmesartan ameliorates urinary dysfunction in the spontaneously hypertensive rat via recovering bladder blood flow and decreasing oxidative stress
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Fumiya Ohmasa, Darryl T. Martin, Motoaki Saito, Shogo Shimizu, Harunori Oiwa, Yukako Kinoshita, Fotios Dimitriadis, Shuhei Tomita, Itaru Satoh, Panagiota Tsounapi, and Ryo Oikawa
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medicine.medical_specialty ,business.industry ,Urology ,Urinary system ,Malondialdehyde ,Angiotensin II ,chemistry.chemical_compound ,Spontaneously hypertensive rat ,Blood pressure ,Endocrinology ,chemistry ,Nifedipine ,Internal medicine ,medicine ,Neurology (clinical) ,Urothelium ,Olmesartan ,business ,medicine.drug - Abstract
Purpose As hypertension (HT) is one of the risk factors for lower urinary tract symptoms, we investigated the effect of an angiotensin II type I receptor blocker, olmesartan, on bladder dysfunction in the spontaneously hypertensive rat (SHR). Materials and Methods Twelve-week-old male SHRs were administered perorally with olmesartan (0, 1, or 3 mg/kg/day) or nifedipine (30 mg/kg/day) for 6 weeks. Wistar rats were used as normotensive controls. The effects of olmesartan or nifedipine on blood pressure (BP), bladder blood flow (BBF), urodynamic parameters, tissue levels of malondialdehyde (MDA), nuclear factor erythroid 2-related factor 2 (Nrf2), and nerve growth factor (NGF) were measured in the bladder. Localization of 4-hydroxy-2-nonenal (4-HNE), Nrf2, and NGF in the bladder was shown by immunohistochemistry. Results The SHRs showed significant increase in BP, micturition frequency, and expression of MDA, 4-HNE, Nrf2, and NGF when compared to the control Wistar rats. Conversely, there was a decrease in BBF and single voided volume in SHRs when compared to Wistar rats. Treatment with olmesartan and nifedipine significantly improved BP. However, only olmesartan significantly ameliorated urodynamic parameters and oxidative damage compared to the non-treated SHR. The immunoreactivities of 4-HNE, Nrf2, and NGF in SHR urothelium and blood vessels were increased compared to the control. Treatment with a high dose of olmesartan decreased the expressions of 4-HNE, Nrf2, and NGF in the bladder. Conclusion Our data suggest that BP, BBF, and oxidative stress may be responsible for the functional changes in HT-related bladder dysfunction. Olmesartan significantly ameliorated this bladder dysfunction. Neurourol. Urodynam. 33:350–357, 2014. © 2013 Wiley Periodicals, Inc.
- Published
- 2013
17. Decreased susceptibility to salt-induced hypertension in subtotally nephrectomized mice lacking the vasopressin V1a receptor
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Satoshi Takeo, Takuya Daicho, Yoshihisa Nasa, Akito Tanoue, Kouichi Tanonaka, Gozoh Tsujimoto, Chihiro Hosoda, Norio Takagi, and Ryo Oikawa
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Male ,Receptors, Vasopressin ,Vasopressin ,medicine.medical_specialty ,Sympathetic Nervous System ,Time Factors ,Arginine ,Physiology ,Hemodynamics ,Blood Pressure ,Nephrectomy ,Mice ,Hormone Antagonists ,Heart Rate ,Receptors, Adrenergic, alpha-1 ,Physiology (medical) ,Internal medicine ,medicine ,Animals ,Sodium Chloride, Dietary ,Injections, Intraventricular ,Mice, Knockout ,Saline Solution, Hypertonic ,business.industry ,Sodium ,Antagonist ,Hypertonic saline ,Arginine Vasopressin ,Mice, Inbred C57BL ,Disease Models, Animal ,Blood pressure ,Endocrinology ,Vasoconstriction ,Hypertension ,Knockout mouse ,Circulatory system ,Cardiology and Cardiovascular Medicine ,business - Abstract
Aims By examining vasopressin V1a receptor (V1aR) knockout (KO) mice, we previously found that the V1aR is critically involved in the regulation of normal blood pressure. The present study was undertaken to elucidate the role of the V1aR in salt-induced hypertension. Methods and results We compared haemodynamic responses induced by subtotal nephrectomy + salt loading in V1aR KO mice with those of wild-type (WT) controls. The time course of changes in the systolic blood pressure and heart rate during the salt loading was attenuated in the KO mice compared with that for the WT mice. The elevation of the plasma norepinephrine level caused by the subtotal nephrectomy + salt loading was also reduced in the V1aR KO mice. A V1aR antagonist markedly lowered the arterial blood pressure in the salt-loaded WT mice but not in the normotensive WT mice or in the salt-loaded or normotensive V1aR KO mice. Whereas arginine vasopressin (AVP) administered to the lateral ventricle of the brain induced pressor and tachycardiac responses accompanied by sympathetic activation in the WT mice, these events were completely abolished in the V1aR KO mice. Also, pressor and tachycardiac responses induced by intraventricularly administered hypertonic saline in the WT mice were diminished in the V1aR KO mice. Moreover, the pressor response induced by intraventricularly administered AVP was reduced in α1d adrenoceptor KO mice, whereas the tachycardiac response did not differ from that of the WT mice. Conclusion These results suggest that the V1aR is involved in the elevation of arterial blood pressure caused by dietary salt and that a V1aR antagonist, in particular regarding its effect in the brain, could have significant therapeutic potential in the treatment of hypertension.
- Published
- 2010
18. V1a vasopressin receptors maintain normal blood pressure by regulating circulating blood volume and baroreflex sensitivity
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Hitoshi Okamura, Tetsuya Adachi, Yoshihisa Nasa, Gozoh Tsujimoto, Akito Tanoue, Taka-aki Koshimizu, Toyoki Mori, Tomoyuki Kuwaki, Yasushi Kiyono, Yuji Kawahara, Toshiki Tanaka, Satoshi Takeo, and Ryo Oikawa
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Receptors, Vasopressin ,medicine.medical_specialty ,Vasopressin ,Baroreceptor ,Hemodynamics ,Blood Pressure ,Blood volume ,Urinalysis ,Baroreflex ,Biology ,Mice ,Heart Rate ,Internal medicine ,medicine ,Animals ,Homeostasis ,Humans ,Receptor ,Vasopressin receptor ,Mice, Knockout ,Blood Volume ,Multidisciplinary ,Arteries ,Biological Sciences ,Arginine Vasopressin ,Endocrinology ,Echocardiography ,Adrenal Cortex ,Vascular Resistance ,hormones, hormone substitutes, and hormone antagonists ,Blood Chemical Analysis - Abstract
Arginine-vasopressin (AVP) is a hormone that is essential for both osmotic and cardiovascular homeostasis, and exerts important physiological regulation through three distinct receptors, V1a, V1b, and V2. Although AVP is used clinically as a potent vasoconstrictor (V1a receptor-mediated) in patients with circulatory shock, the physiological role of vasopressin V1a receptors in blood pressure (BP) homeostasis is ill-defined. In this study, we investigated the functional roles of the V1a receptor in cardiovascular homeostasis using gene targeting. The basal BP of conscious mutant mice lacking the V1a receptor gene (V1a −/− ) was significantly ( P < 0.001) lower compared to the wild-type mice (V1a +/+ ) without a notable change in heart rate. There was no significant alteration in cardiac functions as assessed by echocardiogram in the mutant mice. AVP-induced vasopressor responses were abolished in the mutant mice; rather, AVP caused a decrease in BP, which occurred in part through V2 receptor-mediated release of nitric oxide from the vascular endothelium. Arterial baroreceptor reflexes were markedly impaired in mutant mice, consistent with a loss of V1a receptors in the central area of baroreflex control. Notably, mutant mice showed a significant 9% reduction in circulating blood volume. Furthermore, mutant mice had normal plasma AVP levels and a normal AVP secretory response, but had significantly lower adrenocortical responsiveness to adrenocorticotropic hormone. Taken together, these results indicate that the V1a receptor plays an important role in normal resting arterial BP regulation mainly by its regulation of circulating blood volume and baroreflex sensitivity.
- Published
- 2006
19. Effects of ACE inhibitor and AT blocker on dystrophin-related proteins and calpain in failing heart
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Teruhiko Toyo-oka, Kouichi Tanonaka, Satoshi Takeo, Takuya Daicho, Ryo Oikawa, Hiroyuki Yoshida, Masaya Takahashi, and Miki Koshimizu
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Trandolapril ,medicine.medical_specialty ,Angiotensin II receptor type 1 ,biology ,Physiology ,business.industry ,Cardiomyopathy ,Calpain ,medicine.disease ,Angiotensin II ,Candesartan ,Endocrinology ,Physiology (medical) ,Internal medicine ,Heart failure ,ACE inhibitor ,medicine ,biology.protein ,Cardiology and Cardiovascular Medicine ,business ,medicine.drug - Abstract
Objectives : Genetic depletion of dystrophin-related protein (DRP) complex causes cardiomyopathy in animals and humans. We found in a previous study that some types of DRP were degraded and that calpain content was increased in rats with non-genetically induced heart failure. The present study was aimed at examining the effects of an angiotensin-I-converting enzyme inhibitor (ACEI) trandolapril (Tra) or an angiotensin II type 1 receptor blocker (ARB) candesartan (Can), both of which are known to improve the pathophysiology of chronic heart failure (CHF) on degradation of DRP in failing hearts. Methods : Coronary artery-ligated (CAL) and sham-operated rats (Sham rats) were treated orally with 3 mg/kg/day trandolapril (Tra) or 1 mg/kg/day candesartan (Can) from the 2nd to 8th week after surgery. Results : Hemodynamic parameters of CAL rats at the 8th week after CAL (8w-CAL) indicated heart failure. α-Sarcoglycan (SG) and dystrophin in the surviving left ventricle (surviving LV) of 8w-CAL rats decreased, whereas β-, γ-, and δ-SGs remained unchanged. Calcium-activated neutral proteases μ-calpain and m-calpain increased in the surviving LV at the 8th week of postmyocardial infarction. Proteolytic activity in the presence of 5 mM Ca2+ markedly increased at the 2nd and 8th weeks, whereas 50 μM Ca2+ slightly but significantly increased proteolysis of casein. Tra or Can treatment improved the hemodynamic parameters, attenuated changes in α-SG and dystrophin, and reversed both calpain contents and activities of the failing heart back to sham levels. Conclusion : These results suggest that attenuation in calpain-induced degradation of DRP complex is a possible mechanism for the Tra- or Can-mediated improvement of the pathogenesis of CHF following myocardial infarction.
- Published
- 2005
20. Preferable Anesthetic Conditions for Echocardiographic Determination of Murine Cardiac Function
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Yoshihisa Nasa, Satoshi Takeo, Takuya Daicho, Ryo Oikawa, Kouichi Tanonaka, Mikio Nawa, and Yuji Kawahara
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Cardiac function curve ,Male ,Xylazine ,Cardiac output ,Pentobarbital ,medicine.medical_treatment ,Intraperitoneal injection ,Mice ,Heart Rate ,Dobutamine ,Heart rate ,medicine ,Animals ,Ventricular Function ,Ketamine ,Cardiac Output ,Rats, Wistar ,Anesthetics ,Pharmacology ,business.industry ,lcsh:RM1-950 ,Adrenergic beta-Agonists ,Echocardiography, Doppler, Color ,Rats ,Mice, Inbred C57BL ,Drug Combinations ,lcsh:Therapeutics. Pharmacology ,Anesthesia ,Phenobarbital ,Anesthetic ,Molecular Medicine ,business ,medicine.drug - Abstract
Ketamine and xylazine are routinely used for measurement of hemodynamics of mice and rats by echocardiography. The anesthetic agents produce low heart rate (HR) in the animals, which may result in misleading data in the hemodynamic profiles of the small animals. The purpose of the present study was to select an appropriate anesthetic condition in the evaluation of mouse and rat cardiac function by echocardiography. Echocardiographic measurement was performed in male C57BL6 mice anesthetized with an intraperitoneal injection of 30 or 40 mg/kg pentobarbital (P30 or P40) or a combination of 60 mg/kg ketamine and 6 mg/kg xylazine (KX) and in male Wistar rats with an intraperitoneal injection of 40 or 50 mg/kg pentobarbital (P40 or P50) or a combination of 100 mg/kg ketamine and 10 mg/kg xylazine (KX). Basal HR of P30-anesthetized mice and P40-anesthetized were comparable to those in the conscious state, whereas KX-anesthetized mice and rats were 38% and 74% of those of the conscious animals, respectively. Fractional shortening (FS) and cardiac output index (COI) of the P30-anesthetized mice or the P40-anesthetized rats were greater than those of KX-anesthetized animals. Intraperitoneal injection of dobutamine at 0.3 and 1 mg/kg increased HR, FS, and COI of the P30-anesthetized mice and the P40-anesthetized rats, respectively, whereas the percent responses of these parameters in KX animals were greater than those in pentobarbital-anesthetized ones due to the lower basal values for the cardiac functional parameters. Anesthesia with P30 for the mouse and P40 for the rat rather than ketamine/xylazine may be relevant to the evaluation of cardiac function using echocardiography. Keywords:: anesthesia, blood flow, cardiac function, echocardiography, heart rate
- Published
- 2005
21. Two α1-Adrenergic Receptor Subtypes Regulating the Vasopressor Response Have Differential Roles in Blood Pressure Regulation
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Yoshihisa Nasa, Tadaichi Kitamura, Taka-aki Koshimizu, Takashi Tomabechi, Chihiro Hosoda, Sayuri Oshikawa, Susanna Cotecchia, Akito Tanoue, Gozoh Tsujimoto, Hitomi Shinoura, Shinya Fukuda, Ryo Oikawa, and Satoshi Takeo
- Subjects
Cardiac function curve ,medicine.medical_specialty ,Hemodynamics ,Aorta, Thoracic ,Blood Pressure ,In Vitro Techniques ,Potassium Chloride ,Norepinephrine (medication) ,Mice ,Radioligand Assay ,Basal (phylogenetics) ,Heart Rate ,Receptors, Adrenergic, alpha-1 ,Internal medicine ,Heart rate ,medicine ,Animals ,Cloning, Molecular ,Mice, Knockout ,Pharmacology ,business.industry ,Prazosin ,Recombinant Proteins ,Blood pressure ,Endocrinology ,Vasoconstriction ,Knockout mouse ,Molecular Medicine ,medicine.symptom ,business ,medicine.drug - Abstract
To study the functional role of individual alpha1-adrenergic (AR) subtypes in blood pressure (BP) regulation, we used mice lacking the alpha1B-AR and/or alpha1D-AR with the same genetic background and further studied their hemodynamic and vasoconstrictive responses. Both the alpha1D-AR knockout and alpha1B-/alpha1D-AR double knockout mice, but not the alpha1B-AR knockout mice, had significantly (p0.05) lower levels of basal systolic and mean arterial BP than wild-type mice in nonanesthetized condition, and they showed no significant change in heart rate or in cardiac function, as assessed by echocardiogram. All mutants showed a significantly (p0.05) reduced catecholamine-induced pressor and vasoconstriction responses. It is noteworthy that the infusion of norepinephrine did not elicit any pressor response at all in alpha1B-/alpha1D-AR double knockout mice. In an attempt to further examine alpha1-AR subtype, which is involved in the genesis or maintenance of hypertension, BP after salt loading was monitored by tail-cuff readings and confirmed at the endpoint by direct intra-arterial recording. After salt loading, alpha1B-AR knockout mice developed a comparable level of hypertension to wild-type mice, whereas mice lacking alpha1D-AR had significantly (p0.05) attenuated BP and lower levels of circulating catecholamines. Our data indicated that alpha1B- and alpha1D-AR subtypes participate cooperatively in BP regulation; however, the deletion of the functional alpha1D-AR, not alpha1B-AR, leads to an antihypertensive effect. The study shows differential contributions of alpha1B- and alpha1D-ARs in BP regulation.
- Published
- 2004
22. Induction of heat shock protein 72 in the failing heart is attenuated after an exposure to heat shock
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Wakako Toga, Masaya Takahashi, Hiroyuki Yoshida, Satoshi Takeo, Kouichi Tanonaka, and Ryo Oikawa
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Male ,Cardiac output ,medicine.medical_specialty ,Hot Temperature ,Heart Ventricles ,Ventricular Dysfunction, Right ,Clinical Biochemistry ,Cardiac Output, Low ,Myocardial Infarction ,Hemodynamics ,HSP72 Heat-Shock Proteins ,In Vitro Techniques ,Left coronary artery ,Right ventricular hypertrophy ,Internal medicine ,medicine.artery ,medicine ,Animals ,Myocardial infarction ,Rats, Wistar ,Molecular Biology ,Heat-Shock Proteins ,business.industry ,Myocardium ,Cell Biology ,General Medicine ,medicine.disease ,Myocardial Contraction ,Rats ,Perfusion ,medicine.anatomical_structure ,Gene Expression Regulation ,Ventricle ,Shock (circulatory) ,Heart failure ,Cardiology ,medicine.symptom ,business ,Heat-Shock Response - Abstract
Induction of heat shock protein (Hsp) 72 in the right ventricular muscle of the rat with heart failure following acute myocardial infarction (AMI) was examined. AMI was induced by the left coronary artery ligation (CAL). The animals at the 8th, but not 2nd, week after CAL revealed a decrease in cardiac output index (COI), suggesting that heart failure had developed by 8 weeks after CAL. Increases in the right ventricular developed pressure and the ratios of right ventricle/body weight and lung/body weight at the 2nd and 8th weeks showed the development of the right ventricular hypertrophy. After measurement of hemodynamic parameters, the hearts isolated from animals at the 2nd and 8th weeks after CAL (2w- and 8w-CAL hearts, respectively) were perfused and subjected to heat shock (at 42 degrees C, for 15 min) followed by 6-h perfusion. At the end of perfusion, Hsp72 content in the left ventricle without infarct area (viable LV) and the right ventricle (RV) was determined by the Western immunoblotting method. The production of myocardial Hsp72 in the viable LV and RV of the 2w-CAL heart increased after an exposure to heat shock. In contrast, induction of Hsp72 in the viable LV and RV of the 8w-CAL heart was blunted. The results suggest that the development of heart failure following AMI may result in a decrease in the ability for Hsp72 induction not only in the viable LV but also in the RV, leading to contractile dysfunction of the heart.
- Published
- 2004
23. Decrease in sarcoglycans and dystrophin in failing heart following acute myocardial infarction
- Author
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Kouichi Tanonaka, Teruhiko Toyo-oka, Hiroyuki Yoshida, Satoshi Takeo, Masaya Takahashi, Ryo Oikawa, and Miki Koshimizu
- Subjects
Male ,medicine.medical_specialty ,Physiology ,Blotting, Western ,Cardiac Output, Low ,Myocardial Infarction ,Cardiomyopathy ,Blood Pressure ,Dystrophin ,Cytosol ,Sarcolemma ,Heart Rate ,Culture Techniques ,Sarcoglycans ,Physiology (medical) ,Internal medicine ,Animals ,Medicine ,Myocardial infarction ,Rats, Wistar ,Dystroglycans ,Calpastatin ,Membrane Glycoproteins ,biology ,Calpain ,business.industry ,Myocardium ,Calcium-Binding Proteins ,medicine.disease ,Rats ,Cytoskeletal Proteins ,Preload ,medicine.anatomical_structure ,Ventricle ,Heart failure ,Models, Animal ,Ventricular pressure ,Cardiology ,biology.protein ,Cardiology and Cardiovascular Medicine ,business - Abstract
Objective: Genetic defects in several sarcoglycans (SGs) and dystrophin (Dys) play a critical role in cardiomyopathy. The present study was designed to determine whether changes in SGs and Dys might occur in animals with chronic heart failure (CHF) induced by acute myocardial infarction (AMI), which have no genetic defects. Methods: AMI was induced by the left coronary artery ligation (CAL) in rats. The hemodynamic parameters of the 2- and 8-week CAL (2w- and 8w-CAL) rats were measured and the myocardial SGs, Dys, calpain, and calpastatin levels were determined by the Western blot method. Myocardial calpain-like protease activity was evaluated as caseinolysis activity. Results: Increases in left ventricular end-diastolic pressure (LVEDP) and right ventricular systolic pressure, and a decrease in ±d P /d t were observed at the 2nd week, whereas cardiac output index (COI) was preserved. In contrast, the 8w-CAL rats showed a further increment in LVEDP with low COI. α-SG of the viable left ventricle (LV), and septum (Sep) of the 8w-CAL rat decreased (60–70% of the control). The α- and β-SGs of the right ventricle (RV) of the 2w- and 8w-CAL rats were reduced, while γ- and δ-SGs in the three regions did not change significantly. Dys in the viable LV and RV of the 8w-CAL rat decreased (75% of the control). The amount of m -calpain in the three regions of the 2w- and 8w-CAL rats increased (140–200% of the control), whereas the endogenous calpain inhibitor, calpastatin, did not change significantly. The in vitro degradation studies using purified m -calpain or cytosolic fractions of the 8w-CAL rat heart suggested a reduction in SGs and Dys by calpain. Conclusion: The results suggest that a decrease in SGs and Dys may play an important role in the pathophysiology of CHF following AMI.
- Published
- 2003
24. Blocking of the ATP sensitive potassium channel ameliorates the ischaemia-reperfusion injury in the rat testis
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Motoaki Saito, Shuhei Tomita, Takehiro Sejima, Keiji Inoue, Panagiota Tsounapi, Masashi Honda, Ryo Oikawa, Takahiro Shimizu, Shogo Shimizu, Darryl T. Martin, and K. Tanaka
- Subjects
Male ,endocrine system ,medicine.medical_specialty ,Cromakalim ,ATP-sensitive potassium channel ,Urology ,Endocrinology, Diabetes and Metabolism ,Ischemia ,Apoptosis ,medicine.disease_cause ,Glibenclamide ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Random Allocation ,Endocrinology ,KATP Channels ,Internal medicine ,Malondialdehyde ,Glyburide ,Testis ,Diazoxide ,medicine ,Potassium Channel Blockers ,Testicular torsion ,Animals ,Peroxidase ,Spermatic Cord Torsion ,business.industry ,medicine.disease ,Rats ,Oxidative Stress ,Reproductive Medicine ,chemistry ,Neutrophil Infiltration ,Reperfusion Injury ,business ,Hydroxy Acids ,Decanoic Acids ,hormones, hormone substitutes, and hormone antagonists ,Oxidative stress ,medicine.drug - Abstract
There is increasing evidence that the effects of administered ATP sensitive potassium (KATP ) channel openers or blockers during ischaemia are still controversial in many organs/tissues. Testicular torsion detorsion which causes ischaemia-reperfusion (IR) injury, cannot be predicted, thus an effective drug should be administered during or after the ischaemia. The aim of this study was to examine whether the administration of KATP channel openers or blockers during ischaemia ameliorates IR injury in the testis. Eight-week-old male Sprague-Dawley rats were subjected to 2 h right testicular ischaemia followed by 24 h reperfusion. The selective mitochondrial (mito) KATP channel blocker, 5-hydroxydecanoate (5-HD) (40 mg/kg), the non-selective KATP channel blocker glibenclamide (5 mg/kg), the selective mito KATP channel opener diazoxide (10 mg/kg) and the non-selective KATP channel opener cromakalim (300 μg/kg) were administered intraperitoneally 15 min prior to the ischaemia or 75 min after the induction of ischaemia. Tissue damage was evaluated by malondialdehyde concentration, myeloperoxidase activity, histological evaluation and TdT-mediated dUTP nick end labelling assay in the testis. There was a significant increase in oxidative stress, neutrophil infiltration, histological damage and apoptosis in the testicular IR model. A significant reduction in the testicular IR injury was observed with the administration of glibenclamide, but not 5-HD, diazoxide or cromakalim during ischaemia. The administration of non-selective KATP channel blocker glibenclamide ameliorated the testicular IR injury. On the other hand, the selective mito KATP channel blocker, 5-HD and KATP channel openers did not reduce the testicular IR injury. These data suggest that blocking of the membrane KATP channel may have a protective effect during the testicular ischaemia. Glibenclamide could be an effective drug to manage the post-ischaemic injury caused by the testicular torsion-detorsion.
- Published
- 2013
25. Prostatic ischemia induces ventral prostatic hyperplasia in the SHR; possible mechanism of development of BPH
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Yukako Kinoshita, Shuhei Tomita, Shogo Shimizu, Masashi Honda, Ryo Oikawa, Panagiota Tsounapi, Motoaki Saito, and Takehiro Sejima
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Male ,medicine.medical_specialty ,Ischemia ,Prostatic Hyperplasia ,Blood Pressure ,Enzyme-Linked Immunosorbent Assay ,Rats, Inbred WKY ,Article ,Transforming Growth Factor beta1 ,chemistry.chemical_compound ,Internal medicine ,Malondialdehyde ,Rats, Inbred SHR ,medicine ,Animals ,Nicorandil ,Multidisciplinary ,business.industry ,Prostate ,Dihydrotestosterone ,Blood flow ,Hypoxia (medical) ,Hyperplasia ,medicine.disease ,Hypoxia-Inducible Factor 1, alpha Subunit ,Actins ,Rats ,Oxidative Stress ,Endocrinology ,Blood pressure ,chemistry ,Regional Blood Flow ,Hypertension ,cardiovascular system ,Fibroblast Growth Factor 2 ,medicine.symptom ,business ,Biomarkers ,medicine.drug - Abstract
In the light of increasing evidence that benign prostatic hyperplasia is associated with cardiovascular disease, we have investigated the relationship between prostatic blood flow and prostatic hyperplasia in the spontaneously-hypertensive-rat (SHR). Twelve-week-old male SHRs were treated with nicorandil for six weeks. Wistar-Kyoto rats were used as controls. Six weeks after nicorandil treatment, blood pressure and the prostatic blood flow were estimated and tissue levels of malondialdehyde, HIF-1α, TGF-β1, bFGF, dihydrotestosterone and α-SMA were measured. SHRs showed significant increases in blood pressure, tissue levels of malondialdehyde, HIF-1α, TGF-β1, bFGF, α-SMA and a significant decrease in the prostatic blood flow. Although treatment with nicorandil failed to alter the blood-pressure and α-SMA, it significantly ameliorated the increased levels of malondialdehyde, HIF-1α, TGF-β1 and bFGF. There were no significant differences in tissue levels of dihydrotestosterone among any groups. These data indicate that development of prostatic hyperplasia may be associated with prostatic hypoxia, which nicorandil prevents via its effect to increase the blood flow.
- Published
- 2013
26. 23 ANGIOTENSIN II RECEPTOR BLOCKER, OLMESARTAN PRESERVES BLADDER BLOOD FLOW AND OXIDATIVE STRESS, AND IMPROVES BLADDER DYSFUNCTION IN THE SPONTANEOUSLY HYPERTENSIVE RAT
- Author
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Panagiota Tsounapi, Yukako Kinoshita, Ryo Oikawa, Motoaki Motoaki, Fumiya Ohmasa, Shogo Shimizu, Harunori Oiwa, and Shuhei Tomita
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Angiotensin receptor ,medicine.medical_specialty ,business.industry ,Urology ,Blood flow ,medicine.disease_cause ,Spontaneously hypertensive rat ,Endocrinology ,Internal medicine ,Medicine ,business ,Olmesartan ,Oxidative stress ,medicine.drug - Published
- 2013
27. System design to reduce disaster risks by installing distributed power resources.
- Author
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Akane Uemichi, Masaaki Yagi, Ryo Oikawa, Yudai Yamasaki, and Shigehiko Kaneko
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- 2018
- Full Text
- View/download PDF
28. Olmesartan ameliorates urinary dysfunction in the spontaneously hypertensive rat via recovering bladder blood flow and decreasing oxidative stress
- Author
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Shogo, Shimizu, Motoaki, Saito, Harunori, Oiwa, Fumiya, Ohmasa, Panagiota, Tsounapi, Ryo, Oikawa, Fotios, Dimitriadis, Darryl T, Martin, Itaru, Satoh, Yukako, Kinoshita, and Shuhei, Tomita
- Subjects
Male ,Aldehydes ,Nifedipine ,NF-E2-Related Factor 2 ,Urinary Bladder ,Imidazoles ,Urinary Bladder Diseases ,Tetrazoles ,Blood Pressure ,Rats ,Disease Models, Animal ,Oxidative Stress ,Urodynamics ,Regional Blood Flow ,Malondialdehyde ,Rats, Inbred SHR ,Hypertension ,Nerve Growth Factor ,Animals ,Rats, Wistar ,Angiotensin II Type 1 Receptor Blockers ,Antihypertensive Agents ,Biomarkers - Abstract
As hypertension (HT) is one of the risk factors for lower urinary tract symptoms, we investigated the effect of an angiotensin II type I receptor blocker, olmesartan, on bladder dysfunction in the spontaneously hypertensive rat (SHR).Twelve-week-old male SHRs were administered perorally with olmesartan (0, 1, or 3 mg/kg/day) or nifedipine (30 mg/kg/day) for 6 weeks. Wistar rats were used as normotensive controls. The effects of olmesartan or nifedipine on blood pressure (BP), bladder blood flow (BBF), urodynamic parameters, tissue levels of malondialdehyde (MDA), nuclear factor erythroid 2-related factor 2 (Nrf2), and nerve growth factor (NGF) were measured in the bladder. Localization of 4-hydroxy-2-nonenal (4-HNE), Nrf2, and NGF in the bladder was shown by immunohistochemistry.The SHRs showed significant increase in BP, micturition frequency, and expression of MDA, 4-HNE, Nrf2, and NGF when compared to the control Wistar rats. Conversely, there was a decrease in BBF and single voided volume in SHRs when compared to Wistar rats. Treatment with olmesartan and nifedipine significantly improved BP. However, only olmesartan significantly ameliorated urodynamic parameters and oxidative damage compared to the non-treated SHR. The immunoreactivities of 4-HNE, Nrf2, and NGF in SHR urothelium and blood vessels were increased compared to the control. Treatment with a high dose of olmesartan decreased the expressions of 4-HNE, Nrf2, and NGF in the bladder.Our data suggest that BP, BBF, and oxidative stress may be responsible for the functional changes in HT-related bladder dysfunction. Olmesartan significantly ameliorated this bladder dysfunction.
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- 2012
29. Characterization of silodosin and naftopidil in the treatment of bladder dysfunction in the spontaneously hypertensive rat
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Panagiota Tsounapi, Ryo Oikawa, Keisuke Satoh, Yukako Kinoshita, Motoaki Saito, Shogo Shimizu, Fumiya Ohmasa, and Fotios Dimitriadis
- Subjects
Male ,medicine.medical_specialty ,Indoles ,Urology ,Urinary system ,media_common.quotation_subject ,Urinary Bladder ,Urination ,Blood Pressure ,Naphthalenes ,Piperazines ,Spontaneously hypertensive rat ,Rats, Inbred SHR ,medicine ,Nocturia ,Animals ,Rats, Wistar ,media_common ,Naftopidil ,business.industry ,Body Weight ,Urinary Bladder Diseases ,Organ Size ,Silodosin ,Hyperplasia ,medicine.disease ,Circadian Rhythm ,Rats ,Overactive bladder ,Adrenergic alpha-1 Receptor Antagonists ,Neurology (clinical) ,medicine.symptom ,business ,medicine.drug ,Muscle Contraction - Abstract
Purpose As increasing evidence suggest that α1-blockers prevent benign prostatic hyperplasia related overactive bladder and nocturia in the human, we investigated the effects of silodosin and naftopidil on hypertension-related bladder dysfunction in the spontaneously hypertensive rat (SHR) model. Materials and Methods Twelve-week-old male SHRs received no treatment or treatment with silodosin (100 µg/kg, p.o.) or naftopidil (10 or 30 mg/kg, p.o.) once daily for 6 weeks. Wistar rats were used as normotensive controls. After 6-week treatment, voiding functions were estimated by metabolic cages (dark- and light-cycle separately) and cystometric studies. Furthermore, the bladder blood flow (BBF) was measured employing the hydrogen clearance method. Results SHRs showed significant increases in micturition frequency, and decreases in BBF and single voided volume in both metabolic cages and cystometrograms compared to the Wistar group. Treatment with silodosin normalized the decreased BBF, and treatment with naftopidil increased the BBF in a dose-dependent manner in the SHR group. Although treatment with silodosin and the high dose of naftopidil significantly inhibited micturition frequency in one day, only treatment with the high dose of naftopidil significantly inhibited micturition frequency and urine production in the light-cycle compared to the non-treated SHRs. Although treatment with silodosin and the high dose of naftopidil significantly increased single voided volume, only treatment with silodosin significantly inhibited non-voiding contractions in the cystometrgrams. Conclusion Our data suggest that both silodosin and naftopidil improve hypertension-related bladder dysfunction in the SHR, and naftopidil but not silodosin improves urinary frequency in the light-cycle due to inhibition of urine production. Neurourol. Urodynam. 32: 393–398, 2013. © 2012 Wiley Periodicals, Inc.
- Published
- 2012
30. Vasopressin V1A receptor enhances baroreflex via the central component of the reflex arc
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Ryo Oikawa, Gozoh Tsujimoto, Rie Ishii, Akito Tanoue, Satoshi Takeo, Yoshihisa Nasa, and Tomoyuki Kuwaki
- Subjects
Chronotropic ,Bradycardia ,medicine.medical_specialty ,Receptors, Vasopressin ,medicine.drug_class ,Blood Pressure ,Baroreflex ,Mice ,Heart Rate ,Internal medicine ,Heart rate ,medicine ,Animals ,Phenylephrine ,Pharmacology ,Mice, Knockout ,business.industry ,Brain ,Vagus Nerve ,Receptor antagonist ,Electric Stimulation ,Mice, Inbred C57BL ,Endocrinology ,Knockout mouse ,cardiovascular system ,Reflex ,medicine.symptom ,business ,circulatory and respiratory physiology ,medicine.drug - Abstract
The neurohypophyseal peptide [Arg 8 ]-vasopressin (AVP) exerts its physiological actions via 3 distinct receptor isoforms designated V1A, V1B, and V2. We recently showed that V1A receptor was involved in the baroreflex control of heart rate using V1A receptor knockout mice. The present study was undertaken to further clarify this finding. In conscious mice, resting blood pressure of the knockout group was lower than that of the wild-type group (wild-type, 108 ± 2.0 mm Hg; knockout, 98 ± 3.8 mm Hg; n = 6–7) without notable change in heart rate. Although phenylephrine and nitroprusside-induced changes in blood pressure did not differ in these strains, the subsequent bradycardia and tachycardia were markedly blunted in the knockout mice (mean slopes for baroreflex curve after phenylephrine treatment; wild-type, − 5.65 ± 0.30 bpm/mm Hg; knockout, − 3.97 ± 0.52 bpm/mm Hg; those after nitroprusside treatment; wild-type, − 0.51 ± 0.10 bpm/mm Hg; knockout, − 0.18 ± 0.05 bpm/mm Hg; n = 6–7). Under urethane anesthesia (1.0–1.2 g/kg, i.p.), electrical stimulation of the vagal afferent nerve evoked frequency-dependent hypotension and bradycardia in the wild-type mice. In contrast, in the knockout mice such stimulation induced a pressor, not a depressor, response and diminished bradycardia. Moreover, electrical stimulation-induced hemodynamic changes through the vagal afferent nerve in the wild-type mice were significantly attenuated by pretreatment with intravenously administered V1A receptor antagonist d(CH 2 ) 5 Tyr(Me)AVP. Electrical stimulation of the vagal efferent nerve-induced hemodynamic changes (depressor and bradycardia) and chronotropic responses to adrenergic and cholinergic stimuli were not different between the 2 strains. These results suggest that the V1A receptor in the central nervous system is involved in the regulation of the heart rate via the baroreflex arc.
- Published
- 2006
31. Vasopressin promotes cardiomyocyte hypertrophy via the vasopressin V1A receptor in neonatal mice
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Akito Tanoue, Ryo Oikawa, Satoshi Takeo, Toshinori Aoyagi, Shuyi Wang, Masami Hiroyama, and Atsushi Sanbe
- Subjects
MAPK/ERK pathway ,Male ,Vasopressin ,medicine.medical_specialty ,Receptors, Vasopressin ,Time Factors ,Transcription, Genetic ,Stimulation ,Cardiomegaly ,Biology ,Cell Enlargement ,Quinolones ,Mice ,Atrial natriuretic peptide ,Piperidines ,Internal medicine ,Arginine vasopressin receptor 2 ,medicine ,Animals ,Vasoconstrictor Agents ,Myocytes, Cardiac ,RNA, Messenger ,Phosphorylation ,Extracellular Signal-Regulated MAP Kinases ,Cells, Cultured ,Pharmacology ,Pressure overload ,Arginine vasopressin receptor 1B ,Mice, Knockout ,Dose-Response Relationship, Drug ,Reverse Transcriptase Polymerase Chain Reaction ,DNA ,Immunohistochemistry ,Arginine Vasopressin ,Disease Models, Animal ,Endocrinology ,Animals, Newborn ,Protein Biosynthesis ,hormones, hormone substitutes, and hormone antagonists ,Homeostasis ,Atrial Natriuretic Factor - Abstract
[Arg8]-vasopressin (AVP) is an essential hormone for maintaining osmotic homeostasis and is known to be a potent vasoconstrictor that regulates the cardiovascular system. In the present study, cardiomyocytes were isolated from neonatal mice and used to investigate the effects of AVP on cardiac hypertrophy. Reverse transcription polymerase chain reaction (RT-PCR) analysis revealed that vasopressin V1A receptor mRNA, but not V1B or V2 receptor mRNA, was expressed in primary cultured neonatal mouse cardiomyocytes. By exposing the cultured neonatal cardiomyocytes to AVP for 24 h, cell surface areas were significantly increased, suggesting that AVP could induce cardiomyocyte growth. We then investigated the expression level of the atrial natriuretic peptide (ANP), which is a marker of cardiac hypertrophy. Stimulation with AVP increased the expression of cardiomyocyte ANP mRNA in a dose- and time-dependent manner. Immunocytochemical studies showed that stimulation with AVP significantly increased the expression of the ANP protein as well. Furthermore, AVP administration activated extracellular signal-regulated kinase (ERK)1/2 in cardiomyocytes. The effects of AVP on these parameters were significantly inhibited by a selective vasopressin V1A receptor antagonist, OPC-21268, and were not observed in cardiomyocytes from mice lacking the vasopressin V1A receptor. In vivo cardiac hypertrophy in response to pressure overload was attenuated in vasopressin V1A receptor-deficient (V1AR-KO) mice. Taken together, our data suggest that AVP promotes cardiomyocyte hypertrophy via the vasopressin V1A receptor, which is in part regulated by the pathway of ERK1/2 signaling.
- Published
- 2006
32. Possible involvement of calpain activation in pathogenesis of chronic heart failure after acute myocardial infarction
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Ryo Oikawa, Masaya Takahashi, Miki Koshimizu, Satoshi Takeo, Kouichi Tanonaka, Takuya Daicho, and Hiroyuki Yoshida
- Subjects
Trandolapril ,Male ,medicine.medical_specialty ,Myocardial Infarction ,Angiotensin-Converting Enzyme Inhibitors ,Blood Pressure ,Cytosol ,Internal medicine ,Medicine ,Animals ,Myocardial infarction ,Rats, Wistar ,Calpastatin ,Pharmacology ,Heart Failure ,biology ,business.industry ,Calpain ,Myocardium ,Calcium-Binding Proteins ,Organ Size ,medicine.disease ,Rats ,Enzyme Activation ,Candesartan ,Heart failure ,ACE inhibitor ,biology.protein ,Cardiology ,Myocardial infarction complications ,Cardiology and Cardiovascular Medicine ,business ,Angiotensin II Type 1 Receptor Blockers ,medicine.drug - Abstract
Changes in proteolytic activity of the myocardium during the development of heart failure after left coronary artery ligation (CAL) of rats were examined. Hemodynamics of the rats at the eighth week (8w-CAL rat), but not at the second week (2w-CAL rat), after CAL showed the symptoms of chronic heart failure. Contents of mu-calpin and m-calpain, but not an intrinsic calpain inhibitor calpastatin, in the viable left ventricular muscle (viable LV) and the right ventricular muscle (RV) of the 2w-CAL and 8w-CAL rats were increased, which was associated with an elevation of intrinsic activities of leupeptin-sensitive, Ca(2+)-activated proteolysis in the cytosolic fractions of the viable LV and RV. Oral administration of 3 mg/kg/d trandolapril or 1 mg/kg/d candesartan from the second to eighth week after CAL improved the hemodynamics of 8w-CAL rats. The drug treatment attenuated the increases in mu-calpain and m-calpain contents and the elevation of the proteolytic activity of the viable LV and RV in the 8w-CAL rat. The drug treatment increased calpastatin content of the RV in the 8w-CAL rat. These results suggest that sustained activation of calpain is involved in the development of chronic heart failure and that trandolapril and candesartan prevent the activation of calpains after CAL.
- Published
- 2006
33. Effects of angiotensin I-converting enzyme inhibitor and angiotensin II type 1 receptor blocker on the right ventricular sarcoglycans and dystrophin after left coronary artery ligation
- Author
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Takuya Daicho, Ryo Oikawa, Miki Koshimizu, Masaya Takahashi, Kouichi Tanonaka, Satoshi Takeo, and Hiroyuki Yoshida
- Subjects
Male ,Indoles ,Time Factors ,Transcription, Genetic ,Myocardial Infarction ,Gene Expression ,Tetrazoles ,Angiotensin-Converting Enzyme Inhibitors ,Blood Pressure ,Dystrophin ,Cytosol ,Heart Rate ,Medicine ,Protein Isoforms ,Myocardial infarction ,Sarcoglycans ,Calpain ,Reverse Transcriptase Polymerase Chain Reaction ,musculoskeletal system ,Coronary Vessels ,medicine.anatomical_structure ,Circulatory system ,Cardiology ,medicine.drug ,musculoskeletal diseases ,Trandolapril ,congenital, hereditary, and neonatal diseases and abnormalities ,medicine.medical_specialty ,Heart Ventricles ,Blotting, Western ,Left coronary artery ,Internal medicine ,medicine.artery ,Animals ,RNA, Messenger ,Rats, Wistar ,Ligation ,Pharmacology ,business.industry ,Biphenyl Compounds ,Body Weight ,Calcium-Binding Proteins ,medicine.disease ,Angiotensin II ,Rats ,Candesartan ,Endocrinology ,Ventricle ,Benzimidazoles ,business ,Angiotensin II Type 1 Receptor Blockers - Abstract
We examined the effects of trandolapril and candesartan on changes in the levels of sarcoglycans and dystrophin in the right ventricle of rats with the left coronary artery ligation. Hemodynamic and morphological alterations suggested the development of hypertrophy of the right ventricle and chronic heart failure by the 8th week. By the end of the 8th week, alpha- and beta-sarcoglycans and dystrophin were decreased. Increases in mu- and m-calpains in the hypertrophied right ventricle were associated with an elevation of casein-proteolytic activity in the cytosolic fraction. Oral administration of 3 mg/kg/day trandolapril or 1 mg/kg/day candesartan from the 2nd to 8th week after the left coronary artery ligation attenuated decreases in alpha-sarcoglycan and dystrophin and reduced the increased proteolytic activity. The results suggest that attenuation of decreases in sarcoglycans and dystrophin is a possible mechanism underlying trandolapril- and candesartan-mediated improvement of structural and functional alterations of the right ventricle in the coronary artery-ligated rat.
- Published
- 2005
34. Effects of ACE inhibitor and AT1 blocker on dystrophin-related proteins and calpain in failing heart
- Author
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Masaya, Takahashi, Kouichi, Tanonaka, Hiroyuki, Yoshida, Ryo, Oikawa, Miki, Koshimizu, Takuya, Daicho, Teruhiko, Toyo-Oka, and Satoshi, Takeo
- Subjects
Heart Failure ,Male ,Indoles ,Calpain ,Reverse Transcriptase Polymerase Chain Reaction ,Myocardium ,Biphenyl Compounds ,Blotting, Western ,Hemodynamics ,Tetrazoles ,Angiotensin-Converting Enzyme Inhibitors ,Receptor, Angiotensin, Type 1 ,Rats ,Cytosol ,Sarcoglycans ,Models, Animal ,Animals ,Protein Isoforms ,Benzimidazoles ,Rats, Wistar - Abstract
Genetic depletion of dystrophin-related protein (DRP) complex causes cardiomyopathy in animals and humans. We found in a previous study that some types of DRP were degraded and that calpain content was increased in rats with non-genetically induced heart failure. The present study was aimed at examining the effects of an angiotensin-I-converting enzyme inhibitor (ACEI) trandolapril (Tra) or an angiotensin II type 1 receptor blocker (ARB) candesartan (Can), both of which are known to improve the pathophysiology of chronic heart failure (CHF) on degradation of DRP in failing hearts.Coronary artery-ligated (CAL) and sham-operated rats (Sham rats) were treated orally with 3 mg/kg/day trandolapril (Tra) or 1 mg/kg/day candesartan (Can) from the 2nd to 8th week after surgery.Hemodynamic parameters of CAL rats at the 8th week after CAL (8w-CAL) indicated heart failure. alpha-Sarcoglycan (SG) and dystrophin in the surviving left ventricle (surviving LV) of 8w-CAL rats decreased, whereas beta-, gamma-, and delta-SGs remained unchanged. Calcium-activated neutral proteases mu-calpain and m-calpain increased in the surviving LV at the 8th week of postmyocardial infarction. Proteolytic activity in the presence of 5 mM Ca2+ markedly increased at the 2nd and 8th weeks, whereas 50 microM Ca2+ slightly but significantly increased proteolysis of casein. Tra or Can treatment improved the hemodynamic parameters, attenuated changes in alpha-SG and dystrophin, and reversed both calpain contents and activities of the failing heart back to sham levels.These results suggest that attenuation in calpain-induced degradation of DRP complex is a possible mechanism for the Tra- or Can-mediated improvement of the pathogenesis of CHF following myocardial infarction.
- Published
- 2004
35. Involvement of vasopressin V1a receptor in the baroreflex arc
- Author
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Akito Tanoue, Rie Ishii, Tomoyuki Kuwaki, Satoshi Takeo, Ryo Oikawa, Yoshihisa Nasa, and Gozoh Tsujimoto
- Subjects
Arc (geometry) ,medicine.medical_specialty ,Endocrinology ,business.industry ,Internal medicine ,medicine ,Baroreflex ,Cardiology and Cardiovascular Medicine ,business ,Molecular Biology ,Vasopressin V1a Receptor - Published
- 2006
36. Prostatic ischemia induces ventral prostatic hyperplasia in the SHR; possible mechanism of development of BPH.
- Author
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Motoaki Saito, Panagiota Tsounapi, Ryo Oikawa, Shogo Shimizu, Masashi Honda, Takehiro Sejima, Yukako Kinoshita, and Shuhei Tomita
- Subjects
PROSTATE hypertrophy ,ANIMAL models in research ,HYPERTENSION ,LABORATORY rats ,BLOOD flow ,CARDIOVASCULAR diseases ,MALONDIALDEHYDE ,STANOLONE - Abstract
In the light of increasing evidence that benign prostatic hyperplasia is associated with cardiovascular disease, we have investigated the relationship between prostatic blood flow and prostatic hyperplasia in the spontaneously-hypertensive-rat (SHR). Twelve-week-old male SHRs were treated with nicorandil for six weeks. Wistar-Kyoto rats were used as controls. Six weeks after nicorandil treatment, blood pressure and the prostatic blood flow were estimated, and tissue levels of malondialdehyde, HIF-1α, TGF-β1, bFGF, dihydrotestosterone, and α-SMA were measured. SHRs showed significant increases in blood pressure, tissue levels of malondialdehyde, HIF-1α, TGF-β1, bFGF, α-SMA and a significant decrease in the prostatic blood flow. Although treatment with nicorandil failed to alter the blood-pressure and α-SMA, it significantly ameliorated the increased levels of malondialdehyde, HIF-1α, TGF-β1, and bFGF. There were no significant differences in tissue levels of dihydrotestosterone among any groups. These data indicate that development of prostatic hyperplasia may be associated with prostatic hypoxia, which nicorandil prevents via its effect to increase the blood flow. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
37. Induction of heat shock protein 72 in the failing heart is attenuated after an exposure to heat shock.
- Author
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Kouichi Tanonaka, Wakako Toga, Masaya Takahashi, Hiroyuki Yoshida, Ryo Oikawa, and Satoshi Takeo
- Abstract
Induction of heat shock protein (Hsp) 72 in the right ventricular muscle of the rat with heart failure following acute myocardial infarction (AMI) was examined. AMI was induced by the left coronary artery ligation (CAL). The animals at the 8th, but not 2nd, week after CAL revealed a decrease in cardiac output index (COI), suggesting that heart failure had developed by 8 weeks after CAL. Increases in the right ventricular developed pressure and the ratios of right ventricle/body weight and lung/body weight at the 2nd and 8th weeks showed the development of the right ventricular hypertrophy. After measurement of hemodynamic parameters, the hearts isolated from animals at the 2nd and 8th weeks after CAL (2w- and 8w-CAL hearts, respectively) were perfused and subjected to heat shock (at 42°C, for 15 min) followed by 6-h perfusion. At the end of perfusion, Hsp72 content in the left ventricle without infarct area (viable LV) and the right ventricle (RV) was determined by the Western immunoblotting method. The production of myocardial Hsp72 in the viable LV and RV of the 2w-CAL heart increased after an exposure to heat shock. In contrast, induction of Hsp72 in the viable LV and RV of the 8w-CAL heart was blunted. The results suggest that the development of heart failure following AMI may result in a decrease in the ability for Hsp72 induction not only in the viable LV but also in the RV, leading to contractile dysfunction of the heart. [ABSTRACT FROM AUTHOR]
- Published
- 2004
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