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Objective: We examined the hypothesis that lipoprotein(a) levels are elevated in preeclampsia and associated with severity of the disease.Study Design: Plasma lipoprotein(a) levels were measured in 24 normal pregnant women, 18 mild, and 8 severe preeclamptic women using an enzyme-linked immunosorbent assay method. Kruskall-Wallis one-way analysis of variance was used to evaluate the difference in plasma lipoprotein(a) among different groups. The Mann-Whitney U test was used to compare the differences between two groups.Results: The plasma lipoprotein(a) levels were increased in pregnant women with both severe preeclampsia (median 826.9 mg/L [interquartile range 590.7, 986.9 mg/L], n = 8, p < 0.0001) and mild preeclampsia (median 357.7 mg/L [interquartile range 208.0, 477.1 mg/L], n = 18, p < 0.0001) compared with normal pregnancy (median 78.5 mg/L [interquartile range 45.2, 127.9 mg/L], n = 24). The lipoprotein(a) level was significantly higher in severe than in mild preeclampsia (p < 0.001).Conclusion: This study has demonstrated that lipoprotein(a) levels are elevated in preeclampsia and associated with severity of the disease. It may serve as a marker of the pathogenic process. [ABSTRACT FROM AUTHOR]

Background: The lactate albumin ratio (LAR), a simple prognostic marker used in intensive care units (ICUs), combines lactate and serum albumin levels to predict patient outcomes. Despite its potential, the predictive accuracy of the LAR remains insufficiently explored. This study aimed to assess the usefulness of the LAR in predicting mortality among patients in the ICU., Methods: This retrospective study conducted a secondary analysis of prospectively obtained clinical data from the Japanese Intensive Care Patient Database. We included all patients admitted to ICUs between 2015 and 2021, excluding those under the age of 16 years. The main outcome was in-hospital mortality. The LAR predictive value for this outcome was assessed by examining the area under the receiver operating characteristic curve and comparing it against prognostic indicators such as age, lactate, albumin and Sequential Organ Failure Assessment score. LAR shape was assessed using unrestricted spline curves, and the optimal cut-off value was identified from sensitivity and negative likelihood ratio. Subgroup analysis was used to evaluate the predictive accuracy of the LAR across different patient attributes and clinical scenarios., Results: Of 2 34 774 cases analysed, in-hospital mortality was 8.8% (20 723 deaths). The LAR had an area under the curve of 0.761 (95%CI 0.757 to 0.765), indicating a fair predictive performance for in-hospital mortality. Unrestricted spline curves demonstrated that LAR can predict mortality through a monotonic positive dose-response relationship with 0.4 as the optimal cut-off value. In subgroup analysis, areas under the curve were significantly higher in subgroups defined by younger age, female sex, unplanned ICU admission, non-surgical patients, non-infectious patients, non-heart failure patients and lack of end-stage renal disease., Conclusions: The LAR might be a useful predictor for screening mortality in ICU patients. However, further research to establish appropriate cut-off values for the LAR and identify the optimal target population is warranted., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Introduction: Hyponatremia, frequently encountered in intensive care (ICU) settings, plays a critical role in shaping patient outcomes. Despite its prevalence, contemporary research into its newly classified severity categories and their implications on mortality, renal function, and length of stay remains limited. This study aims to fill this gap by examining the impact of hyponatremia severity on these critical outcomes., Methods: A retrospective analysis of ICU patients aged >18 years who were admitted between March 2019 and December 2022 was conducted at Hamamatsu University Hospital, Shizuoka, Japan. Patients who were readmitted or had incomplete data were excluded. Hyponatremia was categorized as mild (130-135 mmol/L), moderate (125-129 mmol/L), or severe (<125 mmol/L), following the criteria set by the European Society of Intensive Care Medicine. This classification utilized the lowest sodium concentration within 24 hours of ICU admission. The outcomes were in-hospital mortality, ICU mortality, newly implemented renal replacement therapy (RRT), and length of hospital and ICU stay. Outcomes were analyzed using multivariable logistic and linear regression models, adjusting for relevant covariates including age, sex, Acute Physiology and Chronic Health Evaluation (APACHE) III scores, and the use of mechanical ventilation., Results: Of the 3,538 patients analyzed, 1,072 (30.3%) experienced hyponatremia: 894 (25.3%) mild, 144 (4.1%) moderate, and 34 (1.0%) severe. Multivariable analysis revealed no significant association between hyponatremia severity and in-hospital mortality rates across normonatremia (3.8%), mild (5.2%), moderate (11.8%), and severe (23.5%) groups, nor with ICU mortality. However, compared to normonatremia, moderate and severe hyponatremia were associated with increased RRT initiation (odds ratios = 3.83 and 6.36, respectively) and prolonged hospital stay (mean difference = 7.06 and 9.66 days, respectively), and ICU stays (mean difference, 1.02 and 2.70 days, respectively). Mild hyponatremia was not significantly associated with RRT or length of stay., Conclusion: Moderate-to-severe hyponatremia did not influence mortality but was associated with increased RRT initiation and prolonged hospital and ICU stay. By contrast, mild hyponatremia was not associated with any clinical outcome. Further research is required to determine if correcting hyponatremia directly improves ICU patient outcomes, given the observational nature of the study., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Itoh et al.)

Cardiopulmonary bypass (CPB) causes systemic inflammation and endothelial glycocalyx damage. Hydrogen has anti-oxidant and anti-inflammatory properties; therefore, we hypothesized that hydrogen would alleviate endothelial glycocalyx damage caused by CPB. Twenty-eight male Sprague-Dawley rats were randomly divided into four groups (n = 7 per group), as follows: sham, control, 2% hydrogen, and 4% hydrogen. The rats were subjected to 90 minutes of partial CPB followed by 120 minutes of observation. In the hydrogen groups, hydrogen was administered via the ventilator and artificial lung during CPB, and via the ventilator for 60 minutes after CPB. After observation, blood collection, lung extraction, and perfusion fixation were performed, and the heart, lung, and brain endothelial glycocalyx thickness was measured by electron microscopy. The serum syndecan-1 concentration, a glycocalyx component, in the 4% hydrogen group (5.7 ± 4.4 pg/mL) was lower than in the control (19.5 ± 6.6 pg/mL) and 2% hydrogen (19.8 ± 5.0 pg/mL) groups (P < 0.001 for each), but it was not significantly different from the sham group (6.2 ± 4.0 pg/mL, P = 0.999). The endothelial glycocalyces of the heart and lung in the 4% hydrogen group were thicker than in the control group. The 4% hydrogen group had lower inflammatory cytokine concentrations (interleukin-1β and tumor necrosis factor-α) in serum and lung tissue, as well as a lower serum malondialdehyde concentration, than the control group. The 2% hydrogen group showed no significant difference in the serum syndecan-1 concentration compared with the control group. However, non-significant decreases in serum and lung tissue inflammatory cytokine concentrations, as well as in serum malondialdehyde concentration, were observed. Administration of 4% hydrogen via artificial and autologous lungs attenuated endothelial glycocalyx damage caused by partial CPB in rats, which might be mediated by the anti-inflammatory and anti-oxidant properties of hydrogen., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Iwata et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Background: This study compared the effects of remimazolam and sevoflurane on intraoperative hemodynamics including intraoperative hypotension (IOH)., Results: This study involved adult patients undergoing noncardiac surgery using remimazolam (Group R) or sevoflurane (Group S) for maintenance anesthesia, and invasive arterial pressure measurements, from September 2020 to March 2023 at our hospital. IOH was defined as a mean blood pressure < 65 mmHg occurring for a cumulative duration of at least 10 min. A 1:1 propensity score-matching method was used. The primary endpoint was the occurrence of IOH, and the secondary endpoints were the cumulative hypotensive time, incidence of vasopressor use, and dose of vasopressor used (ephedrine, phenylephrine, dopamine, and noradrenaline). Group R comprised 169 patients, Group S comprised 393 patients, and a matched cohort of 141 patients was created by propensity score matching. There was no significant difference in the incidence of IOH between the two groups (85.1% in Group R vs. 91.5% in Group S, p = 0.138). Patients in Group R had a significantly lower cumulative hypotension duration (55 [18-119] vs. 83 [39-144] min, p = 0.005), vasopressor use (81.6% vs. 91.5%, p = 0.023), and dose of ephedrine (4 [0-8] vs. 12 [4-20] mg, p < 0.001) than those in Group S. There were no significant differences in the doses of other vasopressors between groups., Conclusions: Compared with sevoflurane, the maintenance of anesthesia with remimazolam was not associated with a decreased incidence of IOH; however, it reduced the cumulative hypotension time, incidence of vasopressor use, and dose of ephedrine., (© 2023. The Japanese Society of Anesthesiologists.)

We report a rare case of rhabdomyolysis in a 64-year-old man who had been receiving long-term statin therapy for hyperlipidemia. The patient initially presented with symptoms of acute appendicitis, which later progressed to acute renal failure and rhabdomyolysis. No commonly identified risk factors for rhabdomyolysis, including drug interactions and statin doses, were observed. The patient was urgently admitted to the intensive care unit where the relevant medications were discontinued in a timely manner and infusion resuscitation was performed. Renal function and serum creatine kinase levels gradually stabilized without the need for hemodialysis. After four days, the patient was transferred to a general ward and was fully discharged from the hospital 13 days after admission. This case highlights the importance of considering rhabdomyolysis as a possible complication among patients receiving statin therapy, even in the absence of traditional risk factors., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Naritaka et al.)

Purpose: This study was performed to examine and compare the incidence of extubation recall in surgical patients who underwent remimazolam anesthesia with flumazenil antagonism during emergence and in those who underwent propofol anesthesia., Methods: One hundred sixty-three patients who underwent surgery using general endotracheal or supraglottic airway anesthesia with propofol (n = 97) or remimazolam (n = 66) were retrospectively analyzed. Remimazolam was antagonized by flumazenil after discontinuation of remimazolam at the end of surgery. The endotracheal tube or supraglottic airway was removed after surgery was complete, and consciousness and adequate spontaneous breathing were confirmed. The incidence of extubation recall was compared between the remimazolam and propofol anesthesia groups using propensity score matching., Results: Extubation recall was observed in 28 patients (17%). After propensity score matching, the incidence of extubation recall did not significantly differ between the remimazolam and propofol anesthesia groups (15.6% vs. 18.8%; p = 1.000)., Conclusion: The incidence of extubation recall after remimazolam anesthesia with flumazenil antagonism during emergence did not significantly differ from that after propofol anesthesia., (© 2022. The Author(s) under exclusive licence to Japanese Society of Anesthesiologists.)

Hemorrhagic shock causes vascular endothelial glycocalyx (EGCX) damage and systemic inflammation. Dexmedetomidine (DEX) has anti-inflammatory and EGCX-protective effects, but its effect on hemorrhagic shock has not been investigated. Therefore, we investigated whether DEX reduces inflammation and protects EGCX during hemorrhagic shock. Anesthetized Sprague-Dawley rats were randomly assigned to five groups (n=7 per group): no shock (SHAM), hemorrhagic shock (HS), hemorrhagic shock with DEX (HS+DEX), hemorrhagic shock with DEX and the α7 nicotinic type acetylcholine receptor antagonist methyllycaconitine citrate (HS+DEX/MLA), and hemorrhagic shock with MLA (HS+MLA). HS was induced by shedding blood to a mean blood pressure of 25-30 mmHg, which was maintained for 30 min, after which rats were resuscitated with Ringer's lactate solution at three times the bleeding volume. The survival rate was assessed up to 3 h after the start of fluid resuscitation. Serum tumor necrosis factor-alpha (TNF-α) and syndecan-1 concentrations, and wet-to-dry ratio of the heart were measured 90 min after the start of fluid resuscitation. The survival rate after 3 h was significantly higher in the HS+DEX group than in the HS group. Serum TNF-α and syndecan-1 concentrations, and the wet-to-dry ratio of heart were elevated by HS, but significantly decreased by DEX. These effects were antagonized by MLA. DEX suppressed the inflammatory response and serum syndecan-1 elevation, and prolonged survival in rats with HS.

Background: We herein present a case of venous thrombosis that developed more than 20 years after diagnosis of granulomatosis with polyangiitis (GPA), although many reports of GPA have described venous thrombosis within 1 year of diagnosis., Case Presentation: A 73-year-old man with GPA was admitted for lower extremity swelling and diagnosed with venous thrombosis and pulmonary embolism. On the second day, catheter-based thrombolysis was unsuccessful, and inferior vena cava filter insertion and anticoagulation were performed. On the third day, respiratory disturbance and loss of consciousness appeared and progressed. The patient died on the fifth day. The autopsy revealed a large thrombus in the inferior vena cava filter, and death of progressive venous thrombosis was suspected., Conclusions: We experienced a case of venous thrombosis that developed 20 years after diagnosis of GPA, although GPA is frequently associated with venous thrombosis immediately after diagnosis. The thrombosis progressed rapidly and was resistant to treatment., (© 2021. The Author(s).)

Abstract: Heat stroke is characterized by excessive oxidative stress and inflammatory responses, both of which are implicated in vascular endothelial glycocalyx shedding and heat-stroke mortality. Although molecular hydrogen has antioxidation and anti-inflammatory potency, its effect on the vascular endothelial glycocalyx in heat stroke has not been examined. Therefore, the aim of this study was to investigate the influence of hydrogen inhalation on the survival and thickness of the vascular endothelial glycocalyx of rats subjected to heat stroke. Altogether, 98 Wistar rats were assigned to the experiments. A heat-controlled chamber set at 40°C temperature and 60% humidity was used to induce heat stroke. After preparation, the anesthetized rats that underwent the heating process were subjected to an hour of stabilization in which 0%, 2%, or 4% hydrogen gas was inhaled and maintained until the experiment ended. In addition to survival rate assessments, blood samples and left ventricles were collected to evaluate the thickness of the vascular endothelial glycocalyx and relevant biomarkers. The results showed that 2% hydrogen gas significantly improved survival in the heat-stroked rats and partially preserved the thickness of the endothelial glycocalyx. In addition, serum levels of endotoxin, syndecan-1, malondialdehyde, and tumor necrosis factor-α decreased, whereas superoxide dismutase levels increased, indicating that inhalation of 2% hydrogen attenuated the damage to the vascular endothelial glycocalyx through its antioxidative and anti-inflammatory effects., Competing Interests: The authors report no conflicts of interest., (Copyright © 2021 by the Shock Society.)

Objective: To compare the effects of remifentanil versus fentanyl during light sedation with dexmedetomidine in adults receiving mechanical ventilation (MV) in the intensive care unit., Methods: In this retrospective cohort study, we compared the use of remifentanil versus fentanyl in adults receiving MV with dexmedetomidine sedation. The primary outcome was the proportion of time under light sedation (Richmond Agitation-Sedation Scale score between -1 and 0) during MV., Results: We included 94 patients and classified 58 into the remifentanil group and 36 into the fentanyl group. The mean proportion of time under light sedation during MV was 66.6% ± 18.5% in the remifentanil group and 39.9% ± 27.3% in the fentanyl group. In the multivariate analysis with control for confounding factors, patients in the remifentanil group showed a significantly higher proportion of time under light sedation than patients in the fentanyl group (mean difference: 24.3 percentage points; 95% confidence interval: 12.9-35.8)., Conclusions: Remifentanil use might increase the proportion of time under light sedation in patients receiving MV compared with fentanyl administration.

Purpose: Hydrogen gas (H 2 ) inhalation improved the survival rate of hemorrhagic shock. However, its mechanisms are unknown. We hypothesized that H 2 protected the endothelial glycocalyx during hemorrhagic shock and prolonged survival time., Methods: 83 Sprague-Dawley rats were anesthetized with isoflurane. The animals were randomly assigned to 5 groups: room air with no shock, 1.2% H 2 with no shock, room air with shock (Control-S), 1.2% H 2 with shock (H 2 1.2%-S), and 3.0% H 2 with shock (H 2 3.0%-S). Shock groups were bled to a mean arterial pressure of 30-35 mmHg and held for 60 min, then resuscitated with normal saline at fourfold the amount of the shed blood volume., Results: The syndecan-1 level was significantly lower in the H 2 1.2%-S [8.3 ± 6.6 ng/ml; P = 0.01; 95% confidence interval (CI), 3.2-35.8] than in the Control-S (27.9 ± 17.0 ng/ml). The endothelial glycocalyx was significantly thicker in the H 2 1.2%-S (0.15 ± 0.02 µm; P = 0.007; 95% CI, 0.02-0.2) than in the Control-S (0.06 ± 0.02 µm). The survival time was longer in the H 2 1.2%-S (327 ± 67 min, P = 0.0160) than in the Control-S (246 ± 69 min). The hemoglobin level was significantly lower in the H 2 1.2%-S (9.4 ± 0.5 g/dl; P = 0.0034; 95% CI, 0.6-2.9) than in the Control-S (11.1 ± 0.8 g/dl). However, the H 2 3.0%-S was not significant., Conclusions: Inhalation of 1.2% H 2 gas protected the endothelial glycocalyx and prolonged survival time during hemorrhagic shock. Therapeutic efficacy might vary depending on the concentration.

Purpose: Heatstroke causes systemic inflammation, followed by vascular endothelial damage. The normal vascular endothelium is coated by endothelial glycocalyx (EGCX). Dexmedetomidine (DEX) has an anti-inflammatory effect, but there has been little investigation on the influence of heatstroke on EGCX and the effect of DEX on this condition. Therefore, we examined whether EGCX was disrupted in heatstroke and if DEX improved survival and preserves EGCX., Methods: Anesthetized Wistar rats were randomly assigned to three groups: a DEX group treated with DEX (5 µg/kg/h) and 0.9% saline infused continuously at 10 ml/kg/h during heat exposure; a NSS group given 0.9% saline during heat exposure; and a SHAM group given 0.9% saline alone without heat exposure. Heatstroke was induced by exposure to an ambient temperature of 40 °C with relative humidity of 60%. The survival rate was assessed up to 2 h after the start of heat exposure. Plasma levels of syndecan-1 and the thickness of EGCX using electron microscopy were measured when the systolic blood pressure fell to less than 80 mmHg., Results: The survival rate after 2 h of heat exposure was significantly higher in the DEX group compared to the NSS group (89% vs. 22%, P = 0.004). Plasma levels of syndecan-1 were 0.6 ± 1.3, 9.7 ± 5.9, and 2.1 ± 3.4 ng/ml in the SHAM, NSS and DEX groups, respectively (P = 0.013). The thickness of EGCX was significantly higher in the DEX group compared with the NSS group (P = 0.001)., Conclusions: EGCX was disrupted in heatstroke, and DEX improved survival and preserved EGCX.

Background: In spinal anesthesia for cesarean section, the addition of fentanyl to the local anesthetic has been reported to improve perioperative analgesia. However, there is only limited knowledge on sedative effects of the added fentanyl. We examined whether the patient state index® (PSI) can detect and present the light sedated level with patients undergoing cesarean section., Findings: We measured respiratory rate (RR), SpO2, and PSI values. Between child delivery and the completion of the operation, the proportions of time with the PSI values <90 and 80 were calculated. RR <8 breaths/min or SpO2 <95 % was defined as respiratory depression. Respiratory depression was not observed in any patient. At fentanyl doses of 10, 15, and 20 μg, the proportions of time with the PSI <90 were 14.5 ± 20.8, 49.4 ± 35.3, and 71.1 ± 22.9 %, respectively ( P < 0.01). There were significant differences between 10 and 15 μg ( P < 0.05), and 10 and 20 μg ( P < 0.01). Similarly, the proportions of time with the PSI values <80 were 0.5 ± 1.8, 21.1 ± 24.1, and 31.8 ± 32.2 %, respectively ( P < 0.05). There was a significant difference between 10 and 20 μg ( P < 0.05)., Conclusions: The PSI values decreased in a dose-dependent manner with increasing dose of fentanyl, but no respiratory depression was observed. The PSI values decreased to less than 90, when fentanyl was administered more than 15 μg. Furthermore, the PSI values decreased to less than 80, when fentanyl was administered 20 μg.

Background: Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) has an extremely poor prognosis and there is currently no effective treatment for this condition. Direct hemoperfusion with a polymyxin B-immobilized fiber column (PMX-DHP) improves oxygenation, but it is unclear whether treatment of AE-IPF with PMX-DHP affects survival. This study elucidated the effectiveness and safety of PMX-DHP for the treatment of AE-IPF., Methods: This study included 31 patients with 41 episodes of AE-IPF. All patients received steroids. Of 31, 14 patients (20 episodes) were treated with PMX-DHP. The laboratory and physiological test results after the start of therapy and survival were retrospectively compared between patients treated with and without PMX-DHP., Results: Patients treated with PMX-DHP had a significantly greater change in PaO2/FiO2 ratio (mean ± SEM, 58.2 ± 22.5 vs. 0.7 ± 13.3, p = 0.034) and a smaller change in white blood cell count (-630 ± 959 /μL vs. 4500 ± 1190 /μL, p = 0.002) after 2 days of treatment than patients treated without PMX-DHP. The 12-month survival rate was significantly higher in patients treated with PMX-DHP (48.2% vs. 5.9%, p = 0.041). PMX-DHP was effective in patients with more severe underlying disease (GAP stages II or III; 12-month survival rate 57.1% with PMX-DHP vs. 0% without PMX-DHP, p = 0.021). Treatment with PMX-DHP was an independent predictor of better prognosis (hazard ratio 0.345, p = 0.037). Mild pulmonary thromboembolism occurred in one patient treated with PMX-DHP., Conclusions: Treatment of AE-IPF with PMX-DHP is tolerable and improves 12-month survival.

Background: Hypocapnia induced following the accidental intravenous infusion of a local anesthetic can mitigate anesthetic toxicity, but the effects of hypocapnia induced prior to local anesthetic infusion are unknown. In this study, we examined the effects of prior hypocapnia on bupivacaine-induced cardiotoxicity in rats., Methods: Eighteen Sprague-Dawley rats were randomly divided into two groups: one receiving sevoflurane with normal ventilation (Control Group) and the other receiving sevoflurane with hyperventilation to induce hypocapnia (Hypocapnia Group). After 30 min, both groups received continuous intravenous infusions of 0.25% bupivacaine at 2 mg · kg(-1) · min(-1). The time taken to reach 25% and 50% reductions in heart rate (HR; HR-25%, HR-50%) and mean arterial pressure (MAP; MAP-25%, MAP-50%) from the start of bupivacaine infusion were recorded. The difference between HR-25% and MAP-25% was calculated. The times of the first ventricular premature beat (VPB) and final systole were also recorded., Results: In the Hypocapnia Group, HR-50%, MAP-25%, and MAP-50% were prolonged compared with the Control Group (P < 0.001). Furthermore, the interval between HR-25% and MAP-25% and the times between the first VPB and final systole were prolonged in the Hypocapnia Group (P < 0.001)., Conclusion: In rats under sevoflurane anesthesia, prior hypocapnia delayed the onset of bupivacaine-induced cardiotoxicity. Prior hypocapnia should be avoided during continuous bupivacaine nerve block under general anesthesia, because it may delay the detection of cardiotoxicity.

We have previously reported that halothane anesthesia increases extracellular concentrations of dopamine (DA) metabolites in rat striatum using in vivo microdialysis techniques. Aging induces many changes in the brain, including neurotransmission. However, the relationship between aging and changes in neurotransmitter release during inhalational anesthesia has not been fully investigated. The aim of the present investigation was to evaluate the effect of sevoflurane on methamphetamine (MAPT)-induced DA release and metabolism in young and middle-aged rats. Male Sprague-Dawley rats were implanted with a microdialysis probe into the right striatum. The probe was perfused with a modified Ringer's solution and 40μl of dialysate was directly injected to an HPLC every 20min. Rats were administered saline, the same volume of 2mgkg(-1) MAPT intraperitoneally, or 5μM MAPT locally perfused. After treatments, the rats were anesthetized with 1% or 3% sevoflurane for 1h. Sevoflurane anesthesia significantly increased the extracellular concentration of DA only in middle-aged rats (52-weeks-old). In young rats (8-weeks-old), sevoflurane significantly enhanced MAPT-induced DA when administered both intraperitoneally and perfused locally, whereas no significant additive interaction was found in middle-aged rats. These results suggest that aging changes DA release and metabolism in rat brains primarily by decreasing the DA transporter., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: We created a system that allows the visualization of breath sounds (visual stethoscope)., Aim: We compared the visual stethoscope technique with auscultation for the detection of bronchial intubation in pediatric patients., Methods: In the auscultation group, an anesthesiologist advanced the tracheal tube, while another anesthesiologist auscultated bilateral breath sounds to detect the change and/or disappearance of unilateral breath sounds. In the visualization group, the stethoscope was used to detect changes in breath sounds and/or disappearance of unilateral breath sounds. The distance from the edge of the mouth to the carina was measured using a fiberoptic bronchoscope., Results: Forty pediatric patients were enrolled in the study. At the point at which irregular breath sounds were auscultated, the tracheal tube was located at 0.5 ± 0.8 cm on the bronchial side from the carina. When a detectable change of shape of the visualized breath sound was observed, the tracheal tube was located 0.1 ± 1.2 cm on the bronchial side (not significant). At the point at which unilateral breath sounds were auscultated or a unilateral shape of the visualized breath sound was observed, the tracheal tube was 1.5 ± 0.8 or 1.2 ± 1.0 cm on the bronchial side, respectively (not significant)., Conclusions: The visual stethoscope allowed to display the left and the right lung sound simultaneously and detected changes of breath sounds and unilateral breath sound as a tracheal tube was advanced., (© 2012 Blackwell Publishing Ltd.)

Pentobarbital (PB) and ketamine (Ket) influence the concentration of neurotransmitters in the brain. PB has been reported to decrease the extracellular nitric oxide (NO) concentration through a decrease in acetylcholine (ACh) release, while Ket has been shown to increase the NO concentration via an increase in ACh release. Here, we investigated effects of PB and Ket on NO release and the relationship between NO and ACh in the rat striatum by in vivo microdialysis experiments. Male Sprague-Dawley rats were used. A microdialysis probe was inserted into the right striatum and perfused with modified Ringer's solution. Samples were collected every 15 min and injected into an HPLC system. The rats were freely moving, and PB and Ket were administered intraperitoneally. Neostigmine (1 and 10 µM) and mecamylamine (100 µM) were added to the perfusate. Calcium and magnesium concentrations were modified for each anesthetic to influence ACh release. PB decreased NO products (NOx) while Ket increased them. While perfusion with neostigmine showed no effect on baseline NOx concentrations, it diminished the PB-induced NOx reduction at low concentrations and abolished it at high concentrations. Magnesium-free perfusion had no effect on baseline NOx concentrations, whereas perfusion at a low magnesium concentration antagonized the PB-induced NOx reduction. Mecamylamine and calcium-free perfusion had no effect on baseline NOx concentrations and Ket-induced NOx increases. PB may decrease NO release through reduction in ACh release, whereas Ket may increase NO release independent of ACh regulation.

Aim: Dexmedetomidine is a highly selective α-2 adrenergic agonist used perioperatively. Dexmedetomidine's cardioprotective effect after myocardial ischaemia remains unknown. In this study, we administered dexmedetomidine after ischaemia to investigate its ability to protect the cardiac muscle from ischaemia-reperfusion injury in isolated rat hearts., Methods: After a 30-min stop of perfusion, isolated rat hearts underwent reperfusion for 120 min. At the initiation of reperfusion, dexmedetomidine was administered for 25 min at concentrations of 0 nM (control group), 1 nM (Dex 1 group), and 10 nM (Dex 10 group). Yohimbine (an α-2 adrenergic antagonist) was administered in the manner as above in another group of isolated rat hearts at a concentration of 1 μM without dexmedetomidine (Yoh group) and at 1 μM with 10 nM dexmedetomidine (Yoh+Dex 10 group). The area of infarction was measured using 2,3,5-triphenyltetrazolium staining., Results: Dexmedetomidine administration did not influence haemodynamics or the coronary flow (CF), but did increase the myocardial infarct size. Neither concentration of dexmedetomidine affected the infarct size as the Dex 1 and Dex 10 groups had almost the same infarct size. The infarct size was 40.5±2.9% in the control group, 60.9±5.3% in the Dex 1 group, and 60.9±2.8% in the Dex 10 group. The infarct size was reduced in the yohimbine groups. The infarct size was 39.2±3.3% in the Yoh+Dex 10 group and 45.0±3.2% in the Yoh group., Conclusion: Dexmedetomidine administration does not influence haemodynamics or CF, but does increase the cardiac infarct size. α-2 Adrenergic stimulation may induce this mechanism., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Purpose: To determine the effect of landiolol on ischemic preconditioned rat hearts., Methods: Isolated perfused rat hearts were divided into 8 groups. In the control group, there was no treatment before the 30-min global ischemia. In the landiolol infused groups, landiolol (100, 300, and 500 microM) was infused without ischemic preconditioning (IPC). In other groups, hearts were pretreated with 2 episodes of 5-min global ischemia and reperfusion before the 30-min ischemia. During the preconditioning, landiolol (0, 100, 300, and 500 microM) was infused., Results: Recoveries of coronary flow (CF) and myocardial oxygen consumption (MVO(2)) at the 120th min after global ischemia to 86 +/- 18 and 112 +/- 19% of the baseline in the IPC group was, respectively, significantly greater than that to 65 +/- 10 and 72 +/- 10% in the control group. Landiolol 300 microM also increased the CF and MVO(2) significantly (97 +/- 19 and 98 +/- 39%) compared to the control. IPC + landiolol 500 microM reduced the increase in LV end-diastolic pressure significantly compared to the control. IPC, landiolol (100, 300, and 500 microM), and IPC + landiolol (100, 300, and 500 microM) all decreased infarct sizes significantly to 23.5 +/- 15.2, 29.8 +/- 12.1, 30.2 +/- 13.3, 22.8 +/- 14.8, 21.6 +/- 7.8, 34.2 +/- 14.7 and 25.5 +/- 11.3% of the total left ventricular mass, respectively, compared to the control (53.3 +/- 12.5%), but there were no significant differences among these groups., Conclusion: IPC and landiolol have cardioprotective effects on ischemia-reperfusion injury in isolated rat hearts, but pretreatment with landiolol does not enhance the cardioprotective effect of IPC.

This study examined the sedative effect of, and hemodynamic response to dexmedetomidine administration in propofol-sedated swine. Sixteen swine were subjects. After anesthetic induction and preparation, the propofol infusion rate was adjusted to maintain a bispectral index (BIS) value between 55 and 65 (i.e., baseline). With the propofol infusion rate fixed at the baseline rate, dexmedetomidine was infused continuously at a rate of 0.2, 0.4, and 0.7 microg.kg(-1).h(-1) for one hour at each rate. The BIS value and hemodynamic parameters were recorded at each step. Dexmedetomidine decreased the BIS value, mean arterial blood pressure, heart rate, cardiac output, and mixed venous oxygen saturation in a dose-dependent manner. The systemic vascular resistance (SVR) did not change, but the pulmonary vascular resistance (PVR) increased. Oxygen delivery (DO(2)) and oxygen consumption (VO(2)) decreased. A small dose of dexmedetomidine (0.2 microg.kg(-1).h(-1)) greatly enhanced the sedative effects of propofol with only small changes in hemodynamics and systemic oxygen balance, suggesting it may be useful in reducing the propofol dose requirement. However, dexmedetomidine 0.4 microg.kg(-1).h (-1) suppressed cardiac contractility, and 0.7 microg.kg(-1).h(-1) induced hemodynamic instability and further systemic oxygen imbalance while the additional sedative effect was limited. A lower dose of dexmedetomidine may be recommended when using it in combination with propofol.

Previously, we have reported that halothane anesthesia increases the extracellular concentrations of dopamine (DA) metabolites in the rat striatum using in vivo microdialysis techniques, and we have suggested that volatile anesthetics affect DA release and metabolism in various ways. The present investigation assesses the effect of isoflurane, widely used in clinical anesthesia, on DA release and metabolism. A microdialysis probe was implanted in the striatum of male Sprague-Dawley rats (n=5-7 per group). After recovery, the probe was perfused with modified Ringer's solution and 40 microl of dialysate were injected into a high performance liquid chromatograph every 20 min. The rats were given saline or the same volume of 10 mg kg(-1) clozapine, risperidone, fluoxetine or citalopram. After the pharmacological treatment, the rats were anesthetized with 1.0% or 2.5% isoflurane for 1h. The data were analyzed using two-way analysis of variance (ANOVA). For each drug with significant (p<0.05) drug-time interactions, the statistical analysis included one-way ANOVA and Newman-Keuls post hoc comparisons. A high concentration of isoflurane (2.5%) anesthesia increased the extracellular concentration of DA metabolites during emergence from anesthesia. The levels of DA metabolites increased in an isoflurane concentration-dependent manner. Isoflurane attenuated DA release induced by clozapine and risperidone. Fluoxetine, but not citalopram, antagonized the isoflurane-induced increase in metabolites. The results of current investigation suggest that isoflurane enhances presynaptic DA metabolism, and that the oxidation of DA might be partially modulated by the activities of the dopaminergic-serotonergic pathway at a presynaptic site in the rat striatum.

The purpose of this study was to examine the changes in activated protein C (APC) anticoagulant activity during pregnancy and determine whether changes in APC could contribute to thrombosis in the placental bed in preeclampsia. We measured APC anticoagulant activity in 150 women with a normal pregnancy and 50 women with preeclampsia. There was a significant reduction in the mean APC sensitivity ratio (APC-SR) during pregnancy (p<0.001). APC resistance in preeclampsia was significantly higher than in normal pregnancy (p<0.01). Amongst women with APC resistance the presence of the factor V Leiden mutation was significantly higher in the preeclampsia group than in the normal pregnancy group (p<0.01). It seems that both factor V Leiden mutation and APC resistance may be associated with the development of preeclampsia. These results suggest that APC resistance may be an important mechanism underlying placental bed pathology in pregnancy and may be associated with an increased tendency to develop preeclampsia in some women. Assay of APC resistance and factor V Leiden mutation should be performed in women with preeclampsia.