Search

The interaction between protein kinase C activity and intracellular Ca2+ ([Ca2+]i) during myogenic contraction was analyzed in isolated rat skeletal muscles and mesenteric small arteries with fura 2. Myogenic contraction in isolated rat skeletal muscles and small arteries was attenuated by the inhibition of PKC with staurosporine without altering [Ca2+]i elevations in the skeletal muscles and small arteries. Furthermore, the effects of staurosporine indicated the cooperative role of PKC and [Ca2+]i elevations in the promotion of myogenic contraction.

Objective: The aim was to elucidate the functional role of the sarcoplasmic reticulum in myogenic contraction. Methods: Small arteries which perfuse the rat gracilis muscle were isolated and cannulated. The inner diameter was measured under no flow condition. Myogenic contraction was induced by increasing transmural pressure from 40 to 100 mm Hg. The diameter transient and the steady state internal diameter were analysed at 40 (ID40) and 100 mm Hg (ID100) of lumen pressure. Results: In control, the vessels dilated immediately after the pressure change, and then constricted over approximately 4 min (the diameter decay). ID40 and ID100 were 120(SEM 16) and 108(12) μm (n = 6, p<0.05), respectively. Ryanodine (10−5 M) decreased ID40 to 82(8) μm. The relative rate of the diameter decay in the first 1 min was lower in the ryanodine treated vessels than in control, at 43(1)% v 74(7)%, n = 6 (p<0.05). While KC1 constriction was similar to that of ryanodine, the diameter decay was identical to that of control. Thus a decrease in baseline diameter was not of itself the cause of the depressed rate of diameter decay in the ryanodine treated vessels. Nisoldipine (10−6 M) abolished myogenic contraction. Conclusions: Ryanodine sensitive sarcoplasmic reticular function is probably involved in the mechanism for developing the myogenic response in rat skeletal muscle small arteries.Cardiovascular Research 1994;28:480-484 [ABSTRACT FROM PUBLISHER]

Objective: The aim was to examine the effects of heart rate on total coronary blood volume with pressure-type plethysmography in isolated and vasodilated canine hearts. Methods: Nine hearts were excised from anaesthetised mongrel dogs (13.1-15.2 kg) and perfused with arterial blood of other dogs (17.0-29.0 kg). The venous blood returning to the right atrium and both ventricles was drained under constant negative pressure (−10 mm Hg). A thin latex balloon filled with water was inserted into the left ventricle to keep the intraventricular volume constant. The pressure difference between the cylinder into which the heart was placed and a compensation chamber was measured as a change in coronary blood volume while heart rate was altered from 120 beats·min−1 (control heart rate) to a target level (60, 90, 150, or 180 beats·min−1). Results: The mean coronary blood volume change compared with that at control heart rate was 1.65(SEM 0.32) ml·100 g−1 at 60 beats·min−1 (p<0.005) and −0.74(0.20) ml·100 g−1 at 180 beats·min−1 (p<0.005) under the perfusion pressure of 70 mm Hg. The mean volume decreased with the increase in heart rate. Diastolic-systolic variations in coronary blood volume also decreased with an increase in heart rate, from 0.61(0.06) ml·100−1 (60 beats·min−1) (p<0.005) to 0.12 ml·100 g−1 (180 beats·min−1). Both mean change and variation were almost linear functions of R-R interval (r=0.88 and r=0.83). Lowering the perfusion pressure from 70 to 40 mm Hg diminished the changes in both mean and variation of the coronary blood volume. Conclusions: Tachycardia reduces the mean coronary blood volume and the diastolic-systolic variations in isolated vasodilated canine hearts.Cardiovascular Research 1993;27:1127-1134 [ABSTRACT FROM PUBLISHER]

Study objective – The aim of the study was to examine the relation between zero flow pressure and intramyocardial pressure in the inner and outer layers of the myocardium.Design – Zero flow pressure was obtained in maximally vasodilated excised hearts by decreasing perfusion pressure (at 2 mm Hg·s−1) during transient heart arrest. Intramyocardial pressures in inner and outer myocardium were measured simultaneously with needle tip pressure transducers at depths of 8.0(SD 2.6) and 3.3(1.2) mm from the epicardium respectively. Ventricular and atrial pressure could be controlled at will.Experimental material – The excised hearts of eight mongrel dogs, body weight 14.0(0.8) kg, were used.Measurements and main results – During left ventricular pressure elevation (0, 15, 30 mm Hg), zero flow pressures were 9.1(2.4), 13.8(2.2), and 19.1(5.1) mm Hg, respectively. Corresponding values of intramyocardial pressure at the outer myocardium were in good agreement with the zero flow pressures, at 9.1(3.4), 13.4(2.8), and 20.8(5.4) mm Hg. Values at the inner myocardium increased from 7.4(2.4) to 18.9(8.6) and 32.9(13.0) mm Hg. The latter two values were significantly higher than the corresponding values of zero flow pressure and intramyocardial pressure at the outer myocardium (p<0.05, p<0.01). In isotransmural pressure elevation, the three pressures increased almost equally.Conclusions – The results show that zero flow pressure is strongly affected by intramyocardial tissue pressure, and if uneven intramyocardial pressure distribution is present the value of zero flow pressure depends on the lower values of intramyocardial pressure. [ABSTRACT FROM PUBLISHER]

To examine how end systole differs from end ejection and also whether the slope of the end systolic pressure-volume relation can be approximated to that of the end ejection pressure-volume relation, nine isolated, perfused, paced canine hearts ejecting into a hydraulic loading system that simulated the aortic input impedance of a dog's arterial tree were studied. To measure left ventricular volume changes the heart was placed in a plethysmograph. Peripheral resistance (Rp) and arterial compliance (C) were independently varied from 1.9 (Rp=1.9) to 3.3, 6.4, and 9.6 × 108 Pa·m−3·s (Rp run) with a constant value of compliance 1.3 × 10−9 Pa−1·m3 (C=1.3), and from C=0.4 to C=0.8, C=1.3 and C=2.3 (C run) with a constant value of resistance (Rp=6.4). Five pressure-volume loops were obtained by changing the end diastolic volume at each value of compliance and peripheral resistance. It was clearly shown that ventricular ejection continued after end systole and the time duration between end systole and end ejection became longer with increasing arterial compliance (24(4) at C=0.4 vs 49(4) ms at C=2.3, p<0.001), while the time duration between end diastole and end systole was constant regardless of afterload impedance change. Regarding the left ventricular pressure-volume relation the end systolic relation was almost linear (r≥0.98) and the slope was not significantly affected by change in any afterload impedance tested. End ejection pressure-volume relation was also linear (r≥0.97) and the slopes in the peripheral resistance and compliance runs were lower than those of the end systolic pressure-volume relation in each corresponding run. The former slopes decreased at smaller values of Rp or larger values of C — namely, 4.4(0.6) at Rp=9.6 vs 3.6(0.6) at Rp=1.9, p<0.05; 4.8(0.6) at C=0.4 vs 3.1(0.5) mm·Hg·ml−1 at C=2.3, p<0.001. Thus it is concluded that end ejection is usually different from end systole and the time difference between them is affected by changes in arterial compliance. In addition, the slope of end ejection pressure-volume relation was dependent on the changes in afterload impedance and cannot be approximated to that of the end systolic pressure-volume relation. [ABSTRACT FROM PUBLISHER]

Background/aims: In extended left hepatectomy including venous resection of proximal portion of the MHV, a simple new venous reconstruction technique was attempted to bypass the long gap between the stump of peripheral portion of MHV and IVC., Methodology: One of the hepatic venous branches in resecting side of the liver was dissected during liver transection. The dissected vein was left attached to the IVC at its proximal portion and the distal end was directly anastomosed with the stump of MHV as an alternative venous drainage rout., Results: Of 282 hepatectomies performed for metastatic liver tumor in Tokyo University Hospital from 1995 to 2004, two patients were treated with the present technique. With the in situ hepatic vein graft method, postoperative venous congestion was successfully avoided in both of two cases and drainage areas of the reconstructed vein showed sufficient parenchymal regeneration., Conclusions: In situ hepatic vein graft might be useful and possibly superior to conventional free venous graft in reconstructing long venous gap in selected patients from the viewpoint of its safety, curative potential, and the long-term patency.

Background: The repolarization properties of the crista terminalis (CT) cells have not been elucidated in patients with sinus node disease (SND). In the present study a new technique of recording the monophasic action potential (MAP) at the CT was used to examine the repolarization of the right atrium (RA) in SND patients., Methods and Results: Symptomatic SND (n=13) patients and age-, sex-matched control patients (n=13) were tested. The MAP duration (MAPD) at a basic cycle length of 600 ms was recorded at the CT in the superior vena cava - RA junction and at the middle - anterior RA with the effective refractory period (ERP) at the high RA. In 6 controls and 4 SND patients, the effect of adenosine triphosphate on the MAPD was examined. The MAPD at the CT exceeded that at the middle - anterior RA in both groups. The MAPD at the CT in the SND group was significantly prolonged compared with the control group (CT: 358+/-39 ms vs 289+/-43 ms). Between the SND and control groups, the MAPD at the middle - anterior RA (278+/-36 ms vs 265+/-39 ms) and ERP (294+/-42 ms vs 266+/-41 ms) did not differ. Both the corrected-sinus node recovery time and sinoatrial conduction time were better correlated with the MAPD at the CT than the MAPD at the middle - anterior RA and ERP. Adenosine triphosphate shortened the MAPD, which was augmented at the CT in the SND patients., Conclusion: A novel method of estimating the MAP at the CT revealed the characteristics of atrial repolarization in SND patients.

We investigated the effectiveness and complications of intrathoracic infusion with a combination of cisplatin, OK-432, and minocycline for malignant pleural effusion. All patients were hospitalized with chest tube drainage of pleural effusion until the daily drainage volume was less than 100 ml. Twenty-five mg of minocycline, 1 to 3 KE of OK-432, and 5 to 10 mg of cisplatin were instilled into the pleural space. The administration was repeated until drainage effusion disappeared. Therapeutic effect was evaluated according to the following criteria: (1) excellent, no fluid reaccumulation for at least 4 weeks as determined by chest radiogram and clinical evaluation; (2) effective, fluid reaccumulation less than 50% of original effusion with no need of thoracentesis for symptomatic relief within 4 weeks after treatment; and (3) failure, reaccumulation of more than 50% of the original effusion requiring thoracentesis to relieve symptoms within 4 weeks of treatment. Twelve patients with malignant effusion received the combination treatment; 11 patients had primary lung cancer and one had metastatic lung tumor from cancer of the rectum. In all cases, the histology or cytology revealed adenocarcinoma. Eleven of the 12 patients had an excellent response with relief of clinical symptoms. The remaining case failed to show any improvement. Complications such as local pain, fever, nausea, and vomiting were mild and transient. We conclude that combination administration of low-dose minocycline, OK-432, and cisplatin into the thoracic cavity for malignant effusion is an effective alternative treatment with the potential for improvement of the general condition and reduced morbidity.