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Comparative effects of verapamil, fendiline, diltiazem and nifedipine on action potential of 3D eembryonic chick ventricle
J Mol
Cell
Cardiol
24 (Supplement
I) (1992)
p-01-13
EZ'FHCT OF ACIDOTIC PERFUSION ON THE DEVELOPHENT OF OXYGEN PARADOX IN SUPPRESSIVE ISOLATED RAT SSART. Takao Okada, Sachiko Xvmada, Rikuo Ochi. Department of Physiology, Juntendo University School of Medicine, Tokyo 113, Japan. In Langendorff-perfused rat heart, effect of perfusate pE on the development of oxygen-paradox was examined. When hearts were reoxygenated after a 40-min hypoxia, creatinkinase (CKI release significantly increased from 0.074K1.028 (SF&l) of prehypoxic level to 1.031tO.410 IU/min (n=B) indicating the development of oxygenparadox. Prostanoids (PG D2, E2, Fz~, TXH2, and 6-oxc PGFla) release, determined by GC-MS, also increased at early phase of reoxygenation from 14.32i2.03 of pre-hypoxic value to 37.206.48 pmol/min suggesting the degradation of membrane phospholipid. Reduction of pH (n=5) of the p-erfusate from 7.4 to 6.4, prevented the increases in CX and prostanoid release during the reoxygenation (0.185d.045 IU/mi.n and 16.08i2.46 pmol/min for CK and prostanoids, respectively). It also improved reoxygenationassociated recovery in contraction; the pressure-rate-product and max dP/dt recovered to 57.0t7.2 and 36.0*5.2% of pre-hypoxic values by 30 min reoxygenation at pA 7.4, while they recovered to 85.0i9.4 and 78.8+12.3% by reoxygenation at pIi 6.4 for 15 min followed by perfusion at pH 7.4 for another 15 min. We conclude that acidotic perfusion suppressed membrane degradation to prevent severe irreversible myocardial damages.
p-01-14
THE EFFECT OF QUERCETIN CN Yurl Kolohin, Aleksei Moibenko Medical Institute, A. A. Bogomolets
REPERFUSION-INDUCED Institute
of
DAMAGE Physiology,
Lugansk,
OF
MYCCARDIUM Ukraine,
USSR
The study was undertaken to evaluabe the effect of lipoxygenase blocker quercetln on the degree oi’ reperfusion-induced damage of the myocardium. The experiments were performed on the male Wistar rats with an occlusion UP coronary at-tat-y eh one hour and a reperfusion during 5, 24 and 48 hours and 2 weeks. In the rats adminisbered 40 mg/kg quercetin oompariscn with the oontrol group, Intraperitoneally exhibited a decrease in the total number of arrhythmias more than 4-fold. a reduction oP LTc4 by 57.312.8% (p
p-01-15
CREATINE KMASE RELEASE FROM RAT HEART IN EARLY REPERFUSION PERIOD IN RELATION TO OXYGEN PARADOX. Gao Tian-Li, Zhang Ying. Section of Physiology, Department of Biology, Peking University, 100871 Beijing, PR CHINA. This study provided a model with which the kinetics of early CK release was able to investigate. Isolated rat heart was perfused by Langendorff method with 10 min equilibrium, 10 min global ischemia, and 3 min reperfusion. Effluents were collected every 15 set for CK activity (U/L) analysis. A charateristic feature of the CK reletTnvzFin 3 min reperfusion was biphasic. n Condition CK in 3 min 1st peak 2nd peak 1. K-H without substrate 14 29ztlO 1182zt374 178*64 137f56 2. K-H with substrate 14 24f12 687f172* * 121k45 * 73f20* * 8 3. 1 plus anoxia 34flO 8541303 * 135&27 * 88+136 * 4. 1 plus low Cal+(O. 05 mM) 42f20 1058f309 204f75 98133 * 8 (M&SD; * p
Cell
Cardiol
24 (Supplement
I) (1992)
p-01-13
EZ'FHCT OF ACIDOTIC PERFUSION ON THE DEVELOPHENT OF OXYGEN PARADOX IN SUPPRESSIVE ISOLATED RAT SSART. Takao Okada, Sachiko Xvmada, Rikuo Ochi. Department of Physiology, Juntendo University School of Medicine, Tokyo 113, Japan. In Langendorff-perfused rat heart, effect of perfusate pE on the development of oxygen-paradox was examined. When hearts were reoxygenated after a 40-min hypoxia, creatinkinase (CKI release significantly increased from 0.074K1.028 (SF&l) of prehypoxic level to 1.031tO.410 IU/min (n=B) indicating the development of oxygenparadox. Prostanoids (PG D2, E2, Fz~, TXH2, and 6-oxc PGFla) release, determined by GC-MS, also increased at early phase of reoxygenation from 14.32i2.03 of pre-hypoxic value to 37.206.48 pmol/min suggesting the degradation of membrane phospholipid. Reduction of pH (n=5) of the p-erfusate from 7.4 to 6.4, prevented the increases in CX and prostanoid release during the reoxygenation (0.185d.045 IU/mi.n and 16.08i2.46 pmol/min for CK and prostanoids, respectively). It also improved reoxygenationassociated recovery in contraction; the pressure-rate-product and max dP/dt recovered to 57.0t7.2 and 36.0*5.2% of pre-hypoxic values by 30 min reoxygenation at pA 7.4, while they recovered to 85.0i9.4 and 78.8+12.3% by reoxygenation at pIi 6.4 for 15 min followed by perfusion at pH 7.4 for another 15 min. We conclude that acidotic perfusion suppressed membrane degradation to prevent severe irreversible myocardial damages.
p-01-14
THE EFFECT OF QUERCETIN CN Yurl Kolohin, Aleksei Moibenko Medical Institute, A. A. Bogomolets
REPERFUSION-INDUCED Institute
of
DAMAGE Physiology,
Lugansk,
OF
MYCCARDIUM Ukraine,
USSR
The study was undertaken to evaluabe the effect of lipoxygenase blocker quercetln on the degree oi’ reperfusion-induced damage of the myocardium. The experiments were performed on the male Wistar rats with an occlusion UP coronary at-tat-y eh one hour and a reperfusion during 5, 24 and 48 hours and 2 weeks. In the rats adminisbered 40 mg/kg quercetin oompariscn with the oontrol group, Intraperitoneally exhibited a decrease in the total number of arrhythmias more than 4-fold. a reduction oP LTc4 by 57.312.8% (p
p-01-15
CREATINE KMASE RELEASE FROM RAT HEART IN EARLY REPERFUSION PERIOD IN RELATION TO OXYGEN PARADOX. Gao Tian-Li, Zhang Ying. Section of Physiology, Department of Biology, Peking University, 100871 Beijing, PR CHINA. This study provided a model with which the kinetics of early CK release was able to investigate. Isolated rat heart was perfused by Langendorff method with 10 min equilibrium, 10 min global ischemia, and 3 min reperfusion. Effluents were collected every 15 set for CK activity (U/L) analysis. A charateristic feature of the CK reletTnvzFin 3 min reperfusion was biphasic. n Condition CK in 3 min 1st peak 2nd peak 1. K-H without substrate 14 29ztlO 1182zt374 178*64 137f56 2. K-H with substrate 14 24f12 687f172* * 121k45 * 73f20* * 8 3. 1 plus anoxia 34flO 8541303 * 135&27 * 88+136 * 4. 1 plus low Cal+(O. 05 mM) 42f20 1058f309 204f75 98133 * 8 (M&SD; * p