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Mechanism of protective effects of Ca++ channel blockers on energy deprivation contracture in cultured ventricular myocytes.

作者信息

Kohmoto O, Barry W H

机构信息

Department of Medicine, University of Utah School of Medicine, Salt Lake City.

出版信息

J Pharmacol Exp Ther. 1989 Feb;248(2):871-8.

PMID:2918484
Abstract

To examine mechanisms of the protective effects of Ca++ channel blockers on energy deprivation contracture, we measured cystolic calcium ion concentration ([Ca++]i) (Indo-1 fluorescence), development of contracture (video motion detector) and ATP contents during exposure of cultured chick embryo ventricular cells to 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG). The time periods required for [Ca++]i to reach 50% of [Ca++]i transient ([Ca++]i-50) and contracture were determined after exposure to 1) CN + 2-DG alone, 2) CN + 2-DG simultaneous with 1 microM verapamil (V-sim) and 3) verapamil followed by CN + 2-DG (V-pre). Time periods required to reach [Ca++]i-50 under these conditions were 4.2 +/- 0.4 min (CN + 2-DG alone), 3.8 +/- 0.4 min (NS vs. CN + 2-DG alone) (V-sim) and 6.4 +/- 1.1 min (P less than .05 vs. CN + 2-DG alone) (V-pre), respectively. Time periods required for contracture development were 4.4 +/- 0.3 min (CN + 2-DG alone), 4.4 +/- 0.6 min (NS vs. CN + 2-DG alone) (V-sim) and 9.3 +/- 1.2 min (P less than .05 vs. CN + 2-DG alone) (V-pre). Three minutes after metabolic inhibition, ATP contents declined from 32.3 +/- 0.7 nmol/mg of protein to 4.2 +/- 1.0 in CN + 2-DG alone, to 4.5 +/- 0.9 (NS vs. CN + 2-DG alone) with V-sim and to 8.3 +/- 2.2 (P less than .05 vs. CN + 2-DG alone) with V-pre.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

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Continuous fluorimetric assessment of the changes in cytoplasmic calcium concentration during exposure of rat isolated myocardium to conditions of simulated ischaemia.在大鼠离体心肌暴露于模拟缺血条件下时,对细胞质钙浓度变化进行连续荧光测定评估。
Br J Pharmacol. 1990 Jul;100(3):477-82. doi: 10.1111/j.1476-5381.1990.tb15832.x.
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Contributions of [Ca2+]i, [Pi]i, and pHi to altered diastolic myocyte tone during partial metabolic inhibition.
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