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心肌从整体缺血和再灌注中的恢复:低钙预缺血和/或后缺血灌注的影响。

Myocardial recovery from global ischemia and reperfusion: effects of pre- and/or post-ischemic perfusion with low-Ca2+.

作者信息

Koomen J M, Schevers J A, Noordhoek J

出版信息

J Mol Cell Cardiol. 1983 Jun;15(6):383-92. doi: 10.1016/0022-2828(83)90322-x.

Abstract

The effects of brief (5 min) pre- and/or post-ischemic treatment with low-Ca2+ (10(-4)M) on cardiac mechanical performance during and after increasing periods of total global ischemia were investigated on isolated perfused rat heart. Mechanical parameters studied were changes in diastolic resting length (delta DRL), ventricular contraction amplitude, its first derivative dL/dtmax, and cardiac responsiveness to variations in extracellular Ca2+. The results demonstrate that pre-ischemic low-Ca2+ may completely prevent: (a) the development of myocardial contracture during 45 min ischemia, (b) the occurrence of post-ischemic contracture and (c) a loss in myocardial contractile activity after 30 min of total ischemia. Post-ischemia low-Ca2+ was clearly less effective in protecting the heart against ischemia-induced loss in contractile function and offered no additional benefit when combined with pre-ischemic low-Ca2+. Post-ischemic mechanical recovery appeared to correlate letter with (end-)reperfusion-contracture than with (end-)ischemic contracture. Cardiac responsiveness to perfusate-Ca2+ decreased with increasing duration of the ischemic period (greater than 30 min), but was not significantly altered by the low-Ca2+-treatments. It was concluded from the results that the protective effect of a pre-ischemic low-Ca2+ treatment is superior to that of a similar post-ischemic treatment. The mechanism of protection and the role of Ca2+ in the ischemic process are discussed in terms of changes in the availability of intracellular free-Ca2+.

摘要

在离体灌注大鼠心脏上,研究了短暂(5分钟)缺血前和/或缺血后用低钙(10⁻⁴M)处理对不同时长全心缺血期间及之后心脏机械性能的影响。所研究的机械参数包括舒张静息长度变化(ΔDRL)、心室收缩幅度、其一阶导数dL/dtmax以及心脏对细胞外钙变化的反应性。结果表明,缺血前低钙可完全预防:(a)45分钟缺血期间心肌挛缩的发展;(b)缺血后挛缩的发生;以及(c)30分钟全心缺血后心肌收缩活性的丧失。缺血后低钙在保护心脏免受缺血诱导的收缩功能丧失方面明显效果较差,且与缺血前低钙联合使用时无额外益处。缺血后机械恢复似乎与(终末)再灌注挛缩的相关性比与(终末)缺血挛缩的相关性更好。随着缺血时间延长(大于30分钟),心脏对灌注液钙的反应性降低,但低钙处理未使其发生显著改变。从结果得出结论,缺血前低钙处理的保护作用优于类似的缺血后处理。根据细胞内游离钙可用性的变化,讨论了保护机制以及钙在缺血过程中的作用。

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