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首页> 外文期刊>Korean Circulation Journal >Effect of Ischemic Preconditioning on Catecholamine Release from the Isolated, Ischemic Reperfused Hearts of Rats
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Effect of Ischemic Preconditioning on Catecholamine Release from the Isolated, Ischemic Reperfused Hearts of Rats

机译：缺血预处理对大鼠离体缺血再灌注心脏释放儿茶酚胺的影响

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Background Ischemic preconditioning reduces the infarct size and the severity of arrhythmia in a post-ischemic reperfused heart although the detailed mechanism is unknown. In the ischemic heart, a large amount of catecholamine is released from the adrenergic nerve terminal and this aggravates cell destruction and arrhythmia. In this study, the possibility for ischemic preconditioning to inhibit the release of endogenous catecholamine from the ischemic heart was tested to investigate the probable cardioprotective mechanism of ischemic preconditioning. Methods In the isolated, Langendorff perfused rat hearts, we observed the protective effect of ischemic preconditioning against post-ischemic reperfusion injury, and measured the amount of catecholamine released into coronary effuent. In addition, we observed the effect of catecholamine depletion on reperfusion injury in non-preconditioned and preconditioned hearts. Results During the reperfusion(20min) after ischemia(30min), the cardiac function was markedly depressed with the development of severe contracture. In the heart preconditioned by three sequential episodes of 5min ischemia and 5min reperfusion, the reperfusion contracture decreased significantly and the cardiac function was almost recovered to normal after 20min reperfusion. The release of lactate dehydrogenase was also decreased in the preconditioned heart. The release of endogenous catecholamine was abruptly increased immediately after the reperfusion and the release was exponentially decreased throughout the reperfusion period. THe pattern of catecholamine release was much different from that of lactate dehydrogenase release. In the preconditioned heart, the release was significantly decreased to about half of that in non-preconditioned theart. Endogenous catecholamine depletion by reserpine treatment did not affect the post-ischemic functional recovery in both non-preconditioned and preconditioned hearts. Conclusion It is suggested from these results that ischemic preconditioning inhibis the release of endogenous catecholamine during ischemic period, which may be partly related to cardioporotective effect of preconditioning in ischemic and reperfused heart.
机译：背景缺血预处理可减轻缺血后再灌注心脏的梗塞面积和心律失常的严重程度，尽管其详细机制尚不清楚。在缺血性心脏中，大量儿茶酚胺从肾上腺素能神经末梢释放出来，这会加剧细胞破坏和心律不齐。在这项研究中，通过缺血预处理来抑制缺血性心脏内源性儿茶酚胺的释放，以研究缺血预处理的可能的心脏保护机制。方法在离体的Langendorff灌注大鼠心脏中，观察缺血预处理对缺血再灌注损伤的保护作用，并测定释放到冠状动脉流出物中的儿茶酚胺的量。此外，我们观察到儿茶酚胺耗竭对未预处理和预处理心脏的再灌注损伤的影响。结果缺血（30min）再灌注（20min）过程中，随着严重挛缩的发展，心功能明显下降。在连续5分钟局部缺血和5分钟再灌注的三个连续事件预处理的心脏中，再灌注20分钟后，再灌注挛缩显着降低，心脏功能几乎恢复正常。预处理心脏中的乳酸脱氢酶的释放也减少了。再灌注后内源性儿茶酚胺的释放突然增加，并且在整个再灌注期间释放呈指数下降。儿茶酚胺释放的模式与乳酸脱氢酶释放的模式有很大不同。在预处理的心脏中，释放显着降低至非预处理的心脏中的释放的一半。利血平治疗导致的内源性儿茶酚胺耗竭，未影响未预处理和预处理心脏的缺血后功能恢复。结论从这些结果表明，缺血预处理可以抑制缺血期间内源性儿茶酚胺的释放，这可能与缺血预处理和再灌注心脏的心脏电复光作用有关。

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