Possible mechanism of cardioprotective effect of ischaemic preconditioning in isolated rat heart
Possible mechanism of cardioprotective effect of ischaemic preconditioning in isolated rat heart
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DOI：
10.1006/phrs.1999.0631
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发表时间：
2000-06-01
影响因子：
9.3
通讯作者：
Singh, M
中科院分区：
文献类型：
--
作者：
Sharma, A;Singh, M
本研究旨在探讨缺血预处理的心脏保护作用的机制。离体灌注大鼠心脏进行30分钟整体缺血，然后再灌注120分钟。分析冠状动脉流出物的 LDH 和 CK 释放，以评估心脏损伤的程度。使用 TTC 染色从宏观上估计心肌梗塞大小。四次缺血预处理显着减少了冠状动脉流出物中 LDH 和 CK 的释放，并减少了心肌梗塞的面积。在全身缺血前给予哌唑嗪（α（1）肾上腺素受体拮抗剂）可减少缺血再灌注引起的心肌损伤的程度。哌唑嗪和秋水仙碱（微管解聚剂）消除了缺血预处理的心脏保护作用。基于这些结果，可以得出这样的结论：缺血预处理的心脏保护作用可能是通过刺激α(1)肾上腺素受体和PKC易位来介导的。 (C) 2000 年学术出版社。
The present study is designed to investigate the mechanism of the cardioprotective effect of ischaemic preconditioning. Isolated perfused rat heart was subjected to global ischaemia for 30 min followed by reperfusion for 120 min. Coronary effluent was analysed for LDH and CK release to assess the degree of cardiac injury. Myocardial infarct size was estimated macroscopically using TTC staining. Four episodes of ischaemic preconditioning markedly reduced LDH and CK release in the coronary effluent and decreased myocardial infarct size. Administration of prazosin (alpha(1) adrenoceptor antagonist) before global ischaemia reduced the extent of ischaemia-reperfusion induced myocardial injury. The cardioprotective effect of ischaemic preconditioning was abolished by prazosin and colchicine (microtubule disaggregator). On the basis of these results, it may be concluded that the cardioprotective effects of ischaemic preconditioning may be mediated through stimulation of alpha(1) adrenoceptors and translocation of PKC. (C) 2000 Academic Press.