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首页> 外文期刊>Pharmacological research: The official journal of The Italian Pharmacological Society >Possible mechanism of cardioprotective effect of ischaemic preconditioning in isolated rat heart.
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Possible mechanism of cardioprotective effect of ischaemic preconditioning in isolated rat heart.

机译:缺血预处理对离体大鼠心脏心脏保护作用的可能机制。

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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. Copyright 2000 Academic Press.
机译:本研究旨在研究缺血预处理的心脏保护作用机理。分离的灌流大鼠心脏经受全脑缺血30分钟,然后再灌注120分钟。分析冠状流出物的LDH和CK释放,以评估心脏损伤的程度。使用TTC染色宏观评估心肌梗塞面积。缺血预处理的四次发作显着降低了冠状流出物中的LDH和CK释放,并减少了心肌梗塞面积。在全局缺血之前给予哌唑嗪(α(1)肾上腺素能受体拮抗剂)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(微管分解剂)取消了缺血预处理的心脏保护作用。根据这些结果,可以得出结论,缺血预处理的心脏保护作用可能是通过刺激α(1)肾上腺素能受体和PKC转运来介导的。版权所有2000学术出版社。

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