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血管紧张素在缺血预处理心脏保护作用中的作用。

Role of angiotensin in cardioprotective effect of ischemic preconditioning.

作者信息

Sharma A, Singh M

机构信息

Department of Pharmaceutical Sciences & Drug Research, Punjabi University, Patiala, India.

出版信息

J Cardiovasc Pharmacol. 1999 May;33(5):772-8. doi: 10.1097/00005344-199905000-00014.

Abstract

This study was designed to investigate the role of angiotensin (Ang II) in the cardioprotective effect of ischemic preconditioning. Isolated perfused rat heart was subjected to global ischemia for 30 min followed by reperfusion for 120 min. Coronary effluent was analyzed for lactate dehydrogenase (LDH) and creatine kinase (CK) release to assess the degree of cardiac injury. Myocardial infarct size was estimated macroscopically by using triphenyl tetrazolium chloride (TTC) staining. Four episodes of ischemic/Ang II preconditioning markedly reduced LDH and CK release in the coronary effluent and decreased myocardial infarct size. The cardioprotective effect of Ang II preconditioning was abolished by CV 11974, AT1-receptor antagonist, whereas no such effect was noted with CV 11974 in ischemic preconditioning. PD 123319, AT2-receptor antagonist, produced no marked effect on Ang II preconditioning and ischemic preconditioning induced reduction in myocardial injury. On the basis of these results, it may be concluded that activation of AT1 receptors may be involved in angiotensin-induced pharmacologic preconditioning. But it may not be involved in the cardioprotective effect of ischemic preconditioning in isolated rat heart.

摘要

本研究旨在探讨血管紧张素(Ang II)在缺血预处理心脏保护作用中的作用。将离体灌注的大鼠心脏进行30分钟的全心缺血,随后再灌注120分钟。分析冠脉流出液中的乳酸脱氢酶(LDH)和肌酸激酶(CK)释放量,以评估心脏损伤程度。使用氯化三苯基四氮唑(TTC)染色宏观估计心肌梗死面积。四次缺血/Ang II预处理明显减少了冠脉流出液中LDH和CK的释放,并减小了心肌梗死面积。CV 11974(一种AT1受体拮抗剂)消除了Ang II预处理的心脏保护作用,而在缺血预处理中CV 11974未产生此作用。AT2受体拮抗剂PD 123319对Ang II预处理以及缺血预处理诱导的心肌损伤减轻均未产生明显影响。基于这些结果,可以得出结论:AT1受体的激活可能参与了血管紧张素诱导的药物预处理。但它可能不参与离体大鼠心脏缺血预处理的心脏保护作用。

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