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尼可地尔对离体灌注大鼠心脏短暂低流量全心缺血后缺血后功能及组织腺嘌呤核苷酸的保护作用。

Protective effect of nicorandil on postischemic function and tissue adenine nucleotides following a brief period of low-flow global ischemia in the isolated perfused rat heart.

作者信息

Pieper G M, Gross G J

机构信息

Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee.

出版信息

Pharmacology. 1989;38(4):205-13. doi: 10.1159/000138539.

Abstract

A new antianginal agent, nicorandil, was tested in an isolated perfused rat heart model. Hearts were subjected to 30 min of low-flow, global ischemia followed by 30 min of reperfusion in the presence or absence of nicorandil. Nicorandil (1,500 micrograms/l) significantly improved isovolumic left ventricular minute-work during reperfusion compared to untreated hearts. Nicorandil also prevented the rebound in cardiac phosphocreatine levels and the loss of total adenine nucleotides as a result of ischemia and reperfusion. The salient effect of nicorandil was independent of any alterations in the release of endogenous prostacyclin. These results suggest that nicorandil may possess a unique cytoprotective effect on the ischemic-reperfused myocardium.

摘要

一种新型抗心绞痛药物尼可地尔,在离体灌注大鼠心脏模型中进行了测试。心脏先经历30分钟的低流量全心缺血,然后在有或没有尼可地尔存在的情况下进行30分钟的再灌注。与未处理的心脏相比,尼可地尔(1500微克/升)在再灌注期间显著改善了等容左心室每分钟做功。尼可地尔还可防止缺血再灌注导致的心肌磷酸肌酸水平反弹以及总腺嘌呤核苷酸的丢失。尼可地尔的显著作用与内源性前列环素释放的任何改变无关。这些结果表明,尼可地尔可能对缺血再灌注心肌具有独特的细胞保护作用。

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