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内皮素-3诱导的大鼠心肌微血管功能不全和线粒体损伤

Endothelin-3-induced microvascular incompetence and mitochondrial damage in rat myocardium.

作者信息

Maxwell L, Pratt K, Gavin J

机构信息

Department of Pathology, University of Auckland School of Medicine, New Zealand.

出版信息

Clin Exp Pharmacol Physiol. 1992 Oct;19(10):683-8. doi: 10.1111/j.1440-1681.1992.tb00404.x.

DOI:10.1111/j.1440-1681.1992.tb00404.x
PMID:1424296
Abstract
  1. To determine the possible role of an endothelin in the development of postischaemic microvascular incompetence, isolated buffer-perfused rat hearts were perfused with endothelin-3 (ET-3) in phosphate buffer. 2. ET-3 produced a reduction in coronary flow rate, heart rate and arrhythmia. There was a marked reduction in the density of competent capillaries, and the myocytes showed vacuolation and mitochondrial damage in regions where microvascular incompetence was most severe. 3. These results indicate that ET-3 can substantially reduce microvascular perfusion in the heart and can also cause damage to the myocyte.
摘要
  1. 为了确定内皮素在缺血后微血管功能不全发展过程中可能发挥的作用,将分离的经缓冲液灌注的大鼠心脏在磷酸盐缓冲液中用内皮素-3(ET-3)进行灌注。2. ET-3导致冠状动脉血流速度、心率降低以及心律失常。有功能的毛细血管密度显著降低,并且在微血管功能不全最严重的区域,心肌细胞出现空泡化和线粒体损伤。3. 这些结果表明,ET-3可大幅降低心脏的微血管灌注,还可导致心肌细胞损伤。

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Pharmaceutics. 2022 Jun 21;14(7):1313. doi: 10.3390/pharmaceutics14071313.
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Endothelin and myocardial ischemia.内皮素与心肌缺血
Cardiovasc Drugs Ther. 1994 Aug;8(4):589-99. doi: 10.1007/BF00877413.