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[尼可地尔对缺氧状态下儿茶酚胺诱导的心肌损伤的保护作用]

[Protective effects of nicorandil against catecholamine induced myocardial damage under hypoxia].

作者信息

Hayashi J, Manabe H, Ohni M, Kasahara M, Watanabe Y

出版信息

Kokyu To Junkan. 1989 Nov;37(11):1231-5.

PMID:2532387
Abstract

Direct myocardial protective effects of Nicorandil (NR) against hypoxic injury were evaluated using an in vitro model of isolated, adult rat myocytes. Ca++-tolerant, trypan blue negative, viable cells were suspended for 1 hour in a hypoxic (Po2 20 mmHg) Eagle's MEM culture medium. Myocytes were then divided into 4 groups and incubated for 3 hours either without (control) or with norepinephrine (NE) (10(-6)M), NR (10(-4)M) or NE+NR. Cell viability ratio (trypan blue staining method) and intracellular ATP contents were measured as indexes of cell damage. NE significantly decreased the cell viability ratio compared to that in control after 1 to 3 hours. Addition of NR prevented the reduction in viability ratio produced by NE. NR markedly attenuated intracellular ATP reduction induced by NE after 1 hour incubation. These results suggest that NR has potent direct effects against hypoxia-induced cell injury in the presence of catecholamines.

摘要

使用成年大鼠分离心肌细胞的体外模型评估了尼可地尔(NR)对缺氧损伤的直接心肌保护作用。将耐Ca++、台盼蓝阴性的活细胞悬浮于缺氧(Po2 20 mmHg)的伊格尔氏MEM培养基中1小时。然后将心肌细胞分为4组,在无(对照)或有去甲肾上腺素(NE)(10(-6)M)、NR(10(-4)M)或NE+NR的情况下孵育3小时。通过台盼蓝染色法测定细胞活力比率,并将细胞内ATP含量作为细胞损伤指标进行测量。与对照相比,NE在1至3小时后显著降低了细胞活力比率。添加NR可防止NE导致的活力比率降低。孵育1小时后,NR显著减轻了NE诱导的细胞内ATP减少。这些结果表明,在儿茶酚胺存在的情况下,NR对缺氧诱导的细胞损伤具有强大的直接作用。

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