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|本期目录/Table of Contents|

“缺氧后处理”对大鼠缺氧2复氧心室肌细胞的保护作用X(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
1999年第4期
页码:
241-242
栏目:
研究快报
出版日期:
1999-07-01

文章信息/Info

Title:
“Hypoxic postconditioning”Protecting cardiac myocyte from hypoxia/reoxygenation injury in adult rats
作者:
高 峰1　Yan WL3　Geng YJ3　蔡振杰2　朱妙章1　臧益民1　马新亮1
第四军医大学　1基础部生理学教研室　2西京医院心血管外科中心, 西安 710032,3Cardiovascular Research Institute,Allegheny University of the Health Sciences, Pittsburgh, PA,USA
Author(s):
Gao Feng1;  Yan WL3;  Geng YJ3;  Cai Zhen-Jie2;  Zhu Miao-Zhang1;  Zang Yi-Min1; Ma Xin-Liang1
1Department of Physiology, Fourth Military Medical University; 2Cardiovascular Surgical Center, Xijing Hospital, Xi’an 710032, China; 3Cardiovascular Research Institute,Allegheny University of the Health Scoences, Pittsburgh, PA ,USA
关键词:
心肌细胞　缺氧-复氧损伤　一氧化氮　凋亡
Keywords:
cardiac myocyte　hypoxia/reoxygenation　intric oxide　apoptosis
分类号:
-
DOI:
-
文献标识码:
-
摘要:
采用模拟再灌的缺氧2复氧模型,在细胞水平直接观察到缺氧2复氧可致心肌细胞产生一氧化氮明显增加,并诱导心肌细胞凋亡; 首次发现“缺氧后处理”可减轻心肌复氧损伤, 明显提高心肌细胞存活率(P<0.05)。为更有效救治心肌缺血提供了新的依据。
Abstract:
Using adult rat cardiac myocyte hypoxia/recoxygenation model, we directly observed the marked elevated nitric oxide production of isolated cardiomyocytes induced by hypoxia/reoxygenation,with was accompanied by the increased myocyte apoptosis. The results of the present study demonstrate, for the first time, that“ hypoxic postconditioning”protect cardiac myocyte from reoxygen injury, and thus significantly increase cardiac myocyte viability.

参考文献/References

［1］Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischem icmyocardium. Circulation, 1986; 74 (5) : 1124.

［2］Kim SJ , Iizuka K, Kelly RA , et al. An alpha-cardiacmyosin heavy chain gene mutation impairs contraction and relaxation function of cardiac myocytes. Am J Physiol, 1999, 276 (5 Pt 2) : H1780.

［3］Webster KA , Discher DJ , Bishopric NH. Cardioprotection in an in vitro model of hypoxic preconditioning. J Mol Cell Cardiol, 1995;27 (1) : 453.

［4］Ma XL , Kumar S, Gao F, et al. Inhibition of p38m itogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion. Circulation, 1999; 99 (13) : 1685.

备注/Memo

备注/Memo:
(收稿1999-06-07)
更新日期/Last Update: 1999-07-01