Emulsified isoflurane postconditioning produces cardioprotection against myocardial ischemia-reperfusion injury in rats

被引:20
|
作者
Hu, Zhao-Yang [1 ,2 ]
Abbott, Geoffrey W. [3 ]
Fang, Ya-Dong [4 ]
Huang, Yue-Sheng [4 ]
Liu, Jin [1 ,2 ]
机构
[1] Sichuan Univ, Dept Anesthesiol, West China Hosp, Chengdu 610041, Peoples R China
[2] Sichuan Univ, Translat Neurosci Ctr, West China Hosp, Chengdu 610041, Peoples R China
[3] Univ Calif Irvine, Sch Med, Dept Pharmacol Physiol & Biophys, Irvine, CA 92717 USA
[4] Third Mil Med Univ, State Key Lab Trauma Burn & Combined Injury, Inst Burn Res, Southwest Hosp, Chongqing, Peoples R China
来源
JOURNAL OF PHYSIOLOGICAL SCIENCES | 2013年 / 63卷 / 04期
基金
中国国家自然科学基金;
关键词
Emulsified isoflurane; Ischemia and reperfusion injury; Cardioprotection; MITOCHONDRIAL PERMEABILITY TRANSITION; K-ATP CHANNELS; VOLATILE ANESTHETICS; INHALED ISOFLURANE; CARDIAC PROTECTION; BCL-2; FAMILY; RABBITS; APOPTOSIS; INFARCTION; INHIBITION;
D O I
10.1007/s12576-013-0261-z
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Emulsified isoflurane (EIso) preconditioning can induce cardioprotection. We investigated whether EIso application after ischemia protects hearts against reperfusion injury and whether it is mediated by the inhibition of apoptosis. Rats were subjected to 30-min coronary occlusion followed by 180-min reperfusion. At the onset of reperfusion, rats were intravenously administered saline (sham, control group), 30 % intralipid (IL group) or 2 ml kg(-1) EIso (EIso group) for 30 min. After reperfusion, infarct sizes, myocardial apoptosis and expression of Bcl-2, Bax and caspase-3 proteins were determined. Hemodynamic parameters were not different among groups. Compared with control and intralipid group, EIso limited infarct size, inhibited apoptosis, increased the expression of Bcl-2, decreased the expression of Bax, cleaved caspase-3, and enhanced Bcl-2/Bax ratio. EIso protects hearts against reperfusion injury when administered at the onset of reperfusion, which may be mediated by the inhibition of apoptosis via modulation of the expression of pro- and anti-apoptotic proteins.
引用
收藏
页码:251 / 261
页数:11
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