Protective effects of remifentanil preconditioning on myocardium against ischemia-reperfusion injury in rats
- VernacularTitle:瑞芬太尼预处理对大鼠离体心脏缺血再灌注损伤的保护作用
- Author:
Ye ZHANG
;
Erwei GU
;
Jian ZHANG
- Publication Type:Journal Article
- Keywords:
Piperidines;
Ischemic preconditioning, myocardial;
Myocardial reperfusion injury
- From:
Chinese Journal of Anesthesiology
1995;0(10):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of KATP channel in cardioprotective effects of remifentanil preconditioning (RFC) against ischemia-reperfusion (I/R) injury.Methods Forty-eight male SD rats weighing 200-250 g were killed and the hearts were immediately removed and perfused retrogradely at 100 cm H2 O with Krebs- Ringer's solution aerated with 95 % O2 and 5 % CO2 in an Langendorff apparatus. Myocardial ischemia was achieved by tightening the snare which was placed around anterior descending branch of left coronary artery and confirmed by the appearance of a regional cyanosis, decrease in coronary flow (CF) and S-T segment changes on ECG. After 15 min stabilization all hearts were subjected to 30 min ischemia followed by 120 min reperfusion. The 48 isolated hearts were randomly divided into 6 group ( n = 8 each): ( I ) I/R group; ( II ) RPC group received 3 episodes of 5 min remifentanil (100 ?g ? L-1 ) perfusion at 5 min interval before ischemia; ( III ) HMR group; (IV ) 5-HD group; ( V ) HMR + RPC group and ( VI) 5-HD + RPC group. Group III and IV received HMR-1098, a selective sarcolemmal KATP channel blocker (1? 10-4 mol?L-1 ) or 5-HD, a selective mitochondrial KATP channel blocker (1 ? 10 3 mol?L-1 ) perfusion for 45 min before ischemia. In group V and \1 HMR-1098 or 5-HD perfusion was started 10 min before RPC. Infarct size (IS) was determined by 2, 3, 5-triphenyl-tetrazolium staining. Coronary outflow was collected and recorded and lactate dehydrogenase (LDH) activity in coronary outflow was measured. Results The infarct size was significantly smaller and significantly less LDH was released in group II (RPC) than in I/R group. The protective effects of RPC was abolished by pretreatrnent with 5-HD but not HMR-1098. RPC and HMR-1098 caused a slight but significant increase in CF, however there was no significant difference in CF among ail groups during ischemia and reperfusion. Conclusion Mitochondrisl KATP channel activation is involved in the protective effect of RPC on myocardium against I/R injury.
