Remifentanil mimics cardioprotective effect of ischemic preconditioning via protein kinase C activation in open chest of rats

• 来源期刊: 中国药理学报（英文版）
• 关键词: remifentanil myocardial ischemia precondi-tioning myocardial reperfusion injury protein kinase C chelerythrine GF109203X
• 年，卷（期）: 2005,（5）
• 页码范围: 546-550
• 页数: 5页
• 语种: 英文

摘要

Aim: To examine whether the protective effect of remifentanil preconditioning (RPC) on postischemic hearts is mediated by protein kinase (PKC) activation in comparison with ischemic preconditioning (IPC). Methods: Male Sprague-Dawley rats were anesthetized and their chests were opened. The experiment was performed with chelerythrine (CHE, 2 mg/kg), GF109203X (0.05 mg/kg) protein kinase C (PKC) inhibitors administered before RPC (remifentanil 6 μg·kg-1.min-1×3 cycle) or IPC, respectively. Infarct size (IS), as a percentage of the area at risk (AAR), was determined by triphenyltetrazolium staining. Results: In groups subjected to IPC and RPC the IS/AAR were significantly reduced (IS/AAR from 52.7%±5.5% to 12.9%±3.4%, P＜0.01 vs CON and 16.2%±6.4%, P＜0.01 vs CON), respectively. CHE and GF, both PKC inhibitors, administered 5 min before RPC or IPC completely abolished the cardioprotective effect of RPC (IS/AAR: CHE+RPC 51.2%±5.0%,GF+RPC 53.6%±6.1%, P＞0.05 vs CON) or IPC (CHE+IPC 53.7%±4.3%, GF+IPC 54.1%±6.2%, P＞0.05 vs CON). The difference was not significant in any of the hemodynamic parameters between control and treatment groups during ischemia and reperfusion. Conclusion: Remifentanil confers myocardial protection against ischemic injury through a mechanism that is similar to IPC and involves PKC activation.