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        Remifentanil은 흰쥐의 국소 허혈-재관류 모델에서 심근 보호 효과가 있는가?

        신일우 ( Il Woo Shin ),조만석 ( Man Seok Cho ),장인석 ( In Seok Jang ),손주태 ( Ju Tae Sohn ),이헌근 ( Heon Keun Lee ),정영균 ( Young Kyun Chung ) 대한마취과학회 2009 Korean Journal of Anesthesiology Vol.57 No.2

        Background: It is known that some opioids protect the myocardial tissue from myocardial ischemia-reperfusion (I/R) injury. The aim of this study was to investigate whether remifentanil, at a clinically relevant concentration that`s during the peri-ischemic period, has a protective effect against a regional I/R injury in an in vivo rat heart model. Methods: Rats were subjected to 25 minutes of coronary artery occlusion and this was followed by 24 hours of reperfusion. A microcatheter was advanced into the left ventricle and the hemodynamic function was evaluated after 24 hours of reperfusion. The infarct size was determined by triphenyltetrazolium staining. The serum level of cardiac troponin-I (cTnI) was determined by ELISA (enzyme-linked immunosorbent assay). Results: Remifentanil administration during the peri-ischemic period didn`t show any identifiable protective effects for the hemodynamic function or to reduce the infarct size. In the control group, the peak rate of the ventricular pressure increase (+dP/dt(max)) (P<0.05) and the peak rate of the intraventricular pressure decline (-dP/dt(max) P<0.05) were significantly decreased as compared to those values for the sham group. In the remifentanil group, the +dP/dt(max) and -dP/dt(max) were not improved compared to those values of the control group. The infarct size was 45.6% of the area at risk in the control group, and the infarct size was reduced by administration of remifentanil to 43.2% in the remifentanil group. The I/R-induced serum level of cTn-I was not reduced by remifentanil infusion during the peri-ischemic period. Conclusions: Remifentanil, at a clinically relevant concentration that`s infused during the peri-ischemic period, has no myocardial protective effect after regional myocardial I/R injury in an in vivo rat heart model. (Korean J Anesthesiol 2009;57:190∼4)

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