Dose remifentanil have a myocardial protective effect against a regional ischemia-reperfusion injury in an in vivo rat heart model?.
10.4097/kjae.2009.57.2.190
- Author:
Il Woo SHIN
1
;
Man Seok CHO
;
In Seok JANG
;
Ju Tae SOHN
;
Heon Keun LEE
;
Young Kyun CHUNG
Author Information
1. Department of Anesthesiology and Pain Medicine, College of Medicine, Gyeongsang National University, Jinju, Korea. ykchung@nongae.gsnu.ac.kr
- Publication Type:Original Article
- Keywords:
Heart;
In vivo;
Ischemia-reperfusion injury;
Remifentanil
- MeSH:
Analgesics, Opioid;
Animals;
Coronary Vessels;
Enzyme-Linked Immunosorbent Assay;
Heart;
Heart Ventricles;
Hemodynamics;
Piperidines;
Rats;
Reperfusion;
Reperfusion Injury;
Salicylamides;
Tetrazolium Salts;
Troponin I;
Ventricular Pressure
- From:Korean Journal of Anesthesiology
2009;57(2):190-194
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
