Effects of Halothane on Endothelin-1 Production in coronary Circulation following Myocardial Ischemia-Reperfusion in Dogs.
10.4097/kjae.1994.27.7.669
- Author:
Byu Rha KIM
1
;
Myung Ha YOON
;
Kyung Yeon YOO
;
Chan Jin PARK
Author Information
1. Department of Anesthesiology, Chonnam National University Medical School, Kwangju, Korea.
- Publication Type:Original Article ; In Vitro
- Keywords:
Endothelin;
Myocardial ischemia;
Halothane
- MeSH:
Anesthesia;
Animals;
Blood Vessels;
Coronary Circulation*;
Coronary Vessels;
Dogs*;
Endothelin-1*;
Endothelins;
Endothelium, Vascular;
Femoral Artery;
Halothane*;
Myocardial Ischemia;
Myocardium;
Plasma;
Reperfusion;
Veins
- From:Korean Journal of Anesthesiology
1994;27(7):669-677
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Endothelin (ET), a vascular endothelium derived contracting factor, provokes a strong and long lasting contraction of blood vessels, including coronary artery. Chemical stirnuli such as Ca++ ionophore (in vitro) and myocardial ischemia (in vivo) are known to promote the production of ET. Since halothane has recently been shown to block Ca++ channel, it might blunt ET-1 release or production from ischemic myocardium. To test this hypothesis, open-chest dogs underwent eitber 15 minutes (n=7) of the left anterior descending coronary artery (LAD) occlusion or 30 minutes (n=7) and 120 minutes of reperfusion under the halothane anesthesia. Plasma concentration of ET-1 in the femoral artery (FA) and the great cardiac vein (CV) draining ischemic myocardium was measured using radioimmunoas-say. ET-1 production (pg/mL) was calculated by substrating the ET-1 levels in FA from those in CV. The results were as follows; 1) Baseline ET-1 levels in FA and CV were similar in both groups. 2) ET-1 levels in FA and CV remained unchanged during myocardial ischemia in both groups. 3) ET-1 production significantly increased from baseline at 30, 60 and 120 min into reperfusion, respectively, in the 30 min group, whereas no significant changes were observed from baseline in the 15 min group. These findings indicate that halothane may blunt, but could not block the production or release of ET-1 completely during myocardial ischemia-reperfusion, especially in the case of prolonged coronary arterial occlusion.
