TITLE

Carvedilol reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel

AUTHOR(S)
Zhao, J. L.; Yang, Y. J.; Pei, W. D.; Sun, Y. H.; Zhai, M.; Liu, Y. X.; Gao, R. L.
PUB. DATE
March 2008
SOURCE
Perfusion;Mar2008, Vol. 23 Issue 2, p111
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
It has been verified that carvedilol can attenuate myocardial no-reflow. However, the effects of carvedilol on adenosine triphosphate-sensitive K+ (KATP) channel and endothelin-1 (ET-1) are unknown. Forty mini-swines were randomized into 5 study groups: 8 control, 8 carvedilol pretreatment, 8 glibenclamide (KATP channel blocker)-treated, 8 carvedilol and glibenclamidepre- treated and 8 sham-operated. An acute myocardial infarction(AMI) and reperfusion model was created with a three-hour occlusion of the left anterior descending coronary artery followed by one-hour reperfusion. Compared with the control group, carvedilol significantly decreased the area of no-reflow (myocardial contrast echocardiography: from 78.5±4.5% to 24.9±4.1%, pathological means: from 82.3±1.9% to 25.8±4.3% of ligation area, respectively; all p < 0.01) and reduced necrosis size from 98.5±1.3% to 74.4±4.7% of ligation area, p < 0.05). It also decreased plasma ET-1 and myocardial tissue ET-1. However, glibenclamide abrogated the protective effect of carvedilol. The beneficial effect of carvedilol on myocardial no-reflow could be due to its effect on ET-1 via the activation of the KATP channel. Perfusion (2008) 23, 111-115.
ACCESSION #
34706127

 

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