Intravenous adenosine reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive KM+ channel

Abstract

It has been verified that adenosine can attenuate myocardial no-reflow. However, the effects of adenosine on adenosine triphosphate-sensitive K+ (KATP) channel and endothelin-1 (ET-1) are unknown.Methods — Forty mini-swines were randomized into 5 study groups: 8 in the control group, 8 in the adenosine pretreatment group, 8 in the glibenclamide (KATP channel blocker)-treated group, 8 in the adenosine and glibenclamide-pretreated group and 8 in the sham-operated group. An acute myocardial infarction and reperfusion model was created with three-hour occlusion of the left anterior descending coronary artery followed by a one-hour reperfusion.Results — Compared with the control group, adenosine significantly decreased the area of no-reflow (myocardial contrast echocardiography: from 78.5 ± 4.5% to 20.7 ± 4.1%, pathological means: from 82.3 ± 1.9% to 21.5 ± 4.3% of ligation area, respectively; all P < 0.01), reduced necrosis size from 98.5 ± 1.3% to 75 ± 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 adenosine.Conclusion — The beneficial effect of adenosine on myocardial no-reflow could be due to its effect on ET-1 via the activation of KATP channel.