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Document Details : Title: Intravenous adenosine reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel Author(s): J. Zhao , Y. Yang , W. Pei , Y. Sun , J. Chen , R. Gao Journal: Acta Cardiologica Volume: 63 Issue: 3 Date: 2008 Pages: 355-359 DOI: 10.2143/AC.63.3.1020313 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. |
