Zhao J L, Yang Y J, Pei W D, Sun Y H, Zhai M, Liu Y X, Gao R L
Department of Cardiology, Cardiovascular Institute and Fu-Wai Heart Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Perfusion. 2008 Mar;23(2):111-5. doi: 10.1177/0267659108094628.
It has been verified that carvedilol can attenuate myocardial no-reflow. However, the effects of carvedilol on adenosine triphosphate-sensitive K(+) (K(ATP)) channel and endothelin-1 (ET-1) are unknown. Forty mini-swines were randomized into 5 study groups: 8 control, 8 carvedilol pretreatment, 8 glibenclamide (K(ATP) channel blocker)-treated, 8 carvedilol and glibenclamide-pre-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 K(ATP) channel.
已证实卡维地洛可减轻心肌无复流现象。然而，卡维地洛对三磷酸腺苷敏感性钾（K(ATP)）通道和内皮素-1（ET-1）的影响尚不清楚。40只小型猪被随机分为5个研究组：8只作为对照组，8只进行卡维地洛预处理，8只接受格列本脲（K(ATP)通道阻滞剂）治疗，8只接受卡维地洛和格列本脲预处理，8只进行假手术。通过闭塞左前降支冠状动脉3小时后再灌注1小时建立急性心肌梗死（AMI）和再灌注模型。与对照组相比，卡维地洛显著减小了无复流面积（心肌对比超声心动图：分别从78.5±4.5%降至24.9±4.1%，病理测量：从结扎面积的82.3±1.9%降至25.8±4.3%；均p<0.01），并将坏死面积从结扎面积的98.5±1.3%降至74.4±4.7%，p<0.05。它还降低了血浆ET-1和心肌组织ET-1。然而，格列本脲消除了卡维地洛的保护作用。卡维地洛对心肌无复流的有益作用可能是由于其通过激活K(ATP)通道对ET-1产生的影响。
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