期刊论文详细信息
Brief antecedent ischemia attenuates platelet-mediated thrombosis in damaged and stenotic canine coronary arteries - Role of adenosine
Article; Proceedings Paper
关键词: CYCLIC FLOW VARIATIONS;    ENDOTHELIAL INJURY;    MYOCARDIAL-ISCHEMIA;    BLOOD-FLOW;    AGGREGATION;    DOGS;    ANGIOPLASTY;    RECEPTORS;    ANGINA;    MODEL;   
DOI  :  10.1161/01.CIR.97.7.692
来源: SCIE
【 摘 要 】

Background-Recent studies suggest that patients with angina before myocardial infarction exhibit improved recovery of coronary perfusion after thrombolysis by an as-yet-unknown mechanism, We therefore proposed that brief antecedent ischemia/reperfusion may, via release of adenosine, improve vessel patency in damaged and stenotic coronary arteries. Methods and Results-Anesthetized dogs underwent coronary injury+stenosis, resulting in repeated cyclic variations in coronary blood now (CFVs) caused by the formation/dislodgment of platelet-rich thrombi. Vessel patency was assessed for 3 hours after stenosis by quantification of the nadir of the CFVs, duration of total thrombotic occlusion (flow=0), and area of the now-time profile (expressed as percent of baseline flowx180 minutes), In protocol 1, dogs received 10 minutes of coronary occlusion+10 minutes of reflow or a comparable 20-minute control period before injury+stenosis, The median nadir of the CFVs was higher (4.0 versus 0.3 mL/min), median zero flow duration per 30-minute time interval was shorter (0.4 versus 15.1 minutes), and mean percent flow-time area was greater (54+/-8% versus 28+9%) in dogs that received antecedent ischemia versus controls (P<.05). These benefits of antecedent ischemia/reperfusion were largely mimicked by a 10-minute intracoronary adenosine infusion (400 mu g/min) in lieu of brief ischemia (protocol 2) and were abolished by administration of the adenosine A(1)/A(2) receptor antagonist PD 115,199 (3 mg/kg IV) before brief antecedent coronary occlusion (protocol 3). Conclusions-Brief antecedent ischemia attenuates subsequent platelet-mediated thrombosis in damaged and stenotic canine coronary arteries, due, in large part, to an adenosine-mediated mechanism.

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