Coronary steal-induced increase in myocardial infarct size after pharmacologic coronary vasodilation. Am J Cardiol 1980 Jul;46(1):83-90
Date
07/01/1980Pubmed ID
7386397DOI
10.1016/0002-9149(80)90609-8Scopus ID
2-s2.0-0018837719 (requires institutional sign-in at Scopus site) 32 CitationsAbstract
This study was performed to determine if maximal coronary arterial vasodilation of nonischemic areas would produce an increase in myocardial infarct size through a "steal" of collateral flow from an ischemic region. Myocardial infarction was produced by a 2 hour occlusion and reperfusion of the distal left anterior descending coronary artery in anesthetized dogs. Five minutes after occlusion, 7 dogs were given saline solution, and in 12 dogs the coronary vasodilator chromonar (8 mg/kg, intravenously) was administered. Chromonar produced a significant increase (p less than 0.05) in blood flow to nonischemic regions and a concomitant decrease in flow to ischemic areas. Associated with these changes in flow was an elevation in total release and peak plasma creatine kinase compared with values in saline-treated control dogs. Myocardial infarct size determined with nitroblue tetrazolium stanining was significantly increased (p less than 0.05). These demonstarte that maximal coronary vasodilation of nonischemic areas can result in an extension of myocardial infarction by a steal of collateral flow away from the ischemic region.
Author List
Warltier DC, Gross GJ, Brooks HLMESH terms used to index this publication - Major topics in bold
AnimalsArterial Occlusive Diseases
Chromonar
Collateral Circulation
Coronary Circulation
Coronary Vessels
Coumarins
Creatine Kinase
Dogs
Hemodynamics
Male
Myocardial Infarction
Vasodilation