Coronary steal-induced increase in myocardial infarct size after pharmacologic coronary vasodilation.
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.
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology; D002866:Chromonar / Q000494:pharmacology*; D003097:Collateral Circulation / Q000187:drug effects; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000503:physiopathology; D003374:Coumarins / Q000494:pharmacology*; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D006439:Hemodynamics; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology*; D014664:Vasodilation / Q000187:drug effects*
D003374:Coumarins; D003402:Creatine Kinase; D002866:Chromonar