A possible role of noradrenaline in the development of myocardial infarction: an experimental study in the isolated rat heart.
Isolated rat hearts were perfused with buffer containing noradrenaline 10(-7) to 10(-4) M. A dose-dependent depletion of glycogen and ATP were seen together with a leakage of ASAT and creatine phosphokinase (CK). The damage induced by noradrenaline could be prevented by addition of a beta-blocker (metoprolol), verapamil, or lidocaine to the perfusion medium. When the endogenous myocardial stores of noradrenaline are rapidly depleted by perfusion with tyramine a similar cell damage was demonstrated. Electron micrographs from hearts subjected to noradrenaline showed three different types of cell damage that could be correlated to earlier described findings. The importance of noradrenaline for the ischemic injury was demonstrated. It was hypothesized that acute myocardial infarction may start because of a sudden release of endogenous noradrenaline.
D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D008297:Male; D008929:Mitochondria, Heart / Q000648:ultrastructure; D009203:Myocardial Infarction / Q000139:chemically induced* / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology / Q000648:ultrastructure; D009210:Myofibrils / Q000648:ultrastructure; D009638:Norepinephrine / Q000494:pharmacology* / Q000502:physiology; D010477:Perfusion; D051381:Rats
D003402:Creatine Kinase; D009638:Norepinephrine