Energy metabolism in the infarcted cardiac muscle: the interaction of contractile protein and mitochondria.
In order to investigate the behavior of the energy-converting system in the myocardium, an experimental in vitro model was developed which consisted of contractile protein (myosin B) and mitochondria (Mit) prepared from canine cardiac muscle. In this system, ATP produced in Mit from added ADP caused the superprecipitation of the myosin B (My-B). One hour after the onset of experimental myocaridal infarction in the dog, the superprecipitation was very low in the system if Mit prepared from the infarcted myocardium were used, regardless of the origin of the myosin B. The respiratory control index of Mit prepared from infarcted was lower than that from noninfarcted myocardium, but the ADP:O ratio in Mit from infarcted myocardium, was little deteriorated. The findings indicate that a transferring process of an energy source from Mit to myosin B was markedly impaired in the infarcted myocardium. They also throw light on the mechanism by which the myocardium ceases its contraction at an early stage of infarction.
D000818:Animals; D000968:Antimycin A / Q000494:pharmacology; D001386:Azides / Q000494:pharmacology; D004140:Dinitrophenols / Q000494:pharmacology; D004285:Dogs; D006321:Heart / Q000503:physiopathology; D007700:Kinetics; D008931:Mitochondria, Muscle / Q000187:drug effects / Q000378:metabolism*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects
D001386:Azides; D004140:Dinitrophenols; D000968:Antimycin A; D009218:Myosins