Factors affecting the loss of mitochondrial function in autolyzing cardiac muscle.
Rates of loss of mitochondrial respiratory function were monitored during autolyses of canine myocardial samples pretreated so as to affect tissue pH and/or tissue ATP content prevailing during tissue autolysis. When autolyses occurred under conditions of differing tissue pH, but at nearly identical tissue ATP levels, the rate of loss of mitochondrial function was virtually unchanged suggesting that tissue acidosis in the absence of a concomitant tissue ATP differential had little or no effect upon the rate of progression of mitochondrial damage. In a second comparison, autolyses were carried out at constant tissue pH, but where tissue ATP content differed dramatically. Here, the rate of loss of mitochondrial function was increased markedly suggesting that tissue ATP depletion in the absence of a concomitant tissue pH differential had a major effect upon the rate of loss of mitochondrial function. Thus, of the two parameters studied, tissue ATP content alone was far more important than tissue pH alone in determining the rate of cell membrane damage during ischemia. Finally, autolyses were carried out where both tissue pH and ATP content differed. Here, an even more dramatic increase in the rate of progression of mitochondrial damage occurred suggesting the operation of synergism between tissue ATP depletion and acidosis in promoting cell injury in ischemic cardiac muscle.
D000138:Acidosis / Q000503:physiopathology; D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001329:Autolysis / Q000503:physiopathology*; D003327:Coronary Disease / Q000503:physiopathology; D004285:Dogs; D005260:Female; D006863:Hydrogen-Ion Concentration; D007461:Iodoacetates / Q000494:pharmacology; D008297:Male; D008929:Mitochondria, Heart / Q000502:physiology*; D010101:Oxygen Consumption
D007461:Iodoacetates; D000255:Adenosine Triphosphate