Is early decline of cardiac function in ischaemia due to carbon-dioxide retention?
There is no satisfactory explanation for the early and rapid decline of cardiac muscle function in ischaemia. Reduction of the energy source for contraction, A.T.P., is insufficient in magnitude and too slow in onset to be the prime cause. It is proposed that a large part of the loss of function is directly attributable to an immediate fall of intracellular pH and results from the accumulation of carbon dioxide and lactic acid; the intracellular acidosis reduces myocardial function by inhibition of that part of the calcium-ion influx associated with contraction.
D000138:Acidosis / Q000209:etiology; D000255:Adenosine Triphosphate / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000378:metabolism; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D013997:Time Factors
D007773:Lactates; D002245:Carbon Dioxide; D000255:Adenosine Triphosphate; D002118:Calcium