Myocardial intracellular pH in a perfused rainbow trout heart during extracellular acidosis in the presence and absence of adrenaline.
Myocardial intracellular pH was measured in a perfused rainbow trout, Salmo gairdneri, with DMO (5,5-dimethyl-2,4-oxazlidinedione), to test the hypothesis that catecholamines promote active regulation of myocardial pH in order to protect contractility during a respiratory acidosis comparable to that observed after exercise. Under control conditions (extracellular pH = 8.0; PCO2 = 2 Torr), myocardial pH was 7.53 +/- 0.01 (N = 5). Acidosis (extracellular pH = 7.45; PCO2 = 8.6 Torr) reduced contractility, mechanical efficiency and intracellular pH (7.25 +/- 0.04), but did not affect myocardial O2 consumption. The addition of 0.5 mumol l-1 adrenaline during extracellular acidosis prevented the loss of contractility, restored mechanical efficiency, but did not change intracellular pH significantly. Thus, adrenaline enabled cardiac contractility to recover, without intracellular pH regulation, possibly by modulation of sarcolemmal calcium changes. The absence of a myocardial acidosis after exercise in vivo is discussed with respect to possible intracellular pH regulation via lactate uptake and metabolism.
D000138:Acidosis / Q000503:physiopathology*; D000818:Animals; D001639:Bicarbonates / Q000032:analysis; D004837:Epinephrine / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion; D014337:Trout
D001639:Bicarbonates; D004837:Epinephrine