Contractility in Isolated Mammalian Heart Muscle after Acid-Base Changes

Abstract

In-vitro experiments performed in cat papillary muscles and strips of rat right ventricle suggest that the changes in myocardial contractility that follow acid-base disturbances are not a function of extracellular pH. Simultaneous changes in Pco₂ and NaHCO₃ concentration, with extracellular pH constant, decreased developed tension and maximal rate of rise of the tension (dT/dt) without significant changes in the time to peak tension when the muscle was exposed to the solution with higher Pco₂ and NaHCO₃ concentration. At an extracellular pH of 7.40, developed tension decreased 0.51 ± 0.13 g/mm² (P < 0.02) and dT/dt decreased 1.29 ± 0.50 g/sec (P < 0.05) with no significant change in time to peak tension (0.038 ± 0.022 sec). Changes in pH produced by increasing Pco₂ at constant NaHCO₃ concentration were followed by a significant decrease in contractility. A change of Pco₂ from 20 to 90 mm Hg that produced a change in extracellular pH from 7.60 to 7.00 was accompanied by a decrease in developed tension of 0.67 ± 0.14 g/mm² (P < 0.01), in dT/dt of 2.63 ± 0.54 g/sec (P < 0.01) with no changes in time to peak tension (0.0017 ± 0.10 seconds). We were unable to show significant variations in contractility when extracellular pH was changed at a constant Pco₂ of approximately 21 mm Hg (NaHCO₃ 7.5, 15, and 30 mM) or at a Pco₂ of approximately 95 mm Hg (NaHCO₃ 15, 30, 60, 80 and 120 mM). Only when extracellular pH reached a value as high as 8.0 (Pco₂ 21 mm Hg, NaHCO₃ 80 mM) a small but significant increase in contractility was evidenced. Either Pco₂ or intracellular pH could be the major determinants of the changes in myocardial contractility that follow acid-base alterations.