1 Institute of Physiology, La Plata School of Medicine, La Plata, Argentina
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.
Submitted on April 29, 1969
Accepted on December 4, 1969
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