Paradoxical effect of hypercapnia on toad heart muscle

Experiments were performed on strips dissected from toad ventricles driven at a constant frequency of 12 beats/min. After equilibration, the PCO₂ of the medium was altered from 25 to 95 mm Hg or from 95 to 25 mm Hg. Developed tension (DT) and maximal rate of tension development (dT/dt(max)) were recorded during a 30 min period after the change in PCO₂. In the first experimental series at 30°C, increasing PCO₂ resulted in a decrease in DT and dT/dt(max), followed by a recovery of contractility that reached levels higher than controls. In the 2nd and 3rd series, performed after the addition to the bath of practolol (1 x 10^-6 M) or after reserpinization, high PCO₂ depressed contractility but the recovery did not surpass control values after 30 min of hypercapnia. In this series, when high PCO₂ was replaced by low PCO₂ there was an increase in DT and dT/dt(max) followed by a decrease that reached control levels within a 30 min period. In the 4th series, at 22°C the significant decreases in DT and dT/dt(max) observed after increasing PCO₂ were followed by a recovery that surpassed control values. These results define the existence in toad cardiac muscle of a mechanism that tends to return contractility to control levels after a change in PCO₂. Within 30 min this mechanism, present even after inhibition of catecholamine action, completely counteracts the primary negative inotropic effect of high PCO₂ and the positive inotropic action of hypocapnia.