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.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine