The positive inotropic effect of glucagon in the chronically failed right ventricle as demonstrated in the isolated cat heart

Previous in vitro studies has provided evidence to show that papillary muscles obtained from cats with chronic right ventricular failure had lost their ability to develop a positive inotropic response to glucagon. Since it is difficult to extrapolate from the isolated papillary muscle to the intact heart, studies were done to assess the effects of glucagon in the perfused isovolumically beating heart obtained from cats four months after surgical banding of the pulmonary artery for the experimental production of chronic right ventricular failure (CRVF). At the peak of the dose-response curve, glucagon increased right ventricular isovolumic pressure 25% (39.00 ± 4.37 to 49.67 ± 5.15 mm Hg; p < 0.001) and right ventricular dp/dt 63% (522.2 ± 93.9 to 852.6 ± 159.9 mm Hg/sec; p < 0.001) in 6 normal hearts. Similar dose related increases in right ventricular isovolumic pressure and dP/dt were obtained in 6 hearts taken from cats with chronic right ventricular failure. The respective increases in right ventricular isovolumic pressure and dP/dt were 43% (30.33 ± 4.01 to 43.67 ± 6.25 mm Hg; p < 0.025) and 73% (317.50 ± 30.29 to 550.83 ± 89.04 mm Hg/sec; p < 0.025). These results provide evidence that glucagon possesses the capacity to augment myocardial contractility in the heart with experimentally induced chronic right ventricular failure.