Many investigators have reported the hemodynamics in acute cor pulmonale clinically and experimentally. However, earlier studies have not made quantitative evaluations of the effects of coronary perfusion pressure and hypoxia on right ventricular contractility. We simulated acute cor pulmonale in nine isolated canine hearts and investigated the relationship of the process to cardiac deterioration and restoration. The afterload and preload of the right ventricle were controlled with a computer-assisted load control servosystem. Coronary perfusion pressure (COPP) was also controlled at either normal or variable levels identical to products of measured cardiac output and assumed values of systemic vascular resistance. Critical state (CS) was defined as a condition with an initial decrease in peak systolic pressure despite increased afterload. Within the normal range of PaO2 (105 +/- 5.3 mmHg), CS developed at a COPP of 51 +/- 5.1 mmHg, while under low PaO2 (51 +/- 2.3 mmHg), it developed at a COPP of 59 +/- 8.8 mmHg. As long as the COPP was normal (90 mmHg), the contractility of the right ventricle did not decrease despite hypoxia (PaO2 51 +/- 2.3 mmHg). An increase in systemic vascular resistance or administration of a beta-stimulant at CS restored the contractility of the right ventricle. However, an increase in preload decreased the contractility of the right ventricle.