Abstract
1. Effbcts of coronary occlusion and subsequent reoxygenation by release of occlusion on ventricular contractility and electrical activity were investigated using the blood-perfused papillary muscle of the canine right ventricle paced at 120/min at a constant temperature of 38-39°C.
2. In the early phase of hypoxia, 60-90 sec after occlusion, the maximal rate of tension development (dT/dt) was accelerated significantly, while the developed tension was decreased as a consequence of the shortening of the contractile process.
3. The acceleration of dT/dt was related to the number of contractions at 120-180 beats after the occlusion and was not affected by propranolol or reserpine pretreatment.
4. During reoxygenation following the release of occlusion the developed tension increased rapidly above control values in 45 sec as a result of a prolongation of the contractile process. The overshoot of developed tension lasted for 900 sec after release of occlusion, and dT/dt was depressed significantly throughout the period of reoxygenation.
5. During reoxygenation following various periods of occlusion from 15 to 180 sec, graded depression of dT/dt and prolongation of contraction occurred. These changes were closely correlated with the magnitudeand duration of reactive hyperemia.
6. The overshoot of contraction was markedly reduced by propranolol or reserpine pretreatment. The maximal response of reactive hypermia was not affected by propranolol, but the responses 30 and 60 sec atter release of occlusion were significantly decreased by propranolol.
7. Electrograms of the muscle (EMG) changed little during hypoxia and subsequent reoxygenation in contrast to the marked and characteristic changes in contraction.
