Incomplete relaxation between beats after myocardial hypoxia and ischemia.
Recovery from hypoxia has been shown to prolong cardiac muscle contraction, particularly the relaxation phase. The present studies were designed to examine whether incomplete relaxation between beats can result from this prolongation of contraction and relaxation in isolated muscle after hypoxia and in the canine heart after both hypoxia and acute ischemia. The relationship between heart rate and the extent of incomplete relaxation is emphasized in view of the known enhancement of the velocity of contraction caused by increasing heart rate. The extent of incomplete relaxation during 10-s periods of pacing at increasing rates was examined before and after hypoxia in isometric cat right ventricular papillary muscle (12-120 beats/min) and in the canine isovolumic left ventricle (120-180 beats/min). Incomplete relaxation was quantified by measuring the difference between the lowest diastolic tension or pressure during pacing and the true resting tension or pressure determined by interruption of pacing at each rate. In eight cat papillary muscles (29 degrees C), there was significantly greater incomplete relaxation 5 min after hypoxia at rates of 96 and 120 beats/min (P < 0.02 vs. before hypoxia). In seven canine isovolumic left ventricles, recovery from hypoxia and higher heart rates also resulted in incomplete relaxation. Incomplete relaxation before hypoxia at a rate of 180 beats/min was 0.8+/-0.5 cm H(2)O and at 5 min of recovery from hypoxia was 12.6+/-3.5 cm H(2)O (P < 0.01). 12 hearts were subjected to a 1.5-3-min period of acute ischemia and fibrillation. There was significant incomplete relaxation at a rate of 140 beats/min for 5 min after defibrillation and reperfusion. These data indicate that incomplete relaxation is an important determinant of diastolic hemodynamics during recovery from ischemia or hypoxia. The extent of incomplete relaxation appears to be a function of the rate of normalization of the velocity of relaxation and tension development after ischemia or hypoxia, the heart rate, and the magnitude of developed tension or pressure.
D000818:Animals; D001794:Blood Pressure; D002415:Cats; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D004285:Dogs; D004554:Electric Countershock; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology; D010210:Papillary Muscles / Q000503:physiopathology; D010477:Perfusion; D014693:Ventricular Fibrillation / Q000503:physiopathology