Weisfeldt M L, Armstrong P, Scully H E, Sanders C A, Daggett W M
J Clin Invest. 1974 Jun;53(6):1626-36. doi: 10.1172/JCI107713.
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.
缺氧恢复已被证明可延长心肌收缩,尤其是舒张期。本研究旨在探讨缺氧后离体肌肉以及缺氧和急性缺血后的犬心脏中,这种收缩和舒张的延长是否会导致心跳之间不完全舒张。鉴于已知心率增加会增强收缩速度,故强调心率与不完全舒张程度之间的关系。在等长收缩的猫右心室乳头肌(12 - 120次/分钟)和犬等容左心室(120 - 180次/分钟)中,分别在缺氧前后,以递增速率起搏10秒期间,检测不完全舒张的程度。通过测量起搏期间最低舒张张力或压力与每次速率下通过中断起搏确定的真实静息张力或压力之间的差异,对不完全舒张进行量化。在八只猫乳头肌(29摄氏度)中,缺氧5分钟后,在96次/分钟和120次/分钟的速率下,不完全舒张明显更大(与缺氧前相比,P < 0.02)。在七个犬等容左心室中,缺氧恢复和较高心率也导致了不完全舒张。缺氧前180次/分钟时的不完全舒张为0.8±0.5厘米水柱,缺氧恢复5分钟时为12.6±3.5厘米水柱(P < 0.01)。对12只心脏进行了1.5 - 3分钟的急性缺血和颤动处理。除颤和再灌注后5分钟,在140次/分钟的速率下存在明显的不完全舒张。这些数据表明,不完全舒张是缺血或缺氧恢复期间舒张血流动力学的一个重要决定因素。不完全舒张的程度似乎是缺血或缺氧后舒张速度和张力发展正常化速率、心率以及所产生张力或压力大小 的函数。