Gorlachev V I, Vizgalin A N
Kosm Biol Aviakosm Med. 1976 Jan-Feb;10(1):31-5.
An experimental impact on the rat chest in the cardiac area induced bradycardia, arrhythmia, ectopic beats, atrio-ventricular blockade that was followed by a fall of the arterial pressure and a rise in the venous pressure, a decrease of the cardiac output and blood volume. Breakages in cardiac myofibers were seen under the microscope. These changes can be brought about by a direct effect of impact accelerations on the heart. It is concluded that tolerance of the animal heart to impact accelerations is limited by bradycardia, arterial pressure fall and a 25% decrease of the cardiac output. Greater effects may produce breakages in myofibers. An active alertness and unloading of the right atrium increase the heart tolerance to impact accelerations and potassium chloride prevents hazardous cardiac arrhythmias.
对大鼠心脏区域胸部进行的实验性撞击诱发了心动过缓、心律失常、异位搏动、房室传导阻滞，随后出现动脉压下降和静脉压上升，心输出量和血容量减少。显微镜下可见心肌纤维断裂。这些变化可能是撞击加速度对心脏的直接作用所致。得出的结论是，动物心脏对撞击加速度的耐受性受到心动过缓、动脉压下降和心输出量减少25%的限制。更大的影响可能会导致肌纤维断裂。右心房的主动警觉和卸载可增加心脏对撞击加速度的耐受性，氯化钾可预防危险的心律失常。
