Fang Xiangshao, Tang Wanchun, Sun Shijie, Huang Lei, Chang Yun-Te, Huang Zitong, Weil Max Harry
Weil Institute of Critical Care Medicine, 35100 Bob Hope Dr., Rancho Mirage, CA 92270, USA.
J Appl Physiol (1985). 2006 Oct;101(4):1091-6. doi: 10.1152/japplphysiol.01487.2005. Epub 2006 Jun 22.
Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.
我们团队已经建立了一种心脏骤停和心肺复苏(CPR)的大鼠模型。然而,当前的大鼠模型使用的是健康成年动物。为了更紧密地模拟患有慢性冠状动脉疾病的人类发生心脏骤停和心肺复苏的情况,我们研究了在心脏骤停和心肺复苏期间冠状动脉缩窄的大鼠模型。在麻醉、机械通气的Sprague-Dawley大鼠中通过手术诱导左冠状动脉缩窄。在手术前及术后4周使用超声心动图测量整体心脏功能。在干预后4周,即诱发心室颤动(VF)之前,冠状动脉缩窄导致射血分数显著降低、左心室舒张末期容积增加以及左心室收缩末期容积增加。在未经处理的室颤6分钟后,对三组动物进行心肺复苏:1)冠状动脉缩窄组,2)假手术组,3)对照组(未进行前期手术)。心肺复苏6分钟后尝试除颤。所有动物均成功复苏。与假手术组和对照组相比,冠状动脉缩窄组复苏后心肌功能(通过左心室压力在40 mmHg时的上升速率和左心室压力下降速率来衡量)受损更显著,左心室舒张末期压力更高。各组成功复苏所需的总电击能量和存活时间没有差异。总之,这种慢性心肌缺血大鼠模型在干预后4周与心室重构和左心室心肌功能障碍相关,随后与严重的复苏后心肌功能障碍相关。该模型为进一步开展与心脏骤停和心肺复苏相关的临床研究提供了思路。