Gazmuri R J, Berkowitz M, Cajigas H
Medical Service, Section of Pulmonary and Critical Care Medicine, North Chicago VA Medical Center, IL 60064, USA.
Crit Care Med. 1999 Aug;27(8):1542-50. doi: 10.1097/00003246-199908000-00023.
Ventricular fibrillation (VF) is known to increase myocardial oxygen requirements and to alter coronary vascular physiology. However, the significance of these effects during cardiac arrest and resuscitation is not well understood. A model was developed in the isolated rat heart to investigate the myocardial effects of VF during a simulated episode of cardiac arrest and resuscitation. We hypothesized that VF would intensify the severity of myocardial ischemia and consequently accentuate postischemic myocardial dysfunction.
Prospective and randomized.
Research laboratory.
Twenty Sprague-Dawley rats.
Hearts were harvested and perfused at a constant flow rate of 10 mL/min using a modified Krebs-Henseleit solution equilibrated with 95% oxygen and 5% CO2. In five hearts, VF was induced by a 0.05-mA current delivered to the right ventricular endocardium. The perfusate flow was then stopped for a 10-min interval and resumed at 20% of baseline flow for another 10 mins. After 20 mins of VF, the perfusate flow was returned to baseline and a sinus rhythm reestablished by epicardial electrical shocks. The studies were randomized and included three additional groups to control for the effects of ischemia without VF (n = 5), the effects of VF without ischemia (n = 5), and the stability of the preparation (n = 5).
Isovolumic indices of left ventricular function were obtained using a latex balloon advanced through the mitral valve and distended to an end-diastolic pressure of 10 mm Hg. The coronary effluent was collected from the right ventricular cavity. VF during myocardial ischemia was associated with a higher coronary effluent PCO2, increased coronary vascular resistance, and development of ischemic contracture as indicated by increases in left ventricular pressure from 9+/-3 to 33+/-6 mm Hg (p < .05). After defibrillation, contractility and relaxation rapidly returned to baseline values, whereas the isovolumic end-diastolic pressure remained elevated for 20 mins. These changes were much less prominent when ischemia was not accompanied by VF.
These findings indicate that VF may adversely affect myocardial ischemia by hastening the development of ischemic contracture, increasing coronary vascular resistance, and favoring the development of diastolic pump failure early after resuscitation from cardiac arrest.
已知室颤（VF）会增加心肌需氧量并改变冠状动脉血管生理功能。然而，在心脏骤停和复苏过程中这些影响的意义尚未得到充分理解。在离体大鼠心脏中建立了一个模型，以研究在模拟心脏骤停和复苏过程中室颤对心肌的影响。我们假设室颤会加剧心肌缺血的严重程度，从而加重缺血后心肌功能障碍。
前瞻性和随机化。
研究实验室。
20只斯普拉格 - 道利大鼠。
取出心脏，使用用95%氧气和5%二氧化碳平衡的改良克雷布斯 - 亨塞尔特溶液以10毫升/分钟的恒定流速进行灌注。在5只心脏中，通过向右心室心内膜施加0.05毫安电流诱导室颤。然后停止灌注10分钟，之后以基线流量的20%恢复灌注10分钟。室颤20分钟后，将灌注流量恢复到基线，并通过心外膜电击重新建立窦性心律。研究是随机的，还包括另外三组，以控制无室颤时的缺血影响（n = 5）、无缺血时的室颤影响（n = 5）以及标本的稳定性（n = 5）。
使用通过二尖瓣推进并膨胀至舒张末期压力为10毫米汞柱的乳胶气球获得左心室功能的等容指标。从右心室腔收集冠状动脉流出液。心肌缺血期间的室颤与冠状动脉流出液中较高的PCO2、冠状动脉血管阻力增加以及缺血性挛缩的发展相关，表现为左心室压力从9±3毫米汞柱增加到33±6毫米汞柱（p < 0.05）。除颤后，收缩性和舒张迅速恢复到基线值，而等容舒张末期压力在20分钟内仍保持升高。当缺血不伴有室颤时，这些变化则不那么明显。
这些发现表明，室颤可能通过加速缺血性挛缩的发展、增加冠状动脉血管阻力以及促进心脏骤停复苏后早期舒张期泵衰竭的发展，对心肌缺血产生不利影响。
