Morris J J, Hamm D P, Pellom G L, Abd-Elfattah A, Wechsler A S
Department of Surgery, Duke University Medical Center, Durham, N.C. 27710.
J Thorac Cardiovasc Surg. 1988 Oct;96(4):590-9.
The hemodynamic manifestations of right ventricular dysfunction after ischemic injury depend not only on the severity of injury but also on the degree of coexistent left ventricular dysfunction. A better understanding of right ventricular failure and of optimal therapies has been hindered in part by lack of suitable experimental models of selective and differential ventricular injury. Therefore, we developed a technique of differential ventricular myocardial protection during a period of global cardiac ischemia and examined the effect of such an injury on intrinsic right and left ventricular myocardial function, metabolism, and regional blood flow. Twenty-six dogs were subjected to 30 minutes of ischemia while being supported by cardiopulmonary bypass. During ischemia, right and left ventricular myocardial temperatures were independently varied by selective ventricular endomyocardial thermal regulation. Nine dogs underwent right and left ventricular normothermic ischemia, eight underwent right and left ventricular hypothermic ischemia, and nine underwent right ventricular normothermic and left ventricular hypothermic ischemia. In both ventricles, normothermic ischemia resulted in greater depression of ventricular ability to generate stroke work as a function of end-diastolic dimension (p less than 0.05), greater depletion of myocardial adenine nucleotide content (p less than 0.05), and greater subendocardial reperfusion hyperemia (p less than 0.05). Myocardial temperature of the contralateral ventricle during ischemia had no effect (p = not significant) on intrinsic ventricular functional, metabolic, or regional blood flow response to injury. For a given degree of right ventricular injury assessed by these parameters, the degree of left ventricular injury could be independently varied by as much as 50%. This is a particularly suitable model for the investigation of acute right ventricular failure.
缺血性损伤后右心室功能障碍的血流动力学表现不仅取决于损伤的严重程度,还取决于并存的左心室功能障碍的程度。部分由于缺乏选择性和差异性心室损伤的合适实验模型,对右心室衰竭及最佳治疗方法的深入理解受到了阻碍。因此,我们开发了一种在全心缺血期间进行差异性心室心肌保护的技术,并研究了这种损伤对右心室和左心室心肌固有功能、代谢及局部血流的影响。26只狗在体外循环支持下经历30分钟的缺血。在缺血期间,通过选择性心室心内膜热调节独立改变右心室和左心室心肌温度。9只狗经历右心室和左心室常温缺血,8只狗经历右心室和左心室低温缺血,9只狗经历右心室常温缺血和左心室低温缺血。在两个心室中,常温缺血导致作为舒张末期容积函数的心室产生每搏功能力的更大降低(p<0.05)、心肌腺嘌呤核苷酸含量的更大消耗(p<0.05)以及更大的心内膜下再灌注充血(p<0.05)。缺血期间对侧心室的心肌温度对心室对损伤的固有功能、代谢或局部血流反应没有影响(p=无显著性差异)。对于通过这些参数评估的给定程度的右心室损伤,左心室损伤程度可独立变化达50%。这是一个特别适合研究急性右心室衰竭的模型。