Murphy C O, Gott J P, Guyton R A
Department of Surgery, Emory University School of Medicine, Atlanta, Georgia, USA.
Ann Thorac Surg. 1995 Oct;60(4):1021-7. doi: 10.1016/0003-4975(95)00580-e.
The effects of three techniques of cardioplegic arrest on endothelium-dependent microvascular function of the right and left ventricles were examined in a canine model of cardiopulmonary bypass.
Oxygenated cold crystalloid cardioplegia and cold blood cardioplegia groups, (n = 11 each) had hypothermic cardiopulmonary bypass (28 degrees C), topical cooling, antegrade arrest, and intermittent antegrade delivery. A warm blood cardioplegia group (n = 11) had normothermic cardiopulmonary bypass (37 degrees C), antegrade arrest, and continuous antegrade delivery. All groups underwent cardioplegic arrest for 1 hour followed by 1 hour of reperfusion. Dogs that did not have instrumentation were used as controls (n = 10). Coronary microvessels (100 to 200 microns in internal diameter) were examined in a pressurized, no-flow state with video microscopic imaging and electronic dimension analysis.
Ischemic arrest with cold crystalloid cardioplegia significantly (p < 0.05) impaired endothelium-dependent relaxations in both ventricles to acetylcholine (left ventricle, 69% +/- 4%, and right ventricle, 73% +/- 5%, versus control left ventricle, 100% +/- 0.3%, and control right ventricle, 100% +/- 0.3%) and the calcium ionophore (left ventricle, 70% +/- 6%, and right ventricle, 68% +/- 3%, versus control left ventricle, 98% +/- 1%, and control right ventricle, 98% +/- 1%). In the cold blood cardioplegia group, endothelium-dependent relaxations to acetylcholine (left ventricle, 96% +/- 1%, and right ventricle, 87% +/- 4%) and the calcium ionophore (left ventricle, 88% +/- 3%, and right ventricle, 78% +/- 7%) were preserved. In the warm blood cardioplegia group, endothelium-dependent responses to acetylcholine (92% +/- 3%) and the calcium ionophore (96% +/- 1%) were preserved in the left ventricle, but the right ventricle showed reduced (p < 0.05) reactivity to the endothelium-dependent acetylcholine (77% +/- 8%) and the calcium ionophore (69% +/- 8%). Endothelium-independent relaxation to sodium nitroprusside was similar to controls in all groups for both ventricles, thus indicating normal smooth muscle responsiveness.
Cardioplegic arrest with cold blood cardioplegia preserved the endothelium-dependent response in the right and left ventricles, whereas cold crystalloid cardioplegia impairs this response. Warm blood cardioplegia preserved the endothelium-dependent response in the left ventricle, but this response was reduced in the right ventricle. This suggests that blood cardioplegia and hypothermia may be important in protection of microvascular endothelium and that the right ventricle may be more vulnerable to damage than the left ventricle.
在犬体外循环模型中，研究了三种心脏停搏技术对左右心室内皮依赖性微血管功能的影响。
氧合冷晶体心脏停搏组和冷血心脏停搏组（每组n = 11）进行低温体外循环（28℃）、局部降温、顺行灌注停搏和间歇性顺行给药。温血心脏停搏组（n = 11）进行常温体外循环（37℃）、顺行灌注停搏和持续顺行给药。所有组均进行1小时心脏停搏，随后再灌注1小时。未进行仪器植入的犬用作对照组（n = 10）。采用视频显微镜成像和电子尺寸分析，在加压无血流状态下检查内径为100至200微米的冠状动脉微血管。
冷晶体心脏停搏的缺血性停搏显著（p < 0.05）损害了两个心室对乙酰胆碱的内皮依赖性舒张功能（左心室，69% ± 4%，右心室，73% ± 5%，而对照左心室为100% ± 0.3%，对照右心室为100% ± 0.3%）以及对钙离子载体的舒张功能（左心室，70% ± 6%，右心室，68% ± 3%，而对照左心室为98% ± 1%，对照右心室为98% ± 1%）。在冷血心脏停搏组中，对乙酰胆碱（左心室，96% ± 1%，右心室，87% ± 4%）和钙离子载体（左心室，88% ± 3%，右心室，78% ± 7%）的内皮依赖性舒张功能得以保留。在温血心脏停搏组中，左心室对乙酰胆碱（92% ± 3%）和钙离子载体（96% ± 1%）的内皮依赖性反应得以保留，但右心室对内皮依赖性乙酰胆碱（77% ± 8%）和钙离子载体（69% ± 8%）的反应性降低（p < 0.05）。所有组两个心室对硝普钠的非内皮依赖性舒张功能与对照组相似，这表明平滑肌反应性正常。
冷血心脏停搏可保留左右心室的内皮依赖性反应，而冷晶体心脏停搏会损害这种反应。温血心脏停搏可保留左心室的内皮依赖性反应，但右心室的这种反应降低。这表明血液心脏停搏和低温可能对微血管内皮保护很重要，且右心室可能比左心室更容易受到损伤。
