SURGICAL CARDIOPULMONARY BYPASS AND CEREBRAL RESISTANCE

术后神经功能缺损是致残和潜在致命的 心脏手术并发症。 虽然栓塞的气体和 在心肺分流术期间已经观察到颗粒物质， 搭桥术期间受损的脑灌注显著有助于 赤字的严重性。 在犬低温旁路的研究中， 复温期间血管阻力意外增加260-380% 所以脑血流量没有改善。 虽然 脑氧摄取明显增加，脑代谢 复温后，氧的速率仍然很低。 病因及 脑血管阻力持续增加意义 尚不清楚，但可能易导致术后神经功能缺损。 随后的实验研究表明，脑灌注不足 低温而非正常体温的旁路，表明 心肺转流术本身不会导致这种缺陷。 拟议的调查将深入分析影响 犬复温过程中脑灌注和代谢缺陷 体外循环模型。 脑血流与脑血管病的关系 血流、血管阻力、氧代谢和脑电图 将在各种条件下进行表征。 颅内压将 直接测量，并通过脑评估颅内水肿形成 水含量和比重。 微栓塞与缺血性损伤 将通过死后视网膜和脑组织病理学进行评估。 复温后脑血管阻力明显增加， 心肺转流术可能是由于区域不平衡， 血管扩张剂和血管收缩剂的影响。 同时严格控制所有 旁路期间的影响因素，四个假设将在 复温：1）高血糖降低脑灌注压， 血流，2）尼莫地平钙通道阻滞剂降低脑血流 血管阻力和改善脑灌注，3）腺苷，输注 直接进入脑脊液腔，增加脑血流量 超过乙酰胆碱和硝普钠，表明 低温转流损害脑血管内皮介导的舒张功能 血管平滑肌; 4）脑血管阻力增加 取决于前期体温过低的持续时间， 在常温脉动流4小时后消退。 体外循环的临床研究受到血流动力学的限制 这些参数可以在实践中或道德上测量。 我们的狗 模型将建立改善脑灌注的指南， 低温旁路

Postoperative neurological deficits are disabling and potentially lethal complications of cardiac surgery. Although embolization of gaseous and particulate matter has been observed during cardiopulmonary bypass, impaired cerebral perfusion during bypass contributes significantly to the severity of the deficit. In studies of canine hypothermic bypass, cerebral vascular resistance increased unexpectedly during rewarming by 260-380% over baseline so that cerebral blood flow failed to improve. Although cerebral oxygen extraction increased significantly, the cerebral metabolic rate for oxygen remained depressed after rewarming. The etiology and significance of this persistent increment in cerebral vascular resistance are not known but may predispose to neurological deficits postoperatively. Subsequent experimental studies show that cerebral hypoperfusion occurs with hypothermic but not normothermic bypass, indicating that cardiopulmonary bypass per se does not cause this defect. The proposed investigation will analyze in depth the factors governing defective cerebral perfusion and metabolism during rewarming in a canine model of cardiopulmonary bypass. The relationships among cerebral blood flow, vascular resistance, oxygen metabolism, and the electroencephalogram will be characterized under various conditions. Intracranial pressure will be measured directly and intracranial edema formation assessed by brain water content and specific gravity. Microembolization and ischemic damage will be assessed by postmortem retinal and cerebral histopathology. The marked increase in cerebral vascular resistance after rewarming on cardiopulmonary bypass may be due to a regional imbalance between vasodilator and vasoconstrictor influences. While tightly controlling all influential factors during bypass, four hypotheses will be tested during rewarming: 1) hyperglycemia decreases cerebral perfusion pressure and blood flow, 2) calcium channel blockade with nimodipine reduces cerebral vascular resistance and improves cerebral perfusion, 3) adenosine, infused directly into the cerebrospinal fluid space, increases cerebral blood flow more than acetylcholine and sodium nitroprusside indicating that hypothermic bypass impairs endothelially mediated relaxation of cerebral vascular smooth muscle, and 4) the increase in cerebral vascular resistance is dependent upon the duration of antecedent hypothermia and only partially resolves after 4 hours of normothermic pulsatile flow. Clinical studies of cardiopulmonary bypass are limited by the hemodynamic parameters which can be measured practically or ethically. Our canine model will establish guidelines to improve cerebral perfusion following hypothermic bypass.