SURGICAL CARDIOPULMONARY BYPASS AND CEREBRAL RESISTANCE

术后神经功能障碍是致残的，并可能致命 心脏手术的并发症。尽管气囊和气囊栓塞术 在体外循环期间观察到了颗粒物， 体外循环期间脑血流灌注受损显著地导致 赤字的严重性。在犬低温转流术的研究中，脑 血管阻力在复温期间意外增加260-380% 超过基线，使脑血流未能改善。虽然 脑氧摄取量明显增加，脑部代谢 复温后氧分压仍然较低。病原学和 脑血管阻力持续增加的意义 都是未知的，但可能会导致术后神经功能障碍。 随后的实验研究表明，脑部出现低灌注量 有低温但不是常温搭桥，表明 体外循环本身并不会导致这种缺陷。 拟议的调查将深入分析影响 犬在复温过程中的脑血流和代谢缺陷 体外循环模型。浅谈脑血的相互关系 血流量、血管阻力、氧代谢和脑电 将在不同的条件下进行表征。颅内压会 直接测量和脑评估颅内水肿的形成 水含量和比重。微栓塞术与缺血性损伤 将通过死后视网膜和脑组织病理学进行评估。 复温后脑血管阻力显著增加 体外循环可能是由于区域间的不平衡 血管扩张剂和血管收缩药的影响。同时严密控制所有 搭桥过程中的影响因素，四个假说将在 复温：1)高血糖降低脑灌流压和 血流，2)尼莫地平阻断钙通道减少脑组织 血管阻力和改善脑血流灌注，3)腺苷，输注 直接进入脑脊液空间，增加脑血流量 比乙酰胆碱和硝普钠更多的表明 低温转流对血管内皮细胞介导的脑血管松弛的影响 血管平滑肌；4)脑血管阻力增加 取决于先期体温过低的持续时间，且仅部分 在常温脉动流动4小时后溶解。 体外循环的临床研究受到血流动力学的限制 可以在实践上或道德上测量的参数。我们的狗 模型将建立指南以改善以下脑血流灌注 低温搭桥术。

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.