体外循环对大鼠脑血管功能的影响

Effects of the cardiopulmonary bypass on cerebral vasomotor changes

目的观察不同体外循环时间和体外循环模式对脑血管功能的影响。方法将30只大鼠平均分为5组，分别建立不同体外循环模型。取右大脑中动脉，在不同压力下进行肌源性活动功能检测，观察在不同浓度乙酰胆碱溶液中内皮细胞相关舒张反应强度和利用硝普钠和血管紧张素观察平滑肌细胞相关血管舒缩反应。取海马区脑组织进行微血管内皮细胞超微结构观察。结果各组大鼠均成功建立和脱离体外循环。代表肌源性活动功能的MCA收缩百分率深低温低流量组为（34．62±2．36）％，深低温停循环组为（33．83±2．28）％，较正常对照组（37．75±1．92）％明显受损（P〈0．05）。在不同乙酰胆碱浓度下，体外循环组内皮细胞相关的血管舒张率为（8．59±1．48）％，较正常组（24．26±1．90）％明显受损（P〈0．05），深低温低流量组和深低温停循环组损伤较常温组明显加重。血管平滑肌相关的收缩舒张功能各组均处于正常范围。结论体外循环早期即可引起脑血管内皮细胞相关的血管舒张功能受损，深低温转流可引起脑血管自主调节功能降低。而这可能是体外循环后脑损伤的重要机制之一。

Objective To study the cerebral vasomotor changes after different cardiopulmonary bypass time and modes. Methods Thirty SD rats were equally divided into 5 groups,which were subjected to CPB for 60 min and 120 rain, deep hypothermic low flow bypass 60 min, deep hypothermic circulatory arrest 60 min, and sham respectively. The right middle cerebral artery was harvested and prepared for assessment of the myogenic tone with different transmural pressure, the endothelial cell response induced by different concentration of acetylcholine, and the vascular smooth muscle cell response induced by the sodium nitroprusside and serotonin. The hippocampus tissue was harvested to observe the uhramicrostructure of endothelial cells in capillary by electron microscope. Results The CPB was performed successfully in all the rats. The deep hypothermic bypass altered the results of myogenic tone test with different transmural pressure compared with the sham group [（34.62 ±2.36）% and （33. 83 ±2.28）% vs （37.75±1.92） % ,P 〈 0.051. Acetylcholine caused a dose-dependent vasodilation in the sham group that was absent in animals undergoing CPB [ （ 24.26 ±1.90 ） % vs （ 8.59 ± 1.48 ） %, P 〈 0.05 ]. Significantly, this was apparent after only 60 min of CPB and the vasodilation response of endothelial cells was worse in DHLF and DHCA groups than in simple CPB. The vascular smooth muscle cell response induced by the sodium nitroprusside and serotonin was intact in all the rats. Conclusion The specific loss of acetylcholine- induced vasodilation suggests endothelial cell dysfunction, which appeares early after the onset of CPB. The deep hypothermie bypass can cause the dysfunction of cerebrovascular autonomic regulation. And these cerebral vasomotor changes may contribute to the neurologie injuries after CPB.