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在地氟烷脑保护作用下颅内动脉瘤夹闭术中不同时间点血管紧张素Ⅱ和内皮素水平的变化
引用本文:王涛,罗芳,赵继宗,张淑珍.在地氟烷脑保护作用下颅内动脉瘤夹闭术中不同时间点血管紧张素Ⅱ和内皮素水平的变化[J].中国组织工程研究与临床康复,2005,9(41):150-151.
作者姓名:王涛  罗芳  赵继宗  张淑珍
作者单位:1. 首都医科大学附属北京天坛医院神经外科,北京市,100050
2. 首都医科大学附属北京天坛医院麻醉科,北京市,100050
基金项目:北京市自然科学基金资助项目(7992021) Natural Science Foundation of Beijing, No. 7992021
摘    要:背景脑血管痉挛是颅内动脉瘤手术围术期主要并发症之一,颅内动脉瘤行开颅夹闭术的麻醉不仅应满足麻醉的基本要求而且要求尽可能预防脑血管痉挛、提供脑功能的保护.目的观察地氟烷麻醉下颅内动脉瘤患者行夹闭术中收缩脑血管物质血管紧张素Ⅱ、内皮素水平的变化,探讨地氟烷的脑保护作用.设计病例分析.单位首都医科大学附属北京天坛医院神经外科和麻醉科.对象选择2002-10/2004-06首都医科大学附属北京天坛医院神经外科64例拟行开颅动脉瘤夹闭术患者,男30例,女34例.方法麻醉诱导后气管插管控制呼吸,地氟烷维持麻醉.分别于麻醉诱导前、剪硬膜、夹闭动脉瘤和动脉瘤夹闭后30 min 4个时点采集动脉血4 mL,应用放免法检测血浆中血管紧张素Ⅱ、内皮素的水平.主要观察指标颅内动脉瘤患者麻醉诱导前、剪硬膜、夹闭动脉瘤和动脉瘤夹闭后30 min血浆中血管紧张素Ⅱ和内皮素的水平.结果2例患者手术中发生动脉瘤破裂,进入结果分析62例.①血管紧张素Ⅱ水平颅内动脉瘤患者术前血管紧张素Ⅱ水平在正常范围,地氟烷麻醉中3个时间点较麻醉诱导前无明显变化(P>0.05).②内皮素水平剪硬膜、夹闭动脉瘤和动脉瘤夹闭后30 min时明显低于麻醉诱导前(40.4±10.3),(40.0±9.6),(40.7±12.3),(49.3±12.7)ng/L,(P=0.002,0.001,0.009)].结论地氟烷麻醉下开颅动脉瘤夹闭术中收缩脑血管物质血管紧张素Ⅱ和内皮素在整个麻醉维持期间均无上升趋势,内皮素甚至明显低于麻醉诱导前水平,且不同手术阶段无明显差异,表明地氟烷麻醉能够避免由于血管紧张素Ⅱ和内皮素释放增加导致的急性脑血管痉挛,降低继发性脑缺血性损害,从而起到脑保护的作用.

关 键 词:颅内动脉瘤  血管紧张素类  内皮缩血管肽类
文章编号:1671-5926-(2005)41-0150-02
修稿时间:2005年3月7日

Changes of angiotensin Ⅱ and endothelin levels under the cerebral protection of desfiurane during the clamp operation of intracranial aneurysm at various time points
Wang Tao,Luo Fang,Zhao Ji-zong,Zhang Shu-zhen.Changes of angiotensin Ⅱ and endothelin levels under the cerebral protection of desfiurane during the clamp operation of intracranial aneurysm at various time points[J].Journal of Clinical Rehabilitative Tissue Engineering Research,2005,9(41):150-151.
Authors:Wang Tao  Luo Fang  Zhao Ji-zong  Zhang Shu-zhen
Abstract:BACKGROUND: Cerebral vascular spasm is the main complication of intracranial aneurysm during perioperative period. Anesthesia of clamp operation of intracranial aneurysm not only meet the basic requirement of anesthesia, but also prevent cerebral vascular spasm and protect cerebral function possibly.OBJECTIVE: To observe the changes of angiotensin Ⅱ and endothelins of paitents with intracranial aneurysm under the anesthesia of desflurane during the clamp operation so as to discuss the effect of desflurane on cerebral protection.DESIGN: Case analysis.SETTING: Department of Neurosurgery and Department of Anesthesiology of Beijing Tiantan Hospital Affiliated to Capital University of Medical Sciences.PARTICIPANTS: Totally 64 patients, 30 males and 34 females, who were prepared for clamp operation of intracranial aneurysm, were selected from Department of Neurosurgery of Beijing Tiantan Hospital Affiliated to Capital University of Medical Sciences between October 2002 and June 2004.METHODS: After anesthesia induction, tracheal cannula was used to control respiration and desflurane was used to maintain the anesthesia. Totally 4 mL arterial blood were collected at the four time points: before anesthesia induction, cutting dura mater, clamp aneurysm and 30 minutes after clamp aneurysm. Levels of angiotensin Ⅱ and endothelins in plasma were assayed with radioimmunoassay.MAIN OUTCOME MEASURES: Levels of angiotensin Ⅱ and endothelins at the four time points: before anesthesia induction, cutting dura mater,clamp aneurysm and 30 minutes after clamp aneurysm.RESULTS: Aneurysm of two patients was disrupted during the operation of angiotensin Ⅱ was ranged normally before operation, and that at the other three time points during the anesthesia of desflurane did not changed endothelins: Level of endothelins at the three time points of cutting dura mater, clamp aneurysm and 30-minutes after clamp aneurysm was lower than that at the time point of pre-an esthesia induction (40.4±10.3),(40.0±9.6), (40.7±12.3), (49.3±12.7) ng/L, (P=0.002, 0.001, 0.009)].CONCLUSION: Levels of angiotensin Ⅱ and endothelins which anesthetizes by desflurane are not increased during the whole clamp operation of intracranial aneurysm. However, level of endothelins is obviously lower than that at the time point of pre-anesthesia induction, and there is not significantly different from that at various time points of the operation. This suggests that anesthesia of desflurane can avoid the onset of acute cerebral vascular spasm induced by the increasing liberation of angiotensin Ⅱ and endothelins and decrease the onset of secondary cerebral ischemic injury so as to protect brain.
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