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背景:缺血早期脑组织损伤是急性脑卒中治疗面临的主要挑战。此期应用高压氧治疗是否对脑组织有明确的保护作用。目的:观察大鼠脑缺血再灌注后,高压氧诱导降钙素基因相关肽和β-内啡肽的动态变化以及高压氧治疗对其的影响,探讨高压氧的治疗作用。设计:随机对照实验。单位:首都医科大学动物科学部。材料:实验于2003-12/2005-02在首都医科大学动物科学部进行。选择清洁级雌性SD大鼠63只按随机数字表分为9组:假手术组7只;缺血再灌注组分别取再灌注6,24,48,96h时相点组,每组各7只;缺血再灌注+高压氧处理组分别取再灌注6,24,48,96h时相点组,每组各7只。干预:除假手术组外,其余各组建立脑缺血再灌注动物模型,夹闭双侧颈总动脉缺血20min后再通血流,假手术组同样手术,但不夹闭颈总动脉。假手术组和缺血再灌注组置于常压空气中,缺血再灌注+高压氧处理组治疗方案为:纯氧洗高压氧舱5min,升压5min,然后稳压在0.2MPa下吸纯氧45min,缓慢减压15min,出舱第1天在再灌注3h后行高压氧处理1次,以后均在3天同一时间作相同处理。缺血再灌注组和缺血再灌注+高压氧处理组分别于再灌注6,24,48,96h取血。主要观察指标:用放射免疫测定法测定各组血浆中降钙素基因相关肽和β-内啡肽的含量。结果:63只大鼠均进入结果分析。①缺血再灌注6h:高压氧组降钙素基因相关肽应激性升高(64.12±18.16)ng/L,出现时间较缺血再灌注组早,高于同时相点缺血再灌注组(32.62±11.72)ng/L和假手术组(49.09±8.59)ng/L(F=6.614,P<0.001,P<0.05);高压氧组β-内啡肽一过性增高。②缺血再灌注24h和48h:高压氧处理组降钙素基因相关肽从24h起即恢复至正常[(43.53±22.73)ng/L,F=0.390;(46.02±10.64)ng/L,F=0.969,P均>0.05]。③缺血再灌注96h:缺血再灌注组降钙素基因相关肽应激性(81.74±20.64)ng/L,高于假手术组(49.09±8.59)ng/L和同时相点高压氧组(40.98±20.52)ng/L(F=6.419,P<0.01);并明显高于6,24,48h的缺血再灌注组组(F=10.806,P均<0.01)。高压氧组β-内啡肽水平降至最低,明显低于假手术组[(370.00±130.15,872.30±403.92)ng/L,(F=3.691,P<0.05)]。结论:①早期高压氧治疗可通过升高血浆降钙素基因相关肽水平和降低β-内啡肽水平以减少梗死区的脑组织损伤。②随高压氧治疗次数的增多,其疗效更好。
Background: Early ischemic brain injury is a major challenge in the treatment of acute stroke. Whether hyperbaric oxygen therapy during this period has a clear protective effect on brain tissue. OBJECTIVE: To observe the dynamic changes of calcitonin gene-related peptide and β-endorphin induced by hyperbaric oxygen and the effect of hyperbaric oxygen therapy on it after cerebral ischemia-reperfusion in rats and to explore the therapeutic effect of hyperbaric oxygen. Design: Randomized controlled experiment. Unit: Animal Science Department of Capital Medical University. Materials: The experiment was performed at Animal Science Department of Capital Medical University from December 2003 to February 2005. Sixty-three female SD rats of clean grade were randomly divided into 9 groups according to random number table: 7 sham-operated group; ischemia-reperfusion group were given 6, 24, 48, ; Ischemia-reperfusion + hyperbaric oxygen treatment group were reperfusion at 6,24,48,96 h point group, each group of seven. Intervention: In addition to the sham operation group, the rest of the groups were established cerebral ischemia-reperfusion animal model, occluded bilateral common carotid artery ischemia 20min and then through the blood flow, sham-operated group the same surgery, but not clamping the common carotid artery. Sham-operation group and ischemia-reperfusion group were placed in atmospheric air, ischemia reperfusion + hyperbaric oxygen treatment group treatment program: pure oxygen wash hyperbaric oxygen chamber 5min, step-up 5min, and then regulated at 0.2MPa sucked pure Oxygen 45min, slow decompression 15min, the first day of storage in the reperfusion after 3h hyperbaric oxygen treatment 1, after 3 days at the same time for the same treatment. Ischemia reperfusion group and ischemia reperfusion + hyperbaric oxygen treatment group were reperfused 6,24,48,96h blood. MAIN OUTCOME MEASURES: Plasma levels of calcitonin gene-related peptide and β-endorphin were determined by radioimmunoassay. Results: All 63 rats were involved in the result analysis. ① Ischemia-reperfusion 6h: The stress of calcitonin gene-related peptide in hyperbaric oxygen group increased (64.12 ± 18.16) ng / L, the appearance time was earlier than ischemia-reperfusion group and higher than that of ischemia-reperfusion group (32.62 ± 11.72) ng / L and sham operation group (49.09 ± 8.59) ng / L (F = 6.614, P <0.001, P <0.05). ② 24h and 48h after ischemia-reperfusion, calcitonin gene-related peptide in hyperbaric oxygen treatment group returned to normal from (24h) [(43.53 ± 22.73) ng / L, = 0.969, P> 0.05]. ③In 96h ischemia / reperfusion group, stress of calcitonin gene related peptide in ischemia reperfusion group was (81.74 ± 20.64) ng / L, higher than that in sham operation group (49.09 ± 8.59) ng / L and hyperbaric oxygen group (40.98 ± 20.52) ng / L (F = 6.419, P <0.01), and significantly higher than that of ischemia reperfusion group at 6, 24 and 48 hours (F = 10.806, P <0.01). The level of β-endorphin in hyperbaric oxygen group was the lowest, which was significantly lower than that in sham-operated group [(370.00 ± 130.15,872.30 ± 403.92) ng / L, F = 3.691, P <0.05). Conclusion: (1) Hyperbaric oxygen therapy can reduce brain injury in infarct area by increasing plasma calcitonin gene-related peptide level and decreasing β-endorphin level. ② With the increase in the number of hyperbaric oxygen therapy, its efficacy is better.