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背景:大鼠局灶性脑缺血模型的制作需要在麻醉状态下通过外科手术完成,但麻醉药物可能影响局灶性脑缺血的结局。目的:观察氯胺酮麻醉对大鼠局灶性脑缺血模型病理结果的影响,并与戊巴比妥进行对照。设计:随机对照动物实验。单位:西安交通大学医学院实验动物中心和西安交通大学医学院第二附属医院病理科。材料:实验于2004-05/2005-03在西安交通大学医学院实验动物中心和第二附属医院病理科进行。取30只雄性SD大鼠,单纯随机分为戊巴比妥组和氯胺酮组,每组15只。方法:戊巴比妥组和氯胺酮组大鼠分别以戊巴比妥40mg/kg,氯胺酮60mg/kg腹腔麻醉。待翻正反射消失后,通过腔内线栓永久性阻塞大鼠大脑中动脉引发脑缺血。主要观察指标:①大脑中动脉阻塞4h时,参照改良的Bederson’s评分方法进行神经功能缺陷评分。②大脑中动脉阻塞24h时,每组选取5只大鼠,处死后取脑,以20g/L的TTC进行染色,计算梗死体积。③大脑中动脉阻塞72h,记录2组死亡率。然后每组取4只大鼠,采用相应的麻醉剂进行麻醉后处死取脑,甲苯胺蓝染色检测半暗带内的存活神经元。结果:30只大鼠全部进入结果分析。①大脑中动脉阻塞4h时,戊巴比妥组和氯胺酮组神经病学评分差异不显著(1.46±0.98,1.38±0.68,P>0.05)。②大脑中动脉阻塞24h时氯胺酮组的脑梗死体积小于戊巴比妥组犤(28.1±4.11)%,(37.8±4.95)%,P<0.05犦。③大脑中动脉阻塞72h,戊巴比妥组和氯胺酮组死亡率差异不显著(42%比33%,P>0.05),但半暗带内的神经元密度氯胺酮组高于戊巴比妥组犤(836±15),(740±24)个/mm2,P<0.05犦。结论:①在制作大鼠局灶性脑缺血模型时,氯胺酮麻醉下产生较轻的脑损伤。②在氯胺酮麻醉下制作的大鼠局灶性脑缺血模型中评价一些药物或方法的神经保护作用时,所研究的药物或方法的神经保护作用可能难以体现。
BACKGROUND: The rat model of focal cerebral ischemia needs to be surgically performed under anesthesia, but anesthetic drugs may influence the outcome of focal cerebral ischemia. Objective: To observe the effects of ketamine anesthesia on the pathological results of focal cerebral ischemia in rats and to compare with pentobarbital. Design: Randomized controlled animal experiments. SETTING: Laboratory Animal Center, Xi’an Jiaotong University School of Medicine and Pathology Department, Second Affiliated Hospital of Xi’an Jiaotong University School of Medicine. MATERIALS: Experiments were performed at Experimental Animal Center of Xi’an Jiao Tong University School of Medicine and Department of Pathology, Second Affiliated Hospital from May 2004 to March 2005. Thirty male SD rats were randomly divided into pentobarbital group and ketamine group, 15 rats in each group. Methods: Rats in pentobarbital group and ketamine group were anesthetized with pentobarbital 40mg / kg and ketamine 60mg / kg respectively. To be inverted after the disappearance of the reflex, through the intraluminal thrombus permanent occlusion of the middle cerebral artery induced cerebral ischemia. MAIN OUTCOME MEASURES: ① After 4 h occlusion of the middle cerebral artery, the neurological deficit score was evaluated according to the modified Bederson’s score method. ② occlusion of the middle cerebral artery 24h, each group selected 5 rats, sacrificed after taking the brain, with 20g / L of TTC staining, infarction volume. ③ middle cerebral artery occlusion 72h, 2 groups were recorded mortality. Then, 4 rats in each group were anesthetized with the corresponding anesthetics and sacrificed for brain injury. Toluidine blue staining was used to detect the survival neurons in the penumbra. Results: All 30 rats entered the result analysis. Neuropathological scores of pentobarbitone group and ketamine group were not significantly different at 4h occlusion of the middle cerebral artery (1.46 ± 0.98, 1.38 ± 0.68, P> 0.05). ② The volume of cerebral infarction in ketamine group was less than that in pentobarbital group (28.1 ± 4.11)%, (37.8 ± 4.95)%, P <0.05 犦, respectively, at 24 h occlusion of middle cerebral artery. ③ After 72 h occlusion of the middle cerebral artery, there was no significant difference in mortality between pentobarbitone group and ketamine group (42% vs. 33%, P> 0.05), but neuronal density in penumbra group was higher than that in pentobarbital group犤 (836 ± 15), (740 ± 24) pieces / mm2, P <0.05 犦. Conclusions: ① In the rat model of focal cerebral ischemia, ketamine anesthesia produces mild brain damage. ② Neuroprotective effects of the drug or method studied may be difficult to assess in evaluating neuroprotective effects of some drugs or methods in a rat model of focal cerebral ischemia produced under ketamine anesthesia.