治疗性高碳酸血症对局灶性脑缺血大鼠神经功能的影响及其机制的研究  

Effects of therapeutic hypercapnia on neurological outcome in a rat focal cerebral ischemia model

作　　者：陶涛[1,2] 张静月[1,2] 赵萌[1,2] 李文志[1,2] 

机构地区：[1]哈尔滨医科大学附属第二医院麻醉科 [2]黑龙江省麻醉与危重病重点实验室,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2013年第4期317-320,共4页Journal of Harbin Medical University

基　　金：哈尔滨市科学技术局优秀学科带头人基金(2012RFXXS064)

摘　　要：目的探讨治疗性高碳酸血症(therapeutic hypercapnia)对大鼠局灶性脑缺血再灌注损伤后神经功能的影响,并探讨其可能的机制。方法 30只雄性SD大鼠随机分为3组:假手术组(Sham组)、缺血再灌注组(ischemia-reperfusion,IR组)和治疗性高碳酸血症组(Hypercapnia组),每组10只。大鼠麻醉后采用大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)法制备局灶性脑缺血再灌注损伤模型,栓塞时间为90 min。Hypercapnia组大鼠吸入外源性二氧化碳使其动脉血二氧化碳分压(PaCO2)维持80～100 mmHg水平并持续2 h。实验过程中检测平均动脉压(mean artery pressure,MAP)、动脉血气以及体温。缺血后24 h进行神经功能评分,评分后将大鼠处死应用蛋白质印迹技术(Western blot)检测各组大鼠缺血皮质线粒体Bcl-2和Bax的表达强度。结果 MCAO导致大鼠出现神经行为学障碍,与IR组相比,Hypercapnia组大鼠神经功能评分明显升高(P<0.05);Western blot结果显示与IR组相比,Hypercapnia组大鼠线粒体Bcl-2和Bax表达分别升高和降低(P<0.05)。结论治疗性高碳酸血症对局灶性脑缺血有一定的保护作用,这种保护作用可能通过调节凋亡蛋白实现的。Objective To investigate the effects of therapeutic hypercapnia in focal cerebral is- chemia in the rat middle cerebral artery occlusion（MCAO） model and the underlying mecha- nism. Methods Adult male Sprague Dawley rats were subjected to 90 minutes of MCAO and subsequently exposed to increased carbon dioxide （CO2 ） levels to maintain arterial blood CO2 tension （PaCO2 ） between 80 and 100 mmHg for 2 hours. Neurological deficits were assessed at 24 hours in 3 groups of animals： sham-operated （Sham）, MCAO （IR） , and MCAO treated with hypercapnia （Hypercapnia）. Apoptosis-related proteins （Bcl-2, Bax） were evaluated by Western blot. Results Therapeutic hypercapnia significantly improved neurological scores after MCAO. Mitochondrial Bcl-2 and Bax cortical explession levels were significantly higher and lower, respectively, in hypercapnia-treated rats. Conclusion Therapeutic hypercapnia pro- motes neurological functional recovery through antiapoptotic mechanisms

关 键 词：局灶性脑缺血 治疗性高碳酸血症 神经元凋亡 

分 类 号：R-332[医药卫生] R743