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作 者:莫文魁[1] 何良勇[1] 陈群清[1] 闫玉生[1] 童健[1] 蒙华[1] 张富丽[1]
机构地区:[1]南方医科大学珠江医院胸心外科,广东广州510282
出 处:《南方医科大学学报》2013年第11期1652-1655,共4页Journal of Southern Medical University
基 金:广东省科技计划项目(2011B061200026);广州市科技计划项目(12A72121524)
摘 要:目的探索建立稳定、可行的兔脑栓塞急性期体外循环(cardiopulmonary bypass,CPB)模型,为研究临床脑栓塞急性期体外循环对脑组织的影响以及手术时机选择提供实验工具。方法 54只兔随机分成A、B二大组,A组为非脑栓塞CPB组(n=18),B组分为B1组(脑栓塞24 h后CPB组,n=18),B2组(脑栓塞1周后CPB组,n=18)。经眶上缘入路,直视下电凝左侧大脑中动脉主干,建立兔大脑中动脉脑栓塞(middle cerebral artery occlusion,MCAO)模型,并分别于脑栓塞24 h、1周进行MRI检查,观察各组脑栓塞情况。胸骨正中切口,升主动脉和右心房分别插管,建立CPB,从而建立脑栓塞急性期CPB模型。观察各组建模成功率,并于CPB后2 h进行MRI检查观察脑部情况。结果 B1、B2两组均成功建立脑栓塞模型,成功率100%,栓塞后兔均存活;A组和B组在建立CPB模型的成功率上无差异(P>0.05)。在CPB术后2 h,A、B两组MRI检查均未发现出血灶或新发栓塞灶。结论采用眶上缘入路及模拟临床实际建立的兔脑栓塞急性期体外循环模型具有成功率高、稳定、可行的特点,是进行脑栓塞急性期体外循环相关脏器损伤机制研究和对其进行干预的较理想模型。兔脑栓塞急性期进行体外循环后未见脑组织出血及新发栓塞灶。Objective To establish a stable and feasible rabbit model of cardiopulmonary bypass (CPB) in acute cerebral embolism phase for studying the effects of CPB on brain tissues and the timing of surgical intervention of acute cerebral embolism. Methods Fifty-four rabbits were randomized into group A (n=18) to receive CPB without middle cerebral artery occlusion (MCAO) and group B to undergo CPB at 24 h (group B1, n=18) or 1 week (group B2, n=18) after MCAO. Through a supraorbital margin approach, electrocoagulation was carried out to occlude the main stem of the left MCA under direct vision to establish MCAO. Magnetic resonance imaging (MRI) was performed at both 24 h and I week after MCAO, and the severity of cerebral embolization was evaluated. CPB was established by cannulation of the ascending aorta and the right atrium through a median sternotomy incision. MRI was performed at 2 h after CPB to observe the brain tissues. Results MCAO was successfully established in groups B1 and B2, and all the rabbits survived after MCAO. In both groups A and B, MRI examination detected no cerebral hemorrhage or new embolism 2 h after CPB. Conclusions We have established a stable and feasible CPB model in rabbits with acute cerebral embolism to allow study of the mechanisms of CPB-related organ damage and its interventions.
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