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作 者:罗俊丽[1,2] 王勇[1,2] 李姗姗[1,2] 窦雪娇[1,2] 韩明[1,2] 张红[1,2]
机构地区:[1]贵州省麻醉与器官保护基础研究重点实验室,563003 [2]遵义医学院附属医院麻醉科,563003
出 处:《中华麻醉学杂志》2014年第6期683-686,共4页Chinese Journal of Anesthesiology
基 金:贵州省科学技术基金
摘 要:目的探讨肺缺血预处理对体外循环(CPB)诱发犬肺缺血再灌注时水通道蛋白1(AQPl)表达的影响。方法健康成年杂种犬12只,体重15~20k,雌雄不拘,采用随机数字表法分为2组(n=6):肺缺血再灌注组(I/R组)和缺血预处理组(IP组)。非停跳CPBl0min时阻断左肺动脉,停止左肺机械通气,60min后开放左肺动脉,恢复左肺机械通气,建立CPB诱发肺缺血再灌注损伤模型。IP组在阻断左肺动脉前进行缺血预处理:阻断5min,开放5min,2个循环。于CPB前(T1)、阻断左肺动脉即刻(T2)、停CPB时(T3)、停CPB后2h(T4)时取肺组织,测定肺组织湿干重(W/D)比值,观察病理学结果,进行肺损伤评分,采用Westernblot法检测AQPl表达;于.T1、T3、T4时点计算呼吸指数(RI)、氧合指数(0I)和肺泡-动脉血氧分压差P(A-a)O2;T4时点计算左肺肺泡液体清除率。结果与I/R组比较,IP组L、T4时P(A-a)q和RI降低,0I升高,肺组织W/D比值和肺损伤评分降低,肺组织AQPl表达上调,左肺肺泡液体清除率升高(P〈0.05)。IP组肺组织病理学损伤较I/R组减轻。结论肺缺血预处理减轻CPB诱发犬肺缺血再灌注损伤的机制与上调肺组织AQPI表达有关。Objective To investigate the effect of lung ischemic preconditioning (IP) on the expression of aquaporin-1 (AQP1) during lung ischemia-reperfusion (I/R) induced by cardiopulmonary bypass i CPB) in dogs. Methods Twelve adult mongrel dogs, weighing 15-20 kg, were randomly divided into 2 groups ( n = 6 each) : lung I/R (group I/R) and ischemic preconditioning group (group IP). The left pulmonary artery was occluded at 10 min of off-pump CPB and mechanical ventilation was stopped in the left lung, 60 min later occlusion was released, and mechanical ventilation was recovered to establish the model of left lung ischemia-reperfusion injury induced by CPB. In group IP, lung ischemic preconditioning was induced by 2 cycles of 5 min ischemia followed by 5 min reperfusion before occlusion of the left pulmonary artery. Before CPB (Tl ), immediately after occlusion of the left pulmonary artery ( T2 ), at the end of CPB ( T3 ), and at 2 h after the end of CPB ( T4 ), pulmonary specimens were collected for determination of wet to dry lung weight ratio (W/D ratio) and expression of AQP1 and for examination of the pathological changes of lungs which were scored. Respiration index ( RI), oxygenation index (OI), and alveolar-arterial oxygen tension difference (P(A-a)02 ) were calculated at Tl , T3 and T4, and the left pulmonary alveolar fluid clearance (AFC) was calculated at T4 ·Results Compared with group I/R, P(A-a) 02 and RI were significantly decreased, OI was increased, W/D ratio and pathological scores were decreased, the expression of AQP1 was up-regulated, and the AFC was increased at T3 and T4 in group IP. The pathological changes of the lung were significantly attenuated in group IP as compared with group I/R. Conclusion The mechanism by which lung ischemic preconditioning mitigates lung I/R injury induced by CPB is related to up- regulation of the expression of AQP1 in dog lung tissues.
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