钙离子拮抗剂对体外循环肺部炎症作用的研究

Reaserch of cadium channel blocker inhibitting culmonary inflammation in cardiopulmonary bypass

目的本实验探讨体外循环过程中,钙离子拮抗剂(尼卡地平)对P38丝裂原激活蛋白激酶(P38MAPK)的作用规律及与肺损伤的关系。方法将12只乳猪随机分为2组,每组6只。Ⅰ组行体外循环,心脏阻断80分钟,主动脉开放后辅助循环15分钟,主动脉阻断,心肌灌注冷停跳液同时,肺脏灌注低温保护液;Ⅱ组体外循环方法同Ⅰ组,在肺低温保护液中加入尼卡地平。分别在不同时段取三组动物之肺脏标本,以免疫印迹方法测量肺组织P38MAPK活性,组织学观察肺损伤改变,估测肺换气功能。结果Ⅰ组肺组织P38MAPK活性增高,Ⅱ组肺组织P38MAPK活性低于I组出现统计学差异。Ⅰ组肺损伤改变与Ⅱ组相比加重,出现统计学差异,肺换气功能Ⅱ组好于Ⅰ组,有统计学差异。结论体外循环过程中,术中应用钙拮抗剂有抑制肺损伤的作用。

Objective Pulmonary injury is produced by inflammatory response during cardiopulmonary bypass （CPB）.phosphoP38MAPK（Mitogcn-activated protein kinases） mediate inflammatory response. Our experiment researched relation between phosphoMAPK （Mitogen-acfivated protein kinases） and Nicardipine Hydrochloride and relation between applying Nicardipine Hydrochloride and pulmonary injury during CPB. Methods 12 pigs randomly distributed two groups（n=6） .The first group and the second group laced on CPB for 100 rain, which included 80 min of cardioplegic arrest, we perfused the lung of the second group with Nicardipine Hydrochloride. Lung samples were collected at baseline, during CPB, and during post-CPB reperfusion. Activated forms of p38 were measured by Wcstem blot. Pulmonary injury was determined by histology. Pulmonary function was measured. Results phosphor-p38 of The first group were increased compared with the second group （ P 〈 0.01）.Lung injury in the first group were evident compared with the second group （ P 〈 0.01）. A-a O2 in the first group was increased compared with the second group （ P 〈0.01） Conclusion results of our study demonstrate that Nicardipine Hydrochloride decreases pulmonary injury.