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山莨菪碱、外源性肺表面活性物质对肺缺血-再灌注损伤的保护作用 被引量:2

PROTECTING EFFECT OF ANISODAMINE(654-2) AND EXOGENOUS PULMONARY SURFACTANT ON PULMONARY FUNCTION DURING ISCHEMIC-REPERFUSION INJURY
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摘要 目的 :探讨山莨菪碱 (6 5 4 - 2 )、外源性肺表面活性物质 (PS)对缺血 -再灌注肺损伤的保护作用及可能机制。方法 :取 4 5d左右幼猪 18只 ,随机分成 3组 :对照组、6 5 4 - 2组、PS组 ,每组 6只 ,于阻断右肺动脉前、阻断后 6 0 ,90 min(开放 )、开放后 6 0 ,90 ,12 0 min等时刻点分别抽取左、右肺静脉血 ,EL ISA法检测 TNF- α含量 ;分别取左、右肺下叶送病检。结果 :各实验组右肺静脉血中 TNF- α质量浓度明显轻于对照组 (P <0 .0 1) ;PS组明显低于 6 5 4 - 2组 (P <0 .0 1)。病检 :肺泡间质水肿、白细胞浸润、肺泡出血等 ,实验组明显轻于对照组 ,以 PS组最轻。结论 :6 5 4 - 2、PS对肺缺血 -再灌注损伤有保护作用 ;PS的肺保护作用优于 6 5 4 - 2。 Objective: To study the protective effect of anisodamine (654 2) and exogenous pulmonary surfactant (PS) on young pig's pulmonary function during ischemic reperfusion injury by measuring tumor necrosis factor α(TNF α) in pulmonary veins and examining lung pathologic changes Methods: 18 pigs ,about 45 day old, were randomly divided into three groups: a control group,a 654 2 group and a PS group The TNF α concentration of every lung was analysed with ELISA methods at the point of pre clamping right pulmonary artery, post clamping 60, 90 min(opening), post unclamping 60,90,120 min We finally examined the pathologic changes of lungs Results: After clamping right pulmonary artery , every experimental group TNF α concentration was significantly lower than that of the control group (P<0 01), TNF α concentration of PS group was significantly lower than that of 654 2 groups (P<0 01), There was significant alveolar edema, leukocyte infiltration and bleeding of the lung in the control group The histological examination proved that the degree of pulmonary injury was significantly less in the experimental groups, especially in the PS group Conclusion: 654 2 and exogenous PS have a protective effect on pulmonary function during ischemic reperfusion injury PS can make better effect than that of 654 2
出处 《广西医科大学学报》 CAS 2002年第3期333-335,共3页 Journal of Guangxi Medical University
关键词 山莨菪碱 外源性肺表面活性物质 肺缺血 再灌注损伤 保护作用 肿瘤坏死因子 pulmonary surfactant ischemic reperfusion pulmonary injury tumor necrosis factor α
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