摘要
目的：探讨缺血再灌注（ＩＲ）损伤过程中磷脂酶Ａ２（ＰＬＡ２）激活介导肿瘤坏死因子（ＴＮＦ）等炎症介质的作用机制。方法：采用大鼠肠ＩＲ损伤模型，用放射免疫分析法测定Ｗｉｓｔａｒ大鼠肠ＩＲ损伤后血浆和肺灌洗液中ＴＮＦ、ＰＬＡ２及肝、肠组织中的ＰＬＡ２水平，并观察大鼠存活情况和脏器损伤的病理变化。结果：ＩＲ损伤后，各用药组大鼠存活时间均明显长于ＩＲ损伤组；假手术组损伤前血浆ＴＮＦ含量较损伤后变化不明显，其余各组损伤后血浆ＴＮＦ及ＰＬＡ２含量均显著高于损伤前，且各用药组血浆ＴＮＦ含量均较损伤组明显下降；损伤后肝和肠组织中ＰＬＡ２与假手术组比较均增高，用药组并无明显下降。ＩＲ损伤组肺灌洗液ＴＮＦ和ＰＬＡ２含量明显高于假手术组；用药组与损伤组比较ＰＬＡ２变化不明显。光镜和电镜下仍可见到肺组织有明显改变，但轻于ＩＲ损伤组，肺泡腔渗出较少，中性粒细胞聚集明显减轻。结论：ＰＬＡ２激活在肠ＩＲ导致的远端脏器肺损伤过程中有着重要的作用，使用ＰＬＡ２阻断剂可减轻肠ＩＲ后肺组织损伤，其机制可能与降低血浆ＴＮＦ以及肺灌洗液中ＴＮＦ和ＰＬＡ２有关。
Objective:To investigate the potential mechanism with regard to phospholipase A 2(PLA 2) activation in mediating tumor necrosis factor (TNF) or other inflammatory mediators release after intestinal ischemiareperfusion(IR) injury.Methods:In a rat model of intestinal IR injury,TNF,PLA 2 levels in plasma and pulmonary lavage fluid,and PLA 2 contents in the liver and intestine were determined by radioimmunoassay.Also,the survival time and pathological changes in vital organs were observed.Results:After intestinal IR injury,the survival time of various treatment groups was significantly longer than that of IR injury group.Plasma TNF and PLA 2 levels were markedly higher in different groups prior to injury compared to baseline values and plasma TNF levels were obviously decreased in treated groups,but no significant changes in TNF levels were observed in shamoperated group (0 65±0 19) ng/L vs.(0 73±0 18)ng/L .Meanwhile,a significant elevation of PLA 2 in the liver and intestine was found in injury group compared to shamoperated group,while it wasn′t influenced by treated with PLA 2 inhibitors.Similarly,TNF and PLA 2 levels in pulmonary lavage fluid were significantly higher in IR injury groups than that in shamoperated group,while no marked difference in pulmonary lavage fluid PLA 2 was observed between treatment group and injury group.Furthermore,it was revealed some pathological changes in the lung in both injury and treatment groups under light microscopy as well as electron microscopy,but relatively minor damage to the lung could be noted in treatment group,such as reduction of alveolar exudate and attenuation of neutrophil infiltration.Conclusions:The activation of PLA 2 plays an important role in the pathogenesis of intestinal IR injury.PLA 2 inhibitors can reduce the pulmonary tissue damage secondary to acute intestinal ischemia,which may be associated with decrease in plasma TNF and pulmonary lavage fluid TNF and PLA 2.
出处
《中国危重病急救医学》
CAS
CSCD
1998年第8期486-489,共4页
Chinese Critical Care Medicine
基金
军队九五指令性课题
关键词
磷脂酶A2
缺血
再灌注损伤
肠
肿瘤坏死因子
phospholipase A 2\ \ intestinal ischemiareperfusion injury\ \ tumor necrosis factor
