摘要
目的 :采用大鼠肠缺血再灌注模型 ,对创伤休克后多系统器官衰竭中肺损伤的发生机制进行研讨。方法 :用动脉夹夹闭肠系膜上动脉根部 ,造成肠道缺血 ,于再灌注后取材。测定肺巨噬细胞分泌的一氧化碳 (NO)与肺组织一氧化碳全酶 (NOS)水平。并抽取左心室抗凝血测 O2 分压和 CO2 分压。结果 :模型组动物肺泡巨噬细胞分泌的 NO水平显著高于对照组 (P<0 .0 0 1) ,模型组肺内 NOS明显高于对照组 (P<0 .0 5 )。模型组动脉血 O2 分压明显低于对照组 ,而 CO2 分压明显高于对照组。结论 :肠道缺血再灌注后引起的肺内巨噬细胞过度活化 ,大量合成并释放 NO,可能是创伤休克后导致肺组织损伤的重要因素。
Objecctive: To explore the pathogenesis of lung injury during multiple system organ failure (MSOF) after traumatic shock by using intestinal ischemia reperfusion model of the rat.Methods: We nipped the root part of the upper mesentery artery to cause intestinal ischemia of the rat,then took the sample after reperfusing.We detected the levels of NO secreted by the alveolar macrophage and NOS in lung tissue; and we also detected the pressure of O 2 and CO 2 in the anticoagulant blood taken from the left ventricle.Results:The level of NO secreted by the alveolar macrphage and NOS in lung tissue in model group were remarkably higher than those in control group(respectively P <0.001, P <0.05).The pressure of O 2 in artery blood in model group was obviously lower than that in control group,but the pressure of CO 2 was higher than that in control group.Conclusion:NO was over synthesized and secreted by the active alveolar macrophage during intestinal ischemia reperfusion of the rat,which may be an important factor of lung injury after traumatic shock.
出处
《山西临床医药》
2001年第10期725-727,共3页
Shanxi Clinical Medicine
