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本实验观察休克时小肠因素在肺损伤中的作用。家兔随机分为SMAO休克组(n=11)和假休克组(n=8),结果发现,肠系膜上动脉夹闭(SMAO)60分钟再灌注,肺毛细血管通透指数(PCPI)和肺组织丙二醛(MDA)含量增加,肺泡和支气管充血、水肿、出血及肺夏型细胞结构损伤,肠病理损伤与肺损伤间有明显相关关系,但未见PaO_2下降。用SMAO 90分钟猫的SMV血血浆灌注离体大鼠肺标本(实验组,n=9;对照组,n=8),致被灌注肺的肺动脉溜注压、PCPI和灌流液中MDA含量及乳酸脱氢酶活性显著升高。提示缺血小肠再灌注时释放的体液因素可直接引起肺损伤。
This experiment observed the role of intestinal factors in lung injury during shock. The rabbits were randomly divided into three groups: SMAO shock group (n = 11) and sham shock group (n = 8). The results showed that SMAO 60 minutes reperfusion, pulmonary capillary permeability index Tissue malondialdehyde (MDA) content increased, alveolar and bronchial congestion, edema, hemorrhage and lung summer cell structure damage, pathological injury and lung injury have a significant correlation between lung injury, but no decline in PaO_2. Pulmonary arterial perfusion pressure, PCPI, and perfusate MDA content in perfusate-evoked lung tissue were measured by perfusion of isolated rat lung specimens (experimental group, n = 9; n = 8) Lactate dehydrogenase activity was significantly increased. It is suggested that the humoral factors released during ischemia reperfusion may directly cause lung injury.