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通过观察血红素氧化酶 (HO)阻断剂锌原卟啉 (ZnPP)对肺组织、肺泡间质多形核白细胞数目、肺组织丙二醛含量和湿重干重之比的影响 ,并对肺组织HO活性和血内碳氧血红蛋白水平 (COHb)进行检测 ,以探讨内源性HO/一氧化碳 (CO)在肢体缺血再灌注 (I/R)所致肺损伤中的作用。结果发现 ,大鼠双侧后肢I/R可导致急性肺损伤 ,同时使肺组织中HO活性和血内COHb水平显著升高 ;应用ZnPP预处理可使HO活性和COHb水平显著降低 ,但肺损伤却进一步加重。上述实验结果表明 ,肢体I/R致肺损伤时 ,肺组织中HO活性和内源性CO生成增多可减轻大鼠肢体I/R所致的肺损伤。
By observing the effect of zinc protoporphyrin (ZnPP), a heme oxygenase (HO) inhibitor, on the number of lung, alveolar interstitial polymorphonuclear leukocytes, the content of malondialdehyde in lung tissue and the ratio of wet weight to dry weight, HO activity and COHb in lung tissue were detected to explore the role of endogenous HO / CO in lung injury induced by limb ischemia-reperfusion (I / R). The results showed that bilateral hindlimb I / R in rats could induce acute lung injury, and at the same time, the HO activity and COHb level in lung tissue were significantly increased. Pretreatment with ZnPP significantly decreased the HO activity and COHb level, but the lung injury But further aggravate. The above experimental results show that limb I / R-induced lung injury, lung tissue HO activity and increased endogenous CO production can reduce rat limb I / R-induced lung injury.