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目的探讨肺泡上皮细胞膜上Na+-K+-ATP酶在盐酸(HCl)和脂多糖(LPS)两种原因致急性肺损伤大鼠肺水生成中的作用及地塞米松(Dex)治疗肺水肿的意义。方法96只雄性SD大鼠随机分为6组(每组16只):生理盐水对照组(NS组)、NS+Dex组、HCl模型组、HCl+Dex组、LPS模型组、LPS+Dex组,每组又分为支气管肺泡灌洗(BAL)亚组和非支气管肺泡灌洗(NBAL)亚组。NBAL组观察肺组织病理改变、湿干重比(W/D)、Na+-K+-ATP酶水解活性和哇巴因与其受体Na+-K+-ATP酶特异性结合位点数量的变化;BAL组观察支气管肺泡灌洗液(BALF)中细胞数及蛋白含量的变化。结果①两种模型组Na+-K+-ATP酶水解活性和酶位点数在激素干预前均显著低于干预后水平,并且显著低于对照组水平。②激素干预前两种模型组BALF中细胞总数、PMN分类计数、蛋白含量显著高于干预后水平,显著低于对照组水平。结论Na+-K+-ATP酶在肺水的转运中起重要作用,ALI时肺泡膜上Na+-K+-ATP酶的活性降低可能是产生肺水肿的重要机制之一,地塞米松可以分别增加两种模型组Na+-K+-ATP酶水解活性和位点数;地塞米松可以减轻LPS组肺水肿(以W/D表示)的程度,但对HCl组无效。
Objective To investigate the role of Na + -K + -ATPase in alveolar epithelial cell membrane in the pulmonary effusion of acute lung injury induced by hydrochloric acid (HCl) and lipopolysaccharide (LPS) in rats and the significance of dexamethasone (Dex) in treating pulmonary edema . Methods Ninety-six male Sprague-Dawley rats were randomly divided into six groups (n = 16): saline control group (NS group), NS + Dex group, HCl model group, HCl + Dex group, LPS model group, LPS + Dex group Each group was further divided into bronchoalveolar lavage (BAL) subgroups and non-bronchoalveolar lavage (NBAL) subgroups. The changes of pathological changes, wet / dry weight ratio (W / D), Na + -K + -ATPase activity and specific binding site of ouabain to its receptor Na + -K + -ATPase in NBAL group were observed. The changes of cell number and protein content in bronchoalveolar lavage fluid (BALF) were observed. Results ① The activity of Na + -K + -ATPase and the number of enzyme sites in both model groups before and after hormone intervention were significantly lower than those after intervention, and were significantly lower than those in control group. ② The total number of cells, PMN count and protein content in BALF of the two models before hormone intervention were significantly higher than those after intervention and significantly lower than those of the control group. Conclusions Na + -K + -ATPase plays an important role in lung water transport. The decrease of activity of Na + -K + -ATPase in alveolar membrane may be one of the important mechanisms of pulmonary edema in ALI. Dexamethasone can increase two Dexamethasone attenuated the degree of pulmonary edema (expressed as W / D) in LPS group, but not in HCl group.