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目的研究血管紧张素Ⅱ(AngⅡ)受体拮抗剂对大鼠内毒素性急性肺损伤(ALI)的保护作用。方法取Wistar大鼠60只,雌雄不拘,随机分为三组:(1)正常对照组(10只),给予大鼠静注等量生理盐水;(2)大肠肝菌脂多糖(LPS)组,分为3、6、12和24 h四个观察组(每组均10只),分别给大鼠注射LPS(10 mg/kg),间隔不同的时间后将大鼠放血活杀,取肺组织待测;(3)LPS+AngⅡ受体拮抗剂组(10只),先给予大鼠静注AngⅡ受体拮抗剂[Sar~1,Ile~8]AngⅡ(20μg/kg)处理,然后观察6 h,放血活杀后取肺组织待测。分别以肺湿/干重比、伊文思蓝法测定肺微血管通透性和肺组织病理变化,观察LPS对大鼠肺组织的急性损伤作用以及AngⅡ受体拮抗剂对该损伤作用的影响。结果与对照组比较,LPS组各时相点大鼠肺组织W/D值显著升高(P<0.01),致大鼠肺血管中伊文思蓝染料向组织中渗漏显著增多(P<0.01),LPS组出现炎性细胞浸润、水肿等损伤表现,总病理评分达(12.00±2.45)分;LPS+AngⅡ受体拮抗剂组大鼠肺组织湿/干重比、肺微血管蛋白渗出量和组织形态学变化均较LPS组显著好转。结论AngⅡ受体拮抗剂对大鼠内毒素性ALI有保护作用。
Objective To study the protective effect of angiotensin Ⅱ receptor antagonist on endotoxin-induced acute lung injury (ALI) in rats. Methods Sixty male Wistar rats were randomly divided into three groups: (1) normal control group (10 rats), rats were given equal volume of normal saline; (2) LPS group , Divided into three observation groups (3, 6, 12 and 24 h) (10 in each group). Rats were injected with LPS (10 mg / kg) respectively. After different time intervals, (3) LPS + AngⅡ receptor antagonist group (10 rats). Ang Ⅱ receptor antagonist [Sar ~ 1, Ile ~ 8] AngⅡ (20μg / kg) 6 h, take the lung tissue after bloodletting to kill. Lung wet / dry weight ratio and Evans blue method were respectively used to detect pulmonary microvascular permeability and lung histopathological changes. The acute injury of LPS to lung tissue and the effect of Ang II receptor antagonist on the injury were observed. Results Compared with the control group, the W / D of lung tissue in LPS group was significantly increased at each time point (P <0.01), and the leakage of Evans blue dye in the pulmonary vessels of rats significantly increased (P <0.01 ), LPS group showed inflammatory cell infiltration, edema and other injuries, the total pathological score (12.00 ± 2.45) points; LPS + Ang Ⅱ receptor antagonist group lung wet / dry weight ratio, pulmonary microvascular protein exudation And histological changes than the LPS group significantly improved. Conclusion Ang Ⅱ receptor antagonist has a protective effect on endotoxin ALI in rats.