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目的探讨肾素-血管紧张素系统(renin-angiotensin system,RAS)中血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)在全氟异丁烯(perfluoroisobutylene,PFIB)吸入性急性肺损伤(acute lung injury,ALI)中的作用。方法使用全身暴露PFIB染毒装置对CD1小鼠实施染毒,采用AngⅡ1型受体(angⅡ1-type receptor,AT1)特异性抑制剂氯沙坦钾作为工具药,以肺系数、支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)总蛋白含量及72 h内存活率为观察指标,评估AT1受抑制状态下肺损伤情况。结果与结论在PFIB染毒前0.5 h、染毒后0.5 h、1 h经腹腔注射方式给予实验CD1小鼠氯沙坦钾(40 mg/kg),虽然对各项ALI指标均有一定的改善趋势,但并不能起到显著的防治效果。以AngⅡ为主要成分的RAS可能并不参与PFIB吸入性急性肺损伤早期炎症反应的扩大过程。
Objective To investigate the role of angiotensin Ⅱ (AngⅡ) in renin-angiotensin system (RAS) in perfluoroisobutylene (PFIB) -induced acute lung injury (ALI) effect. Methods CD1 mice were exposed to systemic exposures to PFIB. Losartan, a specific inhibitor of angiotensin Ⅱ type 1 receptor (angiotensin Ⅱ type 1 receptor, AT1), was used as a tool. Lung function, bronchoalveolar lavage fluid (BALF) total protein content and the survival rate within 72 h were observed to evaluate the lung injury induced by AT1. RESULTS AND CONCLUSION Losartan potassium (40 mg / kg) was administered intraperitoneally at 0.5 h prior to PFIB exposure and at 0.5 h and 1 h after exposure to PFIB, although ALI was improved to some extent Trend, but can not play a significant control effect. RAS, which is mainly composed of AngⅡ, may not participate in the expansion of early inflammatory reaction in PFIB-induced acute lung injury.