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目的初步探讨血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)在大鼠全氟异丁烯(PFIB)急性吸入性肺损伤中的作用。方法 28只雄性Wistar大鼠,随机分为空白对照组(0 h)和PFIB染毒后1、2、4、8、16和24 h活杀组(n=4)。其中PFIB染毒组头部暴露动态吸入PFIB染毒(剂量为145 mg/m3×8 min),空白对照组于过滤空气暴露8min。分别在染毒后相应时间点收集大鼠肺组织、血浆和支气管肺泡灌洗液(brochoalveolar lavage fluid,BALF)等样本,测定肺湿/干重比(W/D)、BALF蛋白含量,并进行肺组织病理学检查;同时测定肺组织匀浆与血浆中AngⅡ含量及肺组织匀浆血管紧张素转换酶(angiotensin converting enzyme,ACE)活性。结果大鼠PFIB染毒后16 h肺W/D和BALF中蛋白含量显著升高,发生急性肺间质与肺泡水肿,伴大量多形核白细胞渗出,染毒后24 h肺损伤程度明显缓解。肺组织AngⅡ含量在染毒后8 h前各时点呈现升高的趋势,但无统计学意义,染毒后16 h与24 h则显著低于空白对照组;血浆中AngⅡ含量与肺组织ACE酶活性在染毒后各时点呈现一定程度的波动,但与对照组比较均无显著性差异。结论大鼠吸入PFIB中毒后肺组织ACE活性及AngⅡ含量与肺损伤程度未见明显关联,其病理学意义有待进一步探讨。
Objective To investigate the role of angiotensin Ⅱ (AngⅡ) in acute lung injury induced by perfluoroisobutylene (PFIB) in rats. Methods Twenty - eight male Wistar rats were randomly divided into control group (0 h) and alive groups (n = 4) at 1, 2, 4, 8, 16 and 24 h after PFIB exposure. PFIB exposure group was exposed to PFIB (dose 145 mg / m3 × 8 min), while the blank control group was exposed to filtered air for 8 min. The lung tissue, plasma and bronchoalveolar lavage fluid (BALF) were collected from rats at the corresponding time points after exposure, and the lung wet / dry weight ratio (W / D) and BALF protein content were determined. Lung histopathological examination was performed. The content of AngⅡ and the activity of angiotensin converting enzyme (ACE) in lung homogenate and plasma were measured simultaneously. Results The protein levels of W / D and BALF were significantly increased at 16 h after PFIB exposure in rats. Acute pulmonary interstitial and alveolar edema occurred with exudation of many polymorphonuclear leukocytes. The severity of lung injury at 24 h after PFIB exposure was relieved . The content of AngⅡin lung tissue showed an upward trend at each time point 8h after exposure, but there was no statistical significance. The content of AngⅡ in plasma was significantly lower than that in control group at 16 h and 24 h Enzyme activity showed a certain degree of fluctuation at various time points after exposure, but no significant difference compared with the control group. Conclusions There is no significant correlation between the activity of ACE and the content of Ang Ⅱ in pulmonary tissue and the severity of lung injury after inhalation of PFIB in rats. The pathological significance needs to be further explored.