摘要
目的研究大鼠内毒素血症时循环肾素血管紧张素系统(RA S)的变化,探讨内毒素血症的病理机制。方法90只雄性W istar大鼠,随机分为正常对照组(n=10)和模型组(n=80),模型组又分为注射脂多糖(LPS)后2、4、8、12、24、48、72 h及7 d 8个时间点,每个时间点10只。分别于腹腔注射LPS后相应时间点处死动物,取心脏血,测定血浆内毒素、肾素活性(PRA)、血管紧张素Ⅱ(AⅡ)以及血清肿瘤坏死因子α(TNFα)、白细胞介素10(IL 10)、血管紧张素Ⅰ转换酶(ACE)的变化,并与正常对照组比较。结果①模型组血浆内毒素和血清TNFα、IL 10水平均在腹腔注射LPS后2 h达高峰,分别在注射LPS后7 d、8 h和8 h降至正常水平。②模型组血浆PRA和血清AⅡ、ACE水平分别在腹腔注射LPS后2、8 h和8 h达高峰,分别于注射LPS后12、72和24 h降至正常水平。结论内毒素血症时,机体产生一系列炎症反应和抗炎反应,释放大量细胞因子和炎症介质,同时循环RA S激活,引起血管收缩,导致微循环障碍,可进一步加重组织细胞缺血、缺氧。研究内毒素血症时RA S改变对阐明内毒素血症的病理机制具有一定价值。
Objective To investigate the changes in circulatory renin -αngiotensin system （RAS） in rats with endotoxernia and explore its mechanism. Methods Ninety Wistar rats were randomly divided into normal control group （n= 10） and endotoxemia groups （n = 80）. The endotoxemia group was further divided into subgroups of 2, 4, 8, 12, 24, 48, 72 hours and 7 days after injection of lipopolysaccharide （LPS） into the abdominal cavity （each n= 10）. The rats were sacrificed at different time points after LPS （10 mg/kg） challenge. Contents of plasma LPS, plasma renin activity （PRA）, plasma angiotensin Ⅱ （A Ⅰ ）, angiotensin - converting enzyme （ACE）, tumor necrosis factor -α （TNF -α）, and interleukin - 10 （IL - 10） were deterininated. Results ① Plasma LPS, TNF a and IL - 10 reached highest levels 2 hours after LPS injection, and they returned to normal levels 7 days, 8 hours and 8 hours after LPS challenge respectively. ② The levels of plasma PRA, A Ⅱ and ACE reached highest levels 2, 8 and 8 hours after LPS challenge respectively, and they returned to normal levels 12, 24 and 72 hours after LPS injection, respectively. Conclusion During endotoxemia, there is a series of inflammatory reactions and anti- inflammatory reactions, and a large number of cytokines and inflammatory mediators are released. At the same time, the circulating RAS is activated, which causes constriction of blood vessel and dysfunction of the microcirculation aggravating hypoxia of cells. The study of the changes in RAS is significant to interpreting the pathogenetic mechanism of endotoxemia in rats.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2006年第2期92-95,共4页
Chinese Critical Care Medicine
基金
北京市自然科学基金资助项目(7032017)
北京市优秀人才培养专项经费资助项目(200410300103)
