摘要
钨酸钠对iv灭活大肠杆菌所致大白鼠内毒素休克时的肺损伤有明显保护作用,表现在喂钨组血压、外周血白细胞总数与中性粒细胞百分数无明显下降,血浆丙二醛(MDA)无明显升高。肺组织中,MDA含量以及黄嘌呤氧化酶(XOD)活性均比不喂钨组低;肺组织干/湿重比值和钨/钼(W/Mo)比值比不喂钨组高。存活率亦增高。NS对照组各项指标无明显变化。其机制可能与钨抑制XOD,使氧自由基(OFRs)生成减少有关。本实验还提示整体条件下,(即PMN和XOD均存在时),内毒素休克所致肺损伤时,XOD是氧自由基产生的始动因素。
The present study was attempted to observe the protective effects of tungsten(W) on the lung injury induced by endotoxin (ET) in rats and to analyze its' mechanisms. 29 male Wistar rats were randomly divided into three groups: (1) ET group(n = 11), given a bolus injection of disintegrated E. coli (5.4×1010 organisms/kg); (2) ET + W group (n=12) , given an equivalent E. coli after being pretreated with Sod. Tungstate rich food and water for 4-5 weeks and (3) Control group (N.S,n = 6). Theresults showed that the following parameters in ET + W group had significant difference at 120 minutes after injection of ET as compared with ET group (P<0.05 or <0.01) , BP (78.2±6.4 vs 31.8±10.0mm Hg) , Total count of WBC (114.8±9.2%) vs 41.6±4.8%) ; PMN% (131.9±6.1 vs 41.6±4.7) ; in the lung tissue, the level of MDA (7.9±1.4 vs 10.4±2.4nMol/mg protein) ; activity of XOD (11.3±7.0 vs 167.0±14.2u/mg protein) ; D W/W W (0.22±0.02 vs 0.15±0.01) ; the ratio of W/Mo (24.89±2.51 vs 0.48±0.02) and survival rate (100% vs 54.5%). Pathological examination also revealed less morpholog ical changes and less infiltration of WBCs in the lung in ET + W group than that in ET group. The results suggested that W could piotect ET induced lung injury in rats.
出处
《基础医学与临床》
CSCD
1993年第4期71-74,共4页
Basic and Clinical Medicine
基金
国家自然科学基因资助课题
