摘要
目的 一氧化氮 (NO)参与休克的血管扩张 ,血压下降 ,但它对组织损伤 ,特别是肠道的损伤及细菌移位的作用仍不十分清楚。本实验以NO合酶 (NOS)底物左旋精氨酸及其抑制剂硝基左旋精氨酸 (LNNA)为工具 ,观察NO对内毒素血症时大鼠肠道损伤及细菌移位的影响。方法 用内毒素 (LPS ,10mg/kg,ip)复制内毒素血症模型 ,给予LNNA或L -arg抑制或促进NO合成 ,测定肠道脂质过氧化物丙二醛 (MDA)的含量 ,二胺氧化酶 (DAO)活性及肠系膜淋巴结细菌培养。结果 LPS可降低肠组织DAO活性 ,增加MDA含量和肠系膜淋巴结细菌移位的发生率和细菌数量 ;用LNNA抑制NO后可加重LPS的上述作用 ,而给予L -arg促进NO合成则可减轻LPS的作用。结论 本实验结果表明在内毒素血症时 ,抑制NO可加重肠道损伤和细菌移位的发生 。
Objective The effects of nitric oxide(NO) on the endotoxin induced tissue damage,especially intestinal injury and bacterial translocation are still poorly known, although its involvement in vasodilatation and hypotenion in shock is much clear. So, the intestinal damage and bacterial translocation were observed in this study in endotoxemic rats after treatment with N ω nitro L arginine(LNNA),the special inhibitor of NO synthase(NOS),and L arginine,the substrate of NOS.Methods The endotoxemia was conducted with administration of lipopolysaccharide(O111B4,10mg/kg,i.p.),animals were treated with LNNA(4mg/kg,i.p.)or L-arg(40mg/kg,i.p.).Intestinal molondialdehyde(MDA) content and Diamine oxidase(DAO) activity were determined,and mesenteric lymph nodes were cultured.Results The results showed that endotoxin decreased intestinal DAO acitivity but increased MDA content and incidence of bacterial translocation to mesenteric lymph nodes.These effects of endotoxin were aggregated by inhibition of NO production with LNNA, but attenuated by L arg.Conclusion We concluded that inhibition of NO formation might enhance endotoxin induced intestinal damage and bacterial translocation,which suggested that NO might play a protective role in this endotoxemia model.
出处
《重庆医学》
CAS
CSCD
2001年第1期4-5,共2页
Chongqing medicine
