摘要
目的 观察外源性正常淋巴液对脂多糖 (LPS)所致大鼠内毒素休克的干预作用 ,初步探讨其作用机制。方法 Wistar雄性大鼠 4 0只 ,随机分为内毒素组、淋巴液组、血浆组、正常组。前 3组复制内毒素休克模型 (LPS ,5mg/kg·bw ,iv) ,正常组以等量生理盐水代替LPS。 15min后 ,淋巴液组输入仅占全血量 1/ 15的无细胞淋巴液。血浆组以血浆代替淋巴液 ,内毒素组和正常组以生理盐水代替淋巴液。给予LPS后 4h,取血浆及心、肝、肾、肺组织匀浆 ,对比观察血浆及组织中肿瘤坏死因子 -α(TNF -α)、一氧化氮 (NO)、一氧化氮合酶 (NOS)、诱导型一氧化氮合酶 (iNOS)、超氧化物歧化酶 (SOD)及丙二醛 (MDA)含量的变化。结果 淋巴液干预后 ,淋巴液组血浆TNF -α水平为 18.81± 3.70fmol/mL、NO含量为 4 6 .0 2± 9.2 9μmol/L、NOS活性为 2 5 .16± 4 .2 0U/mL、SOD活性为 10 2 .15± 17.88NU/mL、MDA水平 8.19± 1.6 4nmol/mL ,与其余 3组相比 ,各项指标差异均有统计学意义 (P <0 .0 5～ 0 .0 1)。结论 外源性正常淋巴液对内毒素休克具有干预作用 ,其机制可能与减少细胞因子及自由基损伤有关。
Objective To observe the effects of exogenous normal lymph on endotoxic shock induced by LPS and discuss its mechanisms. Methods Forty male Wistar rats were randomly divided into four groups: endotoxin group, lymph group, plasma group and normal group. The rats in the preceding three groups were injected intravenously with lipopolysaccharide(LPS,5 mg/kg.bw,iv)to duplicate endotoxic shock model. LPS was replaced by equivalent normal saline in the normal group. 15 minutes later, lymph without cell components was infused in lymph group. The amount of lymph was one fifteenth of blood volume. In plasma group, lymph was replaced by plasma. In normal and endotoxin groups, lymph was replaced by normal saline. When 4 hours passed after the infusion of LPS, we prepared the plasma fraction and homogenate from tissues of heart, liver, kidney and lung. Subsequently, we detected the changes of tumor necrosis factor-alpha(TNF-α),nitric oxide(NO),nitric oxide synthases(NOS),inducible nitric oxide synthases(iNOS),superoxide dismutase(SOD) and malondialdehyde(MDA). Results After lymph infusion, all parameters including the plasma TNF-α level (18.81±3.70 fmol/mL), NO concentration(46.02±9.29 μmol/L),NOS activity(25.16±4.20 U/mL),SOD activity(102.15±17.88 NU/mL)and MDA level(8.19±164 nmol/mL) in lymph group showed significant statistically difference when compared with three other groups (P<0.05～0.01).Conclusion Exogenous normal lymph may be of value in the process of interfering in endotoxic shock. Alleviating the production of cell factors and inhibiting lipid peroxidation may be the relevant mechanisms.
出处
《中国急救医学》
CAS
CSCD
北大核心
2004年第9期661-664,共4页
Chinese Journal of Critical Care Medicine
