摘要
目的 :探讨一氧化氮 (NO)在肝缺血再灌注损伤中的作用。方法 :利用大肠杆菌内毒素 (LPS)和N 单甲基 L 精氨酸 (L NAME)激发和抑制兔体内NO合成 ,检测血清中亚硝酸盐 (NO2 )、脂质过氧化产物 (LPO)、谷丙转氨酶(GPT)的含量 ,观察肝组织病理学改变。结果 :LPS能激发NO合成 ,6h达高峰 (P <0 .0 1) ,而L NAME则能抑制NO合成 ,NO上升导致肝缺血再灌注时的GPT上升 (P <0 .0 1) ,加重肝组织缺血再灌注损伤 ,现时伴随LPO显著升高 ,而L NAME测能逆转这种现象。病理组织学变化与GPT变化一致。结论
Aims:t o investigates the role of Nitric Oxide (NO) in hepatic Ischemia-Reperfusion injury. Methods: 50 rabbits were randomly divided into 5 groups, Blood was sampled for testing nitrate, Glutamic Pyruvic transaminase (GPT) and for Lipid Peroxide(LPO), liver tissue was sampled for pathological mophology. Results: NO production was induced by pretreatment with Escherichia Coli Lipopo Lysaccharide(LPS). The induction leads to an increase in hepatic injury during Ischemia-Reperfution and was ameliorated by the NG Monomethyl L Arginine(L NAME). LPO during Ischemia Reperfution,a measure of lipid peroxidation, was increased and was also decreased by L NAME.Conclusions:the data suggest that NO may increase rabbit liver injury during Ischemia Reperfusion by increasing lipid peroxidation.
出处
《江西医学院学报》
2001年第4期13-15,共3页
Acta Academiae Medicinae Jiangxi
