一氧化氮在大鼠肝缺血再灌注损伤中的作用

• 作 者: 陈玺华 李正中 鲍民生 郑绘霞
• 机 构: 山西医科大学第一医院普外科
• 出 处: 世界华人消化杂志
• 发表日期: 1999年04期
• 关键词: 一氧化氮 大鼠

目的探讨一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）在大鼠肝缺血再灌注（Ｉ／Ｒ）损伤中的作用．方法采用大鼠肝脏原位Ｉ／Ｒ模型，预先经伤寒菌内毒素脂多糖（ＬＰＳ，５００μｇ／ｋｇ）处理，术前腹腔注射Ｌ精氨酸（ＬＡｒｇ，５００ｍｇ／ｋｇ）或Ｌ硝基精氨酸（ＬＮＮＡ，２０ｍｇ／ｋｇ）分别观察分析血清ＮＯ，ＡＬＴ，ＡＳＴ；肝组织ＮＯ、脂质过氧化物（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）以及肝组织病理损伤．结果经ＬＰＳ预处理后引起肝脏ＮＯ的大量合成（ＮＯ，μｍｏｌ／Ｌ，１０８±２１ｖｓ２５±６，Ｐ＜００１，μｍｏｌ／ｇ，０８０９±０１２５ｖｓ０２０８±００７１，Ｐ＜００１）．肝脏经过２０ｍｉｎ缺血和３０ｍｉｎ再灌注后导致明显的肝损伤（ＡＬＴ，ｎｍｏｌ／ｓ，７５５２±７８３ｖｓ１３１７±３６７，Ｐ＜００１，ＡＳＴ，ｎｍｏｌ／ｓ，６５３５±１８６７ｖｓ２４１７±８６７，Ｐ＜００１）．注射ＬＮＮＡ后，抑制了ＮＯ合成，同时更进一步加重了肝损伤（ＡＬＴ，ｎｍｏｌ／ｓ，１９７５４±６３８５ｖｓ７５５２±７８３，Ｐ＜００１，ＡＳＴ，ｎｍｏｌ／ｓ，１９９３７±５９８５ｖｓ６５３５±１８６７，Ｐ＜００１）．而施加Ｌ?

Objective To investigate the role of nitric oxide (NO) in hepatic ischemia-reperfusion (I / R) injury in rats. Methods Rat liver in situ I / R model was pretreated with lipopolysaccharide (LPS, 500μg / kg), and intraperitoneal injection of LArg (500μg / kg) or LArg Nitric arginine (LNNA, 20mg / kg) were used to observe the levels of serum NO, ALT, AST, liver NO, LPO, SOD, . Results LPS pretreatment resulted in massive synthesis of NO in the liver (NO, μmol / L, 108 ± 21 vs 25 ± 6, P <001, μmol / g, 0809 ± 0125 vs 0208 ± 0071, P <001). Hepatic ischemia and reperfusion after 20 min resulted in significant liver injury (ALT, nmol / s, 7552 ± 783 vs 1317 ± 367, P <001, AST, nmol / s, 6535 ± 1867 vs 2417 ± 867, P < 01). After injection of LNNA, NO synthesis was inhibited and liver injury was further aggravated (ALT, nmol / s, 19754 ± 6385 vs 7552 ± 783, P <001, AST, nmol / s, 19937 ± 5985 vs 6535 ± 1867, P <001). While applying L?