Boughton-Smith N K, Hutcheson I R, Deakin A M, Whittle B J, Moncada S
Department of Pharmacology, Wellcome Research Laboratories, Beckenham, Kent, U.K.
Eur J Pharmacol. 1990 Dec 4;191(3):485-8. doi: 10.1016/0014-2999(90)94185-z.
Macroscopic jejunal damage and plasma leakage induced within 15 min by E. coli lipopolysaccharide (LPS 50 mg kg-1 i.v.) in the rat was enhanced by the inhibitor of nitric oxide (NO) formation, NG-monomethyl-L-arginine (L-NMMA 50 mg kg-1 i.v.). The nitro-vasodilator, S-nitroso-N-acetyl-penicillamine (SNAP; 10 micrograms kg-1 min-1 i.v.), which generates NO, attenuated both LPS-induced intestinal damage and the enhancement of such damage and plasma leakage produced by L-NMMA. Endogenous NO may thus have a protective role in the intestinal vasculature that can be mimicked by generators of NO.
在大鼠中，大肠杆菌脂多糖（静脉注射50毫克/千克）在15分钟内引起的宏观空肠损伤和血浆渗漏，被一氧化氮（NO）生成抑制剂N-甲基-L-精氨酸（静脉注射50毫克/千克）增强。生成NO的硝基血管扩张剂S-亚硝基-N-乙酰青霉胺（SNAP；静脉注射10微克/千克/分钟）减轻了LPS诱导的肠道损伤以及L-NMMA所产生的这种损伤和血浆渗漏的增强。因此，内源性NO可能在肠道血管系统中具有保护作用，这种作用可被NO生成剂模拟。
