Calignano A, Whittle B J, Di Rosa M, Moncada S
Wellcome Research Laboratories, Beckenham, Kent, UK.
Eur J Pharmacol. 1992 Dec 15;229(2-3):273-6. doi: 10.1016/0014-2999(92)90567-n.
The effect of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on the motility of the small intestine in an acute model in the anaesthetised rat was determined by changes in jejunal intraluminal pressure. L-NAME (0.5-10 mg kg-1 i.v.) caused a dose-dependent increase in intraluminal pressure and initiated phasic intestinal contractions. These responses were inhibited by concurrent administration of L-arginine (200 mg kg-1 i.v.) but not by D-arginine (200 mg kg-1). The increase in jejunal motility induced by L-NAME was attenuated by atropine (4 mg kg-1), although even high doses of atropine (16 mg kg-1) did not abolish these responses. This indicates that although there are interactions between NO and muscarinic cholinergic mechanisms, other processes are also involved in these contractile events following administration of L-NAME. These observations in the rat suggest that endogenous NO plays a role in the modulation of intestinal motility in vivo.
通过空肠腔内压力的变化，测定了一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）对麻醉大鼠急性模型小肠运动的影响。L-NAME（0.5 - 10 mg kg-1静脉注射）导致腔内压力呈剂量依赖性增加，并引发小肠阶段性收缩。同时给予L-精氨酸（200 mg kg-1静脉注射）可抑制这些反应，但给予D-精氨酸（200 mg kg-1）则无此作用。阿托品（4 mg kg-1）可减弱L-NAME诱导的空肠运动增加，尽管即使高剂量的阿托品（16 mg kg-1）也不能消除这些反应。这表明，虽然NO与毒蕈碱胆碱能机制之间存在相互作用，但在给予L-NAME后的这些收缩事件中，其他过程也参与其中。在大鼠中的这些观察结果表明，内源性NO在体内小肠运动的调节中发挥作用。
