Kaneko H, Tomomasa T, Tabata M, Morikawa A
Department of Pediatrics, Gunma University School of Medicine, Japan.
J Perinat Med. 1998;26(4):308-12. doi: 10.1515/jpme.1998.26.4.308.
Previous studies have suggested that the mechanisms involved in gastric mucosal protection in newborn rats are different from those in adult rats. The aim of this study was to determine whether nitric oxide (NO) has protective effects against ethanol-induced gastric mucosal damage in newborn rats. In 1-week-old rats, (1) pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, increased gastric mucosal damage induced by 35% ethanol dose-dependently (0.3-30 mg/kg), (2) concurrent administration of 300 mg/kg L-arginine (L-Arg) inhibited the L-NAME induced-increase in damage completely, and (3) pretreatment with low dose L-Arg (30 mg/kg) decreased the mucosal damage induced by 60% ethanol. We concluded that endogeneous NO is involved in the protective mechanism of the gastric mucosa in neonatal rats.
先前的研究表明，新生大鼠胃黏膜保护机制与成年大鼠不同。本研究旨在确定一氧化氮（NO）对新生大鼠乙醇诱导的胃黏膜损伤是否具有保护作用。在1周龄大鼠中，（1）用NO合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）预处理，35%乙醇诱导的胃黏膜损伤呈剂量依赖性增加（0.3-30mg/kg），（2）同时给予300mg/kg L-精氨酸（L-Arg）可完全抑制L-NAME诱导的损伤增加，（3）低剂量L-Arg（30mg/kg）预处理可减轻60%乙醇诱导的黏膜损伤。我们得出结论，内源性NO参与新生大鼠胃黏膜的保护机制。
