Iwata F, Endoh K, Leung F W
Research Service, Sepulveda Veterans Administration Medical Center, Los Angeles, California 91343.
Dig Dis Sci. 1994 Feb;39(2):347-52. doi: 10.1007/BF02090207.
We tested the hypotheses that the protective effect of intragastric nicotine against ethanol-induced gastric mucosal injury is dependent on endogenous nitric oxide or peripheral sympathoadrenal mechanisms. Rats were pretreated with NG-nitro-L-arginine methyl ester (3 mg/kg subcutaneous, 1 h prior to study) to block endogenous nitric oxide synthesis or with adrenal medullectomy (three weeks prior to study) to ablate the effect of the adrenal medulla. At 1-h intervals, vehicle or nicotine (4 mg/kg) and 40% ethanol were then given intragastrically. The total lengths of the linear gastric corpus mucosal lesions were measured unbiasedly. The protective effect of intragastric nicotine was not modified by either pretreatment. We conclude that the mechanism mediating intragastric nicotine protection against 40% ethanol-induced gastric mucosal injury is independent of endogenous nitric oxide or the adrenal medulla.
胃内尼古丁对乙醇诱导的胃黏膜损伤的保护作用取决于内源性一氧化氮或外周交感肾上腺机制。大鼠在研究前1小时皮下注射NG-硝基-L-精氨酸甲酯（3毫克/千克）以阻断内源性一氧化氮合成，或在研究前三周进行肾上腺髓质切除术以消除肾上腺髓质的作用。然后每隔1小时给大鼠胃内注射溶媒或尼古丁（4毫克/千克）以及40%乙醇。无偏测量胃体部线性黏膜损伤的总长度。两种预处理均未改变胃内尼古丁的保护作用。我们得出结论，介导胃内尼古丁对40%乙醇诱导的胃黏膜损伤保护作用的机制独立于内源性一氧化氮或肾上腺髓质。
