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内源性血管加压素在束缚和水浸诱导的胃溃疡形成中的作用。

Role of endogenous vasopressin in development of gastric ulcer induced by restraint and water immersion.

作者信息

Honda K, Fukuda S, Ishikawa S E, Kuzuya T, Saito T

机构信息

Department of Medicine, Jichi Medical School, Tochigi, Japan.

出版信息

Am J Physiol. 1994 May;266(5 Pt 2):R1448-53. doi: 10.1152/ajpregu.1994.266.5.R1448.

DOI:10.1152/ajpregu.1994.266.5.R1448
PMID:8203619
Abstract

To elucidate the role of arginine vasopressin (AVP) in the development of stress-induced gastric ulcer, the mucosal lesions after restraint and water immersion were examined in Brattleboro strain rats with hereditary hypothalamic diabetes insipidus (DI) and in Long-Evans rats (LE) used as controls. Restrained animals were immersed in water for 2 h, and the size of lesion was expressed as percentage of the lesion area to the total glandular mucosal area, which were defined as ulcer index (UI). In DI rats, UI was significantly higher than in control LE rats, despite the attenuated responses of plasma adrenocorticotropic hormone (ACTH) to stress. Although subcutaneous injection of selective antidiuretic analogue 1-desamino-8-D-AVP did not affect UI, intracerebroventricular (icv) administration of AVP reduced UI in DI rats, and icv administration of V1 antagonist [d(CH2)5Tyr(Me)]AVP elevated UI in LE rats. These results indicate that endogenous AVP plays a role in preventing the formation of gastric ulcers induced by stress via a central V1 receptor. Furthermore, we suggest that elevation of ACTH in plasma is not essential in the development of stress-induced gastric ulcer in rats.

摘要

为阐明精氨酸加压素(AVP)在应激性胃溃疡发生发展中的作用,我们检测了遗传性下丘脑尿崩症(DI)的Brattleboro品系大鼠以及作为对照的Long-Evans大鼠(LE)在束缚和浸水后的黏膜损伤情况。将受束缚的动物浸入水中2小时,损伤大小以损伤面积占总腺性黏膜面积的百分比表示,定义为溃疡指数(UI)。在DI大鼠中,尽管血浆促肾上腺皮质激素(ACTH)对应激的反应减弱,但UI显著高于对照LE大鼠。虽然皮下注射选择性抗利尿类似物1-去氨基-8-D-AVP对UI无影响,但向DI大鼠脑室内(icv)注射AVP可降低UI,而向LE大鼠脑室内注射V1拮抗剂[d(CH2)5Tyr(Me)]AVP可升高UI。这些结果表明,内源性AVP通过中枢V1受体在预防应激诱导的胃溃疡形成中发挥作用。此外,我们认为血浆ACTH升高在大鼠应激性胃溃疡的发生发展中并非必需。

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