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成人乳糜泻患者空肠对前列腺素E1反应时水和离子分泌减少。

Depressed jejunal secretion of water and ions in response to prostaglandin E1 in adult celiac disease.

作者信息

Modigliani R, Matchansky C, Bernier J J

出版信息

Dig Dis Sci. 1979 Oct;24(10):763-8. doi: 10.1007/BF01317209.

Abstract

In order to test in man the concept that intestinal fluid secretion originates from the crypts of Lieberkühn, we assessed the jejunal secretory effect of intraluminal prostaglandin E1 (PGE1) (0.9 microgram/kg/min) in untreated adult celiac disease (ACD, N = 7), treated ACD (N = 4) and normal subjects using the intestinal perfusion technique. In untreated ACD (1) water and solutes were malabsorbed (or secreted) in the basal period; (2) fluid and ion secretion seen during PGE1 infusion and net secretory effect of PGE1 (difference in transport between basal and PGE1 periods) were reduced (P less than 0.01); (3) the effects of PGE1 inhibition of sodium insorption, and stimulation of sodium exsorption, were decreased and abolished, respectively. In treated patients PGE1-induced secretion returned towards normal values. Our finding of a depressed secretory response to PGE1 in the face of marked crypt hypertrophy do not support the concept that crypt cells are the major site of intestinal fluid secretion.

摘要

为了在人体中验证肠液分泌源自利伯kühn隐窝这一概念,我们采用肠道灌注技术,评估了腔内前列腺素E1(PGE1)(0.9微克/千克/分钟)对未经治疗的成年乳糜泻(ACD,N = 7)、已治疗的ACD(N = 4)和正常受试者空肠的分泌作用。在未经治疗的ACD中:(1)基础期水和溶质吸收不良(或分泌);(2)PGE1输注期间观察到的液体和离子分泌以及PGE1的净分泌作用(基础期和PGE1期之间的转运差异)降低(P < 0.01);(3)PGE1抑制钠吸收和刺激钠排泄的作用分别降低和消失。在已治疗的患者中,PGE1诱导的分泌恢复到正常值。我们发现,尽管隐窝明显肥大,但对PGE1的分泌反应仍降低,这并不支持隐窝细胞是肠液分泌主要部位的概念。

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