Modigliani R, Matchansky C, Bernier J J
Dig Dis Sci. 1979 Oct;24(10):763-8. doi: 10.1007/BF01317209.
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.
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。