Munck L K, Mertz-Nielsen A, Westh H, Bukhave K, Beubler E, Rask-Madsen J
Department of Medicine G, Bispebjerg Hospital, University of Copenhagen, Denmark.
Gut. 1988 Oct;29(10):1337-41. doi: 10.1136/gut.29.10.1337.
Studies in the rat jejunum in vivo have shown that 5-hydroxytryptamine (5-HT) causes secretion of fluid and luminal release of prostaglandin (PG) E2. These effects can be blocked by indomethacin and ketanserin, which suggests that PGE2 may be an important intermediate in the transduction mechanism leading to 5-HT induced fluid secretion. To test this hypothesis in man 'steady state' perfusions (9 ml/min) were done in eight healthy volunteers using the triple lumen technique. The proximal jejunum was perfused with Ringer's solution which contained 51Cr-EDTA as a non-absorbable marker. Before and after the administration of indomethacin (1.0 mg/kg iv) the effects of exogenous 5-HT (10 micrograms/kg/min iv) on jejunal net transport of fluid and electrolytes and jejunal flow rate (JFR) of PGE2 were measured in 15-min periods for 2 x 60 minutes after a 60 minute control period. 5-HT reversed fluid and electrolyte absorption into profuse secretion (p less than 0.01, Duncan's multiple range test) and significantly increased JFR of PGE2 (p less than 0.01). Indomethacin partly restored fluid and electrolyte absorption (p less than 0.01) and inhibited JFR of PGE2 (p less than 0.05). These results provide further evidence in favour of the theory that PGs are involved in 5-HT induced intestinal fluid secretion.
对大鼠空肠进行的体内研究表明,5-羟色胺(5-HT)可引起液体分泌以及前列腺素(PG)E2的肠腔释放。吲哚美辛和酮色林可阻断这些效应,这表明PGE2可能是5-HT诱导液体分泌的转导机制中的重要中间体。为了在人体中验证这一假设,采用三腔技术对8名健康志愿者进行了“稳态”灌注(9毫升/分钟)。用含有51Cr-EDTA作为不可吸收标记物的林格氏液对空肠近端进行灌注。在给予吲哚美辛(1.0毫克/千克静脉注射)之前和之后,在60分钟的对照期后,以15分钟的时间段测量外源性5-HT(10微克/千克/分钟静脉注射)对空肠液体和电解质净转运以及PGE2的空肠流速(JFR)的影响,共进行2×60分钟。5-HT使液体和电解质吸收逆转,变为大量分泌(p<0.01,邓肯多重极差检验),并显著增加PGE2的JFR(p<0.01)。吲哚美辛部分恢复了液体和电解质吸收(p<0.01),并抑制了PGE2的JFR(p<0.05)。这些结果为PG参与5-HT诱导的肠液分泌这一理论提供了进一步的证据。