Jaffe B M
World J Surg. 1979 Sep 20;3(5):565-78. doi: 10.1007/BF01654761.
Prostaglandins and serotonin are vasoactive compounds with profound effects on the gastrointestinal tract. Both cause inhibition of gastric acid secretion (although serotonin stimulates gastric pepsin secretion), stimulation of intestinal motility, and conversion of small intestinal mucosa from absorption to secretion of water and electrolytes. Their effects on pancreatic and biliary function are still not clear. Although prostaglandins appear to elicit their effects primarily by a paracrine mode of action, and serotonin is primarily a neurotransmitter (neurocrine), it is clear that even under normal conditions both can function as humoral agents. For example, we have shown that serotonin plays a physiologic role as a humoral inhibitor of gastric acid secretion. However, the effects of these agents become more pronounced in patients with humorally mediated diarrheogenic syndromes. Serotonin (and related indoles, particularly 5-hydroxytryptophan) has been firmly implicated as a cause of diarrhea in patients with carcinoid syndrome; our recent studies suggest that the diagnosis can be more effectively made by measuring circulating immunoreactive serotonin concentrations than urinary excretion of 5-HIAA; that some circulating serotonin escapes hepatic inactivation and, thus, large intestinal tumors can cause carcinoid syndrome in the absence of hepatic metastases; and that large amounts of serotonin are produced by some noncarcinoid diarrheogenic tumors, including medullary carcinomas of the thyroid and tumors associated with the WDHA syndrome. A large number of tumors of probable neural crest origin, including medullary thyroid carcinoma, carcinoids, and tumors associated with the WDHA syndrome, secrete large amounts of prostaglandins, particularly PGE2. The clinical response of at least some of the patients harboring these tumors to inhibitors of prostaglandin synthesis (particularly indomethacin) suggests that prostaglandins play a role in the etiology of these diarrheogenic syndromes.
前列腺素和血清素是对胃肠道有深远影响的血管活性化合物。两者均可抑制胃酸分泌（尽管血清素会刺激胃蛋白酶分泌），刺激肠道蠕动，并使小肠黏膜从吸收水和电解质转变为分泌水和电解质。它们对胰腺和胆汁功能的影响尚不清楚。尽管前列腺素似乎主要通过旁分泌作用方式发挥其作用，而血清素主要是一种神经递质（神经分泌），但很明显，即使在正常情况下，两者都可作为体液因子发挥作用。例如，我们已经表明血清素作为胃酸分泌的体液抑制剂发挥生理作用。然而，在患有体液介导的腹泻综合征的患者中，这些物质的作用更为明显。血清素（以及相关的吲哚，特别是5-羟色氨酸）已被确凿地认为是类癌综合征患者腹泻的原因；我们最近的研究表明，通过测量循环免疫反应性血清素浓度比测量5-羟吲哚乙酸的尿排泄量能更有效地进行诊断；一些循环血清素逃避了肝脏的灭活作用，因此，大肠肿瘤在没有肝转移的情况下也可导致类癌综合征；并且一些非类癌性腹泻肿瘤，包括甲状腺髓样癌和与WDHA综合征相关的肿瘤，会产生大量血清素。许多可能起源于神经嵴的肿瘤，包括甲状腺髓样癌、类癌和与WDHA综合征相关的肿瘤，会分泌大量前列腺素，尤其是前列腺素E2。至少一些患有这些肿瘤的患者对前列腺素合成抑制剂（特别是吲哚美辛）的临床反应表明，前列腺素在这些腹泻综合征的病因中起作用。
