Jaffe B M, Kopen D F, Lazan D W
Surgery. 1977 Jul;82(1):156-63.
In three dogs with Heidenhain pouches (HP), gastric fistulas (GF), and duodenal cannulas, acidification of the duodenum with 0.1N HC1 (5 ml/minute) resulted in significant inhibition of GF output (preacidification, 8.66+/-0.58 mEq/30 minutes; postacidification, 5.47+/-0.66 mEq/30 minutes) and elevated peripheral venous blood levels of serotonin (basal, 226+/-64 ng/ml; peak, 521+/-168 ng/ml). Infusion of exogenous serotonin to comparable blood levels (basal, 208+/-38 ng/ml; mean postacidification, 571+/-153 ng/ml) resulted in similar GF inhibition (preacidification, 9.17+/-0.92 mEq/30 minutes; postacidification, 6.49+/-0.56 mEq/30 minutes). Per increment in peripheral blood serotonin of 1 ng/ml, endogenous serotonin inhibited 54.59+/-12.99 muEq/hour and exogenous serotonin inhibited 46.54+/-10.39 muEq/hour, p greater than 0.05. Neither endogenously released nor exogenous serotonin inhibited HP acid output. Using mesenteric venous infusions of serotonin, significant amounts of immunoreactive serotonin were found to escape hepatic inactivation; basal peripheral venous levels of serotonin, 233+/-103 ng/ml, increased to 455+/-127 ng/ml at 10 minutes. During release of endogenous serotonin, 92+/-21% of portal venous serotonin was bound to platelets; in contrast, during intraportal serotonin infusion, only 59+/-18% of serotonin was platelet bound.
在三只装有海登海因袋（HP）、胃瘘（GF）和十二指肠插管的狗身上，用0.1N盐酸（5毫升/分钟）酸化十二指肠导致胃瘘输出量显著抑制（酸化前，8.66±0.58毫当量/30分钟；酸化后，5.47±0.66毫当量/30分钟），并使外周静脉血中血清素水平升高（基础值，226±64纳克/毫升；峰值，521±168纳克/毫升）。输注外源性血清素至可比的血药浓度（基础值，208±38纳克/毫升；酸化后平均值，571±153纳克/毫升）导致类似的胃瘘抑制（酸化前，9.17±0.92毫当量/30分钟；酸化后，6.49±0.56毫当量/30分钟）。外周血血清素每增加1纳克/毫升，内源性血清素抑制54.59±12.99微当量/小时，外源性血清素抑制46.54±10.39微当量/小时，p>0.05。内源性释放的血清素和外源性血清素均未抑制海登海因袋酸分泌。通过肠系膜静脉输注血清素，发现大量免疫反应性血清素逃脱了肝脏的灭活作用；血清素的基础外周静脉水平为233±103纳克/毫升，10分钟时升至455±127纳克/毫升。在内源性血清素释放期间，92±21%的门静脉血清素与血小板结合；相比之下，在门静脉内输注血清素期间，只有59±18%的血清素与血小板结合。
