ENDOGENOUS SEROTONIN IN CONTROL OF GASTRIC-ACID SECRETION

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 82  (1) , 156-163
Abstract
In 3 dogs with Heidenhain pouches (HP), gastric fistulas (GF) and duodenal cannulas, acidification of the duodenum with 0.1 N HCl (5 ml/min) resulted in significant inhibition of GF output (preacidification, 8.66 .+-. 0.58 meq/30 min; postacidification, 5.47 .+-. 0.66 meq/30 min) 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 min; postacidification, 6.49 .+-. 0.56 meq/30 min). Per increment in peripheral blood serotonin of 1 ng/ml, endogenous serotonin inhibited 54.59 .+-. 12.99 .mu.eq/h and exogenous serotonin inhibited 46.54 .+-. 10.39 .mu.eq/h, P > 0.05. Neither endogenously released nor exogenous serotonin inhibited HP acid output. Using mesenteric venous infusions of serotonin, significant amounts of immunoreactive serotonin escaped hepatic inactivation; basal peripheral venous levels of serotonin, 233 .+-. 103 ng/ml, increased to 455 .+-. 127 ng/ml at 10 min. 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.