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Acid Secretion Following Portacaval Shunting:  Role of Vagus, Gastrin, Intestinal Phase, and Histamine

Philip H. Newman, MD; David D. Reeder, MD; Warren D. Davidson, MD; Edward Schneider; James H. Miller; James C. Thompson, MD
Arch Surg. 1969;99(3):369-375. doi:10.1001/archsurg.1969.01340150077015.
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Although certain facts have been demonstrated experimentally about gastric hypersecretion in dogs following portacaval transposition, the exact cause remains unclear.1,2 Hypersecretion has been shown to occur independently of hepatic parenchymal damage3 is not suppressed by elimination of the cephalic and antral phases of gastric secretion.4,5 Decreased hepatic catabolism or inactivation of a gastric secretagogue elaborated in the small intestine has been suggested by some investigators,5-8 and histamine has been suggested to be this secretagogue.9 Day and associates10 have shown increased levels of circulating and gastric mucosal histamine in rats with portacaval shunts. Recently, Fischer and Snyder11,12 have shown increased enzymatic activity of histidine decarboxylase in the gastric mucosa of rats with portacaval shunts and have been able to inhibit the gastric hypersecretion following portacaval shunt with brocresine (NSD-1055), a histidine decarboxylase inhibitor. The changes in gastric secretion brought about by portacaval shunting have

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