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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

AMA Arch Surg. 1969;99(3):369-375.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 Snyder^11,12 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 . . . [Full Text PDF of this Article]

Author Affiliations
Torrance, Calif

From the departments of surgery and medicine, Harbor General Hospital, Torrance, and the School of Medicine, University of California at Los Angeles.

Footnotes
Submitted for publication March 10, 1969.

Read before the annual meeting of the Southern California Chapter of the American College of Surgeons, Jan 19, 1969.

Reprint requests to 1000 W Carson St, Torrance, Calif 90509 (Dr. Thompson).

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