The cephalic and gastric phases of gastric secretion during H2-antagonist treatment
| Autor: | Clive H. Wilder-Smith, Robert Walt, Fred Halter, Hans Simon Merki |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Adult
Male medicine.medical_specialty Time Factors medicine.medical_treatment Ranitidine Placebo H2 antagonist Gastric Acid Histamine H2 receptor Internal medicine Gastrins medicine Humans Ingestion Infusion Pumps Gastrin Hepatology business.industry digestive oral and skin physiology Gastroenterology Vagus Nerve Fasting Pirenzepine Hydrogen-Ion Concentration Sham feeding Endocrinology Food Female business medicine.drug |
| Zdroj: | Gastroenterology. 101:599-606 |
| ISSN: | 0016-5085 |
| DOI: | 10.1016/0016-5085(91)90515-m |
| Popis: | The antisecretory effects of H 2 -receptor antagonists are limited by food ingestion. The contributions of the cephalic-vagal and gastrinergic mechanisms to this interaction were examined in two 14-hour randomized, cross-over studies in 24 healthy volunteers. In the first study, either ranitidine or placebo was administered IV by a pH-feedback-controlled infusion pump during fasting, modified sham feeding, or food ingestion. Sham feeding resulted in a well-defined and abrupt interaction with the antisecretory effect of ranitidine (lasting 2–3 hours), after which fasting pH levels were regained. The second study, with the same design, showed that gastrin release occurred during this cephalic-vagal phase but was not attenuated by the additional infusion of the anticholinergic pirenzepine. Following eating, intragastric acidity increased and remained elevated for more than 6 hours. This increase was accompanied by prolonged hypergastrinemia, which was not diminished by pirenzepine. Pirenzepine did, however, enhance the antisecretory effect of ranitidine after both sham feeding and food ingestion. The interaction of food or sham feeding with the antisecretory effect of H 2 antagonists is a consistent phenomenon. In both the cephalic-vagal and the gastric phases of secretion, this interaction appears to be partially mediated by a noncholinergic release of gastrin. |
| Databáze: | OpenAIRE |
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