Trophic effect of histamine on the stomach.

On the basis of clinical observations and experimental animal studies it has been established that gastrin has a trophic effect on the oxyntic mucosa. On the other hand, histamine, being at least as efficient as gastrin as an acid secretagogue, has experimentally been reported not to have such trophic effect. However, during the last few years both endogenously and exogenously induced hypergastremia have been shown to have a specific trophic effect on the enterochromaffin-like (ECL) cell and a less pronounced and later detectable general trophic effect on the oxyntic mucosa. Moreover, in the rat (the species in which most of the trophic studies have been done) the acid-stimulatory effect of gastrin may be solely explained by stimulation of histamine release from ECL cells. Therefore, it seemed natural to evaluate whether the general trophic effect of gastrin could also be caused by histamine or another substance released from the ECL cells. In this review we challenge the concept that maximal pentagastrin-stimulated acid secretion only reflects the parietal cell mass, since the acid-stimulatory effect of gastrin is mediated by histamine release. Therefore, maximal pentagastrin-stimulated acid secretion reflects both the ECL cell mass and the parietal cell mass. With regard to the possible trophic effect of histamine, we show that the doses previously used have been inadequate. Furthermore, histamine has been reported to have a trophic effect on the parietal cell in the dog; some patients with hyperhistaminemia have an increased maximal histamine-stimulated acid secretion, suggesting an increase in the parietal cell mass; and there is parietal cell hyperplasia in the oxyntic mucosa surrounding the histamine-producing carcinoids in mastomys.(ABSTRACT TRUNCATED AT 250 WORDS)