No abstract

No abstract

No abstract

The influence of antrectomy and antrum exclusion on the enterochromaffin like cell kinetics in the gastric mucosa of the rat was studied using a combination of histamine immunocytochemistry and autoradiography after in vivo labelling with tritiated thymidine. In all experimental groups, the enterochromaffin like cells were found to incorporate the DNA precursor, thus indicating an ability to divide. The serum gastrin concentration was raised by antrum exclusion and reduced by antrectomy. After antrum exclusion, the enterochromaffin like cell proliferation rate increased as indicated by a doubling of the labelling index and by the resulting enterochromaffin like cell hyperplasia (after six weeks). After antrectomy, the enterochromaffin like cell labelling index decreased to reach 25% of the control value; at this time the enterochromaffin like cell density had not decreased significantly. The observed correlation between the enterochromaffin like cell labelling indices and the serum gastrin concentration supports the hypothesis that enterochromaffin like cell proliferation is influenced by serum gastrin.

The renewal mechanisms for enterochromaffin-like (ECL) cells, the predominating endocrine cell population in the oxyntic mucosa of the stomach, were investigated in the mouse. The ECL cells were selectively demonstrated by immunostaining using histamine antibodies. Under basal conditions, when observed during the night, ECL cells in mitosis could be seen. This observation proved their ability to divide. Autoradiography after a single pulse and after multiple injections of ³H-thymidine made it possible to study some of their cytokinetic characteristics. The observed replication rate of the labeled ECL cells suggested that self-replication is the main mechanism by which the ECL cell population is renewed. The time interval between two successive divisions of labeled ECL cells was estimated to be around 60 days. Since ECL cells proliferate through mitosis, it may be expected that specific mitogenic stimuli might promote the induction of ECL cell hyperplasia and eventually ECL cell tumors (gastric carcinoids).