Enhanced hyperplasia of gastric enterochromaffinlike cells in response to omeprazole-evoked hypergastrinemia in rats with portacaval shunts. An immunocytochemical and chemical study

Abstract

The histamine-storing enterochromaffinlike cells, which are numerous in the oxyntic mucosa of the rat stomach, are known to proliferate in response to long-lasting hypergastrinaemia. In addition, portacaval shunting, which is not associated with elevated serum gastrin, causes an increase in enterochromaffinlike cell density. The present study shows that the combination of portacaval shunting and omeprazole-evoked, long-lasting hypergastrinemia results in enhanced enterochromaffinlike cell hyperplasia despite the fact that the hypergastrinemia was not significantly greater than in intact omeprazole-treated rats. The mechanism behind the enhanced response to gastrin of the enterochromaffinlike cells in rats with portacaval shunts is unknown. When results from untreated and omeprazole-treated rats were plotted, there was a linear correlation between the serum gastrin concentration and the enterochromaffinlike cell density in both sham-operated rats and rats with portacaval shunts. We conclude that gastrin plays a role in the development of enterochromaffinlike cell hyperplasia following omeprazole treatment in rats with portacaval shunts but that other as yet unidentified agents may also promote the response.