Axelson J, Ekelund M, Sundler F, Håkanson R
Department of Pharmacology, University of Lund, Sweden.
Gastroenterology. 1990 Sep;99(3):635-40. doi: 10.1016/0016-5085(90)90948-z.
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.
组胺储存肠嗜铬样细胞在大鼠胃的泌酸黏膜中数量众多,已知其会因长期高胃泌素血症而增殖。此外,与血清胃泌素升高无关的门腔分流会导致肠嗜铬样细胞密度增加。本研究表明,尽管门腔分流与奥美拉唑诱发的长期高胃泌素血症相结合导致肠嗜铬样细胞增生增强,但高胃泌素血症并不比完整的奥美拉唑治疗大鼠显著更高。门腔分流大鼠肠嗜铬样细胞对胃泌素反应增强的机制尚不清楚。绘制未治疗和奥美拉唑治疗大鼠的结果时,假手术大鼠和门腔分流大鼠的血清胃泌素浓度与肠嗜铬样细胞密度之间均存在线性相关性。我们得出结论,胃泌素在门腔分流大鼠奥美拉唑治疗后肠嗜铬样细胞增生的发展中起作用,但其他尚未确定的因素也可能促进这种反应。