Miura Y, Yoshikawa I, Ohe K
Third Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
J UOEH. 1989 Sep 1;11(3):313-22. doi: 10.7888/juoeh.11.313.
Effect of intravenous infusion of 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) on the alkaline secretion of the proximal duodenal mucosa was investigated using a lumen perfusion system of the duodenal loop in rats. The following results were obtained: 1) 0.001 to 1 microgram/kg/hr of 16,16-dmPGE2 increased the alkaline secretion significantly and dose-dependently. 2) Indomethacin (5 mg/kg) inhibited the alkaline secretion and 16,16-dmPGE2 (0.1 microgram/kg/hr) completely repaired this inhibition. 3) In cysteamine-treated rats, 16,16-dmPGE2 (1 microgram/kg/hr) completely repaired the inhibition of the alkaline secretion induced by cysteamine. 4) Prostaglandin was a potent stimulator of alkaline secretion of the proximal duodenal mucosa not only in cysteamine-treated rats but also in normal rats. This is in contrast to our previous report which showed that secretin repaired the alkaline secretion in cysteamine-treated rats without affecting it in normal rats. We have concluded that prostaglandin and secretin may be involved differently in the mechanism of alkaline secretion of the proximal duodenal mucosa. Further investigation is required to elucidate the mechanism.
采用大鼠十二指肠袢腔内灌注系统,研究静脉输注16,16-二甲基前列腺素E2(16,16-dmPGE2)对十二指肠近端黏膜碱性分泌的影响。结果如下:1)0.001至1微克/千克/小时的16,16-dmPGE2显著且剂量依赖性地增加碱性分泌。2)吲哚美辛(5毫克/千克)抑制碱性分泌,而16,16-dmPGE2(0.1微克/千克/小时)完全修复了这种抑制作用。3)在半胱胺处理的大鼠中,16,16-dmPGE2(1微克/千克/小时)完全修复了半胱胺诱导的碱性分泌抑制。4)前列腺素不仅在半胱胺处理的大鼠中,而且在正常大鼠中都是十二指肠近端黏膜碱性分泌的有效刺激物。这与我们之前的报告相反,之前的报告显示促胰液素在半胱胺处理的大鼠中修复碱性分泌,而在正常大鼠中不影响碱性分泌。我们得出结论,前列腺素和促胰液素可能在十二指肠近端黏膜碱性分泌机制中发挥不同作用。需要进一步研究以阐明其机制。