Takeuchi K, Niida H, Minami M, Okabe S
Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.
Jpn J Pharmacol. 1990 Feb;52(2):225-32. doi: 10.1254/jjp.52.225.
We set up a system to measure the luminal pH, potential difference (PD) and bicarbonate output in the anesthetized rat duodenum, and investigated these responses caused by prostaglandins (PGs) and cholinergic agents. When the proximal duodenum (1.7 cm) was perfused at a flow rate of 0.7 ml/min with saline adjusted to pH 4.5, the duodenal pH, PD and HCO3- output were 5.5 to 6.0, -4 to -6 mV and 1.2 to 1.6 muEq/10 min, respectively; they were markedly reduced by i.v. injection of saturated KCl. Both natural (PGE1, PGE2) and synthetic (PGE2, PGl2) PGs, given either s.c. or i.v., significantly elevated all these parameters, while indomethacin (s.c.) decreased the pH as well as the PD. Small but significant increases of the pH were observed after i.v. administration of cholinergic agents (carbachol, bethanechol), a GABAergic agent (baclofen) and an analogue of thyrotropin releasing hormone (YM-14673), with a temporal elevation of the PD; the degree of net HCO3- output caused by these agents was 20-50% of the values obtained with PGE2 (100 micrograms/kg, i.v.), and they were significantly reduced in the presence of atropine. These results suggest that (a) the system using pH deflections can be used to sensitively detect HCO3- output in the rat duodenum, and (b) duodenal acid neutralizing capacity may be regulated by central and peripheral cholinergic systems as well as endogenous PGs.
我们建立了一个系统来测量麻醉大鼠十二指肠的管腔pH值、电位差(PD)和碳酸氢盐输出,并研究了前列腺素(PGs)和胆碱能药物引起的这些反应。当以0.7 ml/min的流速用pH值调至4.5的生理盐水灌注十二指肠近端(1.7 cm)时,十二指肠pH值、PD和HCO3-输出分别为5.5至6.0、-4至-6 mV和1.2至1.6 μEq/10 min;静脉注射饱和KCl可使其显著降低。天然(PGE1、PGE2)和合成(PGE2、PGI2)PGs,无论是皮下注射还是静脉注射,均能显著提高所有这些参数,而吲哚美辛(皮下注射)则降低了pH值和PD。静脉注射胆碱能药物(卡巴胆碱、贝胆碱)、GABA能药物(巴氯芬)和促甲状腺激素释放激素类似物(YM-14673)后,观察到pH值有小幅但显著的升高,同时PD有短暂升高;这些药物引起的净HCO3-输出程度为静脉注射PGE2(100 μg/kg)所得值的20-50%,且在阿托品存在的情况下显著降低。这些结果表明:(a)利用pH值变化的系统可用于灵敏检测大鼠十二指肠的HCO3-输出;(b)十二指肠的酸中和能力可能受中枢和外周胆碱能系统以及内源性PGs的调节。