Effect of dexamethasone on electrolyte transport in the large intestine of the rat.
Effect of dexamethasone on electrolyte transport in the large intestine of the rat.
复制标题
地塞米松对大鼠大肠电解质转运的影响。
DOI：
10.1016/0016-5085(78)90404-3
复制
发表时间：
1978
期刊：
影响因子：
29.4
通讯作者：
H. Binder
中科院分区：
文献类型：
--
作者：
H. Binder
我们研究了糖皮质激素对大鼠结肠液体和电解质运动的影响。地塞米松600 μg/100 g体重，连续给药3天，可显著增加水钠吸收、钾分泌、电位差（PD）和Na-K-ATP酶活性。更接近生理剂量的地塞米松剂量（分别为10和25 μg/100 g体重）也可显著增加PD和Na-K-ATP酶活性。此外，增加PD观察到尽快3小时后，地塞米松给药，并持续24至48小时。5小时后，地塞米松给药，Na-K-ATP酶活性没有增加，尽管钠吸收，K分泌，和PD显着增加。地塞米松增加液体和钠的吸收在生理盐水和脱氧胆酸灌注。与胆汁酸灌注期间对照组的净水和钠分泌相反，地塞米松给药动物中存在净吸收。这些研究扩展了以前观察到的糖皮质激素对大肠中水和电解质运动的影响，并提供了关于糖皮质激素与离子转运相互作用的最小剂量和时间过程的数据。这些观察结果表明，糖皮质激素可能提供重要的调节控制结肠离子转运，这些糖皮质激素的作用机制是不介导的钠-钾-ATP酶。
We examined the effect of glucocorticosteroids on fluid and electrolyte movement in the rat colon. Dexamethasone, 600 μg per 100 g of body weight daily for 3 days, significantly increased water and sodium absorption, potassium secretion, the electrical potentional difference (PD), and Na-K-ATPase activity. Significant increases in PD and Na-K-ATPase activity were also produced by doses of dexamethasone (10 and 25 μg per 100 g of body weight, respectively) that more closely approximate a physiological dose. Further, the increase in PD was observed as soon as 3 hr after dexamethasone administration and persisted for 24 to 48 hr. Five hours after the administration of dexamethasone, Na-K-ATPase activity was not increased despite significant increments in Na absorption, K secretion, and PD. Dexamethasone increased fluid and sodium absorption during both saline and deoxycholic acid perfusions. In contrast to the net water and sodium secretion in the control group during bile acid perfusions, net absorption was present in the dexamethasone-treated animals. These studies extend previous observations of the effect of glucocorticoids on water and electrolyte movement in the large intestine and provide data concerning the minimal dose and time course of the interaction of glucocorticoids with ion transport. These observations indicate that glucocorticoids may provide important regulatory control of colonic ion transport, and that the mechanism of these glucocorticoid effects is not mediated by Na-K-ATPase.