Oliw E, Anggård E
Acta Physiol Scand. 1979 Mar;105(3):367-73. doi: 10.1111/j.1748-1716.1979.tb06352.x.
The effect of a constant infusion of furosemide (130 micrograms/min i.v. for 60 min, n = 8) was studied on urinary excretion of water, electrolytes and immunoreactive prostaglandin E2 (iPGE2) and iPGF2alpha in chloralose-urethane anesthetized rabbits. During the furosemide infusion sodium and water excretion increased ten-fold and the excretion of potassium and iPGE2 two to three times. The excretion of iPGF2alpha (0.06 +/- 0.03 micrograms/min/100 g kidney weight) was not significantly changed during the furosemide infusion but increased markedly after the infusion and reached a maximum (1.0 +/- 0.6 microgram/min/100 g) 30 to 45 min later, while the small increase in iPGE2 excretion at this time could be attributed to cross-reaction with PGF2alpha. The results indicate that PGE2 might possibly be involved directly in the action of furosemide, while PGF2alpha might participate in sodium and water conserving mechanisms in the rabbit kidney, activated by the drug induced diuresis.
研究了持续静脉输注速尿(130微克/分钟,静脉注射60分钟,n = 8)对水合氯醛 - 乌拉坦麻醉兔尿液中水分、电解质以及免疫反应性前列腺素E2(iPGE2)和iPGF2α排泄的影响。在输注速尿期间,钠和水的排泄增加了10倍,钾和iPGE2的排泄增加了两到三倍。iPGF2α的排泄(0.06±0.03微克/分钟/100克肾脏重量)在速尿输注期间没有显著变化,但在输注后显著增加,并在30至45分钟后达到最大值(1.0±0.6微克/分钟/100克),而此时iPGE2排泄的小幅增加可能归因于与PGF2α的交叉反应。结果表明,PGE2可能直接参与速尿的作用,而PGF2α可能参与兔肾中由药物诱导利尿激活的钠和水的保存机制。