Starbuck E M, Lane J R, Fitts D A
Department of Psychology, University of Washington, Seattle 98195-1525, USA.
Behav Neurosci. 1997 Feb;111(1):206-13.
The authors tested whether the level of hydration after furosemide diuresis and 22 hr of sodium depletion affects the amount of water or 0.3 M NaCl solution consumed by rats with intact brains or with lesions of the subfornical organ (SFO). Rats received 2 (underhydrated) or 10 (euhydrated) ml/kg water by gavage as the only fluid input 2, 4, and 20 hr after 10 mg/kg furosemide. These hydration treatments had little or no effect on the amount of saline consumed in 2 hr by intact rats. SFO lesions reduced water intake regardless of hydration condition. Euhydrated, SFO-lesioned rats drank a normal amount of saline, but underhydrated, lesioned rats drank less saline than any other group. Thus, euhydration may facilitate salt appetite in SFO-lesioned rats, and the deficits in salt appetite noted in SFO-lesioned rats may result from deficits in water ingestion rather than from a destruction of angiotensin II receptor sites that directly provoke salt appetite.
作者测试了速尿利尿和22小时钠缺失后的水合水平是否会影响大脑完整或穹窿下器官(SFO)受损的大鼠消耗的水量或0.3M NaCl溶液量。大鼠在接受10mg/kg速尿后2、4和20小时,通过灌胃接受2(轻度脱水)或10(正常水合)ml/kg水作为唯一的液体输入。这些水合处理对完整大鼠在2小时内消耗的盐水量几乎没有影响。无论水合状态如何,SFO损伤都会减少水的摄入量。正常水合的SFO损伤大鼠饮用正常量的盐水,但轻度脱水的损伤大鼠饮用的盐水比其他任何组都少。因此,正常水合可能会促进SFO损伤大鼠的盐食欲,而SFO损伤大鼠中观察到的盐食欲缺陷可能是由于水摄入不足,而不是直接引发盐食欲的血管紧张素II受体位点的破坏。