Enhanced drinking after excitotoxic lesions of the parabrachial nucleus in the rat

Previous reports indicate the lateral parabrachial nucleus (IPBN) is important in the regulation of fluid intake. After electrolytic lesions of the IPBN, rats consume increased amounts of water when challenged with pharmacological stimuli that mimic depletion of the extracellular fluid space. Nonetheless, it is possible that neurons within the IPBN are not responsible for the overingestion of water during extracellular thirst challenges, since electrolytic lesions damage fibers of passage as well as neurons within the IPBN. Thus we used the excitatory neurotoxin ibotenic acid to lesion cell bodies within the IPBN. After recovery from surgery, water consumption by lesioned rats was significantly greater than consumption by vehicle or uninjected control rats when challenged with subcutaneous angiotensin II or isoproterenol to stimulate drinking. However, when injected with subcutaneous hypertonic saline to produce cellular dehydration, or when water deprived for 24 h, the water intake of rats with lesions was not different from the intake of control rats. Anatomical examination of the lesion sites revealed that ibotenic acid injection caused a notable loss of neurons in the IPBN with little or no damage to surrounding structures. Moreover, injection of an anterograde tracer into the dorsomedial medulla resulted in labeling of fibers that traverse the ibotenic acid lesion site. Together, these data suggest neurons within the IPBN are involved in the regulation of fluid intake, particularly challenges that involve depletion of the extracellular fluid space.

Oral administration of radioactive sulfate to measure extracellular fluid space in man

Radioactive sulfate-35 (35S) was administered to eight human subjects intravenously and orally, to compare respective kinetics of distribution. Intravenously administered 35S attained equilibration within 60–90 min. Orally administered 35S attained equilibration within 60–105 min and thereafter achieved plasma activity equivalent to the intravenously administered tracer. Eighty percent or greater of the 35S dose was recovered in the 24-h urine, following either intravenous or oral administration. The mean extracellular fluid space demonstrated less than 9% mean difference between routes of administration. It is concluded that 35S is completely absorbed at tracer doses, and may be administered orally as a reliable substitute for intravenously administered 35S for measuring extracellular fluid space.