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PubMed1990

Polydipsia in rhesus monkeys deficient in omega-3 fatty acids.

Omega-3 fatty acids are a major component of neural membranes. They are essential nutrients for normal biochemical development of the brain and retina and may affect behavior. In our studies of long-term dietary omega-3 fatty acid deficiency, we have found a new effect of this deficiency in rhesus monkeys. Deficient monkeys visited the home cage drinking spout more frequently than controls (Experiment 1), and drank more water over 24 hours (Experiment 2). The increase in intake was mirrored by increased combined output of urine + feces over 24 hours (Experiment 3), and was not due to spillage (Experiment 4). The dietary deficiency greatly reduced omega-3 fatty acids in red blood cells but did not affect serum electrolyte levels. The changes in fluid intake and output may be related to direct or indirect effects on central or peripheral control mechanisms for drinking or excretion, which may be mediated by altered composition of neural or other membranes or changes in eicosanoid metabolism.

Animals↗
PubMed1979

Effect of addition of ethanol and NaCl on saccharin + glucose polydipsia.

Rats received an ad lib choice of food, water, and a solution containing saccharin, glucose, and NaCl solutes either as single stimuli or in combinations. Ethanol was gradually added to these vehicles or water from 0.5--15% w/v. Ethanol intakes of all groups with vehicles containing glucose were higher than intakes of the water vehicle group. Ethanol intakes of the 0.125% saccharin + 3.0% glucose + 1.0% NaCl + ethanol group were highest, peaking at greater than 9.0 g/kg/day, and this group displayed the highest blood ethanol levels. However, there was no evidence of withdrawal syndrome, nor of increased intake of unflavored ethanol by groups previously receiving flavored ethanol. It is suggested that ethanol eliminative capacity limits free-choice ethanol intake when maximized by the addition of sapid congeners.

Animals↗
PubMed1982

Complete reversal of chronic ethanol polydipsia by schedule withdrawal.

Rats exposed to daily 3-hr intermittent food delivery sessions (binging) chronically ingested excessive amounts of either H2O or 5% EtOH (mean 7.1 g/kg/3-hr). Withdrawing the intermittency of the feeding schedule once every 10 days (single-ration probe session) resulted in reduction of fluid intakes (both H2O and EtOH) to the level of animals always given daily single-ration sessions. This complete dependence of elevated fluid intake levels on the intermittent feeding schedule was unaffected by either the number of probes previously administered (0 to 11) or the duration the feeding schedule was maintained before introduction of the first probe session (29 or 109 days). The results of the probe sessions demonstrated that a history of ethanol overindulgence was not a sufficient condition for the maintenance of overdrinking. Continued overindulgence required the continued presence of the original inducing conditions. Ethanol-polydipsic animals exposed to periodic probe sessions also developed a slow rise in binge session intake. No such increase was observed in the water-polydipsic animals.

Animals↗
PubMed1992

Effects of drugs on the temporal distribution of schedule-induced polydipsia in rats.

Drinking was induced in food-deprived rats by a fixed-time 1-min schedule of food presentation. With three rats, d-amphetamine (0.25, 0.5, 1.0, and 2.0 mg/kg) led to a dose-related increase in licking early in the interfood intervals, the peak of the temporal distribution of licking being shifted to earlier values. These effects were seen even when d-amphetamine had no effect on overall rates of licking and drinking. With another three rats, however, diazepam (0.5, 1.0, 2.0, and 4.0 mg/kg) did not shift the peak of the temporal distribution of licks in interfood intervals, even at doses that produced small increases in overall rates of licking and drinking. However, diazepam did reduce the peak of the distributions of licks at doses that did not decrease water intake and licks per minute.

Animals↗
PubMed2005

Is polydipsia sometimes the cause of oxcarbazepine-induced hyponatremia?

Hyponatremia is a commonly encountered clinical problem with potentially severe complications. Among the underlying implicated etiologies are medications such as oxcarbazepine, which has been well documented and attributed to the syndrome of inappropriate antidiuretic hormones (SIADH). We report the case of a 28-year-old woman with a diagnosis of secondary antiphospholipid syndrome who presented with asymptomatic hyponatremia secondary to excessive water intake after oxcarbazepine ingestion, suggesting a new mechanism for oxcarbazepine-induced hyponatremia.

Journal Article↗
PubMed1998

Olfactory deficits in patients with schizophrenia and severe polydipsia.

BACKGROUND: The present study was designed to assess olfactory function in severely polydipsic/hyponatremic patients with schizophrenia who also had intermittent water intoxication. METHODS: The University of Pennsylvania Smell Identification Test and an olfactory acuity battery were administered to three groups of male subjects: 9 patients with schizophrenia and severe polydipsia/hyponatremia, 9 control nonpolydipsic/normonatremic patients with schizophrenia, and 9 normal controls. RESULTS: Male patients with severe polydipsia/hyponatremia and intermittent water intoxication had marked olfactory acuity and identification deficits when compared to the patient control group of similar age and age at illness onset, and to normal controls. CONCLUSIONS: The finding of deficient acuity (detection threshold) in the polydipsic/hyponatremic group but not the nonpolydipsic, normonatremic group suggests that for this subgroup, abnormalities of olfactory sensory function may occur in a pattern previously reported for other brain disorders such as Alzheimer's disease.

1-Butanol↗