Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Polydipsia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources
PubMed1989

Cytophotometric assessment of T-2 toxin induced alterations in azure B-RNA and Coomassie-protein in supraoptic-magnocellular neurons of rat hypothalami.

Quantitative cytophotometry was used to monitor T-2 toxin-induced alterations in azure B-RNA and Coomassie-total cell protein in supraoptic-magnocellular neurons of rat hypothalami. Thirty male Sprague-Dawley rats (200-220g) were given a single i.p. injection of T-2 toxin (0.5, 0.75, 1.00 and 1.50 x LD50), a trichothecene mycotoxin; rats were decapitated 8 hours post-dosing. After stoichiometric azure B-RNA and Coomassie-protein staining of brain sections, scanning-integrating microdensitometry was used to quantify toxin-induced alterations in these well established indices of neuronal toxicity. Within the magnocellular neurons of the supraoptic nuclei, significant reductions in azure B-RNA reactivity were observed in the 0.75, 1.00 and 1.50 x LD50 groups (i.e. 11%, 13% and 8%, respectively); no differences in RNA levels were observed between controls and the 0.50 x LD50 group. In addition, a decrease in Coomassie-total cell protein was seen in animals receiving 0.50, 0.75 and 1.50 x LD50 T-2 toxin (i.e. 33%, 21% and 12%, respectively); however, toxin administration did not alter protein levels in the 1.00 x LD50 group. Furthermore, a dose-dependent decrease in systolic blood pressure was observed at 8 hr. post-injections (i.e., approximately -39%, -52%, -66% and -64% for the 0.50, 0.75, 1.00 and 1.50 x LD50 groups, respectively). Additional observations include pronounced polydipsia, ascites, abdominal and subdural hemorrhage, and horripilation (piloerection) in experimental groups. It is postulated that the T-2 toxin-induced reductions in azure B-RNA and Coomassie-protein represent an early indication of impaired metabolic activity. Since these neurons are important sites of vasopressin (antidiuretic hormone) synthesis, these data suggest an impaired osmoregulatory ability. The pronounced polydipsia which occurred shortly after intoxication is further evidence of this impairment. Although these findings do not provide insight relating to the mechanism of osmoregulatory disruption, it is advanced that the supraoptic-magnocellular compartment represents an important site in T-2 toxin mycotoxicosis. Moreover, these findings support previous claims that T-2 toxin intoxication may critically impair the vasopressinergic response to toxin-induced cardiovascular collapse.

Animals↗
PubMed1989

Cytophotometric analysis of T-2 toxin induced alterations in chromatin condensation and neuronal nuclear volume of rat supraoptic-magnocellular neurons.

Quantitative cytophotometry and ocular filar micrometry were used to monitor T-2 toxin induced alterations in chromatin and neuronal nuclear volume in supraoptic-magnocellular neurons of rat hypo-thalami. Thirty male Sprague-Dawley rats (200-220g) were given a single i.p. injection of T-2 toxin (0.5, 0.75, 1.0 and 1.5 X LD50), a trichothecene mycotoxin; rats were decapitated 8 hours post-dosing. After stoichiometric Feulgen-DNA staining of brain sections, scanning-integrating microdensitometry was used to quantify changes in the susceptibility of chromatin to Feulgen acid hydrolysis. Changes in neuronal nuclear volumes were also determined histometrically. Within the magnocellular neurons of the supraoptic nuclei, significant reductions in F-DNA reactivity were observed in the 0.5, 0.75, and 1.0 X LD50 groups (i.e. 3.7%, 4.4% and 2.5%, respectively); however, rats receiving 1.5 X LD50 T-2 toxin showed no difference in F-DNA reactivity compared to controls. In addition, ocular filar micrometry demonstrated increased neuronal nuclear volumes in all groups receiving T-2 toxin, and following an inverse trend to that seen with F-DNA stainability. Additional observations included pronounced polydipsia, polyphagia and horripilation in the experimental groups, independent of the dosages employed; these changes were evident within 1 hour post-injection. It is postulated that the T-2 toxin induced reduction in the susceptibility of chromatin to Feulgen acid hydrolysis and concomitant increases in neuronal nuclear volumes represent an early indication of impaired metabolic activity. Since these neurons are important sites of vasopressin (antidiuretic hormone) synthesis, these data suggest an impaired osmoregulatory ability. The pronounced polydipsia which occurred shortly after intoxication is further evidence of this impairment. Although these findings do not provide insight relating to the mechanism of osmoregulatory disruption, it is evident that an impaired ability to osmoregulate is among the earliest indications of acute T-2 toxin mycotoxicosis.

Animals↗
PubMed1983

Patterns of drinking in the rat following the administration of opiate antagonists.

Durations of drinking were recorded for water-deprived rats as they drank to satiety, following SC injections of naloxone (0.1-10.0 mg/kg), naltrexone (0.1-10.0 mg/kg) or saline vehicle. The results provided evidence for the effects of opiate antagonists on the temporal pattern of drinking exhibited by water-deprived animals. A separate, time-sampling procedure was used to supplement the drinking duration data, and showed that the opiate antagonists may suppress water consumption during a period 2.5-7.5 min after the start of the initial drinking bout. A second experiment confirmed that the pattern of drinking displayed during schedule-induced polydipsia in the rat is resistant to any suppressant effect of a moderate dose of an opiate antagonist. The similarity between opiate receptor blockade and water preloading in their effect on drinking in response to water deprivation, and lack of effect on schedule-induced polydipsia is discussed. Opiate antagonists may affect drinking principally by imposing a thirst satiety signal.

Animals↗
PubMed1983

Production of physical dependence on ethanol by a short drinking episode each day.

A 3-hr schedule-induced ethanol polydipsia regimen was used in rats to elevate blood alcohol concentration to a single intoxicating peak each day. After 3 weeks, and again after 3.5 months, animals were tested for the presence of physical dependence by exposure to a brief auditory stimulus (key shaking) at 7 and 11 hr after ethanol polydipsia. Withdrawal signs were observed only at 11 hr when blood ethanol levels had returned to zero. No such signs were observed when animals were made water polydipsic. While sufficient, continuous elevation of blood ethanol concentration is not necessary for the development of a demonstrable physical dependence. A limited daily ethanol binge was sufficient.

Alcohol Drinking↗
PubMed1986

Effects of benzodiazepines on taste aversions in a two-bottle choice paradigm.

Diazepam (DZ) and chlordiazepoxide (CDP) were tested for their ability to antagonize LiCl-established conditioned taste aversions (CTAs) to saccharin in a two-bottle free-choice paradigm. CTAs to saccharin were established in male Sprague-Dawley rats on a chronic fluid-deprivation schedule by the administration of LiCl (3 mEq/kg, IP) following a forced-choice exposure to a novel saccharin solution (0.1%, w/v). Three days later, rats were provided with a two-bottle choice presentation of saccharin and distilled water. Conditioned rats drank distilled water almost exclusively while unconditioned animals preferred saccharin. Pretreatment with DZ (6, 9, 12 mg/kg, IP) and CDP (12 mg/kg, IP) significantly increased the saccharin intake of conditioned rats indicating an attenuation of the manifestation of the CTA. While these results are consistent with the known disinhibitory effects of benzodiazepines, alternative mechanisms involving polydipsia or interactions with the taste characteristics of saccharin could not be excluded. Both hypertonic saline (16%, w/v NaCl) and Barbital Sodium (100 mg/kg) produced polydipsia without attenuating CTAs suggesting that the two-bottle procedure is capable of distinguishing between polydipsic effects and anti-aversion effects for these drugs.

Animals↗
PubMed1994

Pharmacological evaluation of methylcarbamylcholine-induced drinking behavior in rats.

Methylcarbamylcholine (MCC), a structural analog of carbachol (an acetylcholine agonist), has been reported to be a specific nicotinic cholinergic receptor ligand. MCC produces a robust polydipsic response shortly following central administration. The purpose of the present study was to pharmacologically characterize this increase in drinking behavior. Male Wistar rats were implanted with intracerebroventricular (ICV) cannula guides directed at the left lateral ventricle. Following a recovery period, animals were injected ICV with saline or various doses of MCC (3-60 micrograms) and water consumption was quantified. MCC produced a dose-related, transient increase in water consumption that peaked at a dose of 30 micrograms. In contrast, nicotine, a potent nicotinic cholinergic receptor agonist, did not produce changes in drinking following ICV administration. MCC-induced increases in drinking were not blocked by pretreatment with several selective nicotinic receptor antagonists including dihydro-beta-erythriodine (DHBE), hexamethonium, and mecamylamine. However, pretreatment with the muscarinic antagonist atropine (0.01 or 1.0 microgram) completely abolished MCC-induced polydipsia. Following a chronic treatment regimen (MCC injected ICV twice daily for 10 days), no tolerance to MCC-induced changes in water consumption was observed. Previous studies have demonstrated that tolerance develops to nicotinic-receptor mediated responses following the identical chronic treatment paradigm. These results suggest that MCC-induced polydipsia is mediated through stimulation of muscarinic rather than nicotinic receptors.

Animals↗
PubMed1982

Schedule-induced self-injection of drugs.

Studies of acquisition and maintenance patterns of drug intake, including dependence, necessitate voluntary intake of drugs. Voluntary intake in animal studies is difficult to achieve because of aversive taste factors associated with most drugs, and involuntary or forced choice methods obscure the behavior which is the object of study. The schedule-induced polydipsia paradigm has been used to induce oral ingestion of large volumes of alcohol, barbiturate and other drug solutions. We have developed a method of schedule-induced self-injection which allows the study of acquisition and maintenance of drug intake behavior with changing environments free from the interference of taste factors or imbalances due to excessive water intake. In this paper we review our findings on the acquisition and maintenance patterns of amphetamine, methadone, heroin, alcohol, nicotine, cocaine, delta 9-THC and haloperidol. For all drugs except amphetamine, the combination of schedule and nutritional deprivation leads to the highest rates of drug intake as compared to controls. The schedule does not appear to be a potent factor at 90% and free feeding weight, and drug intake is the result of interaction of environmental factors and pharmacological properties of the drugs, rather than the effects of drug or environmental factors separately. The maintenance patterns of nicotine, cocaine, heroin and alcohol are also discussed and the advantages of schedule-induced self-injection over schedule-induced polydipsia methods are presented.

Amphetamine↗
PubMedDate not supplied

Vasopressin and ethanol preference. II. Altered preference in two strains of diabetes insipidus rats and nephrogenic diabetes insipidus mice.

In the first paper of this series, the influence of a single gene (di) for vasopressin deficiency on ethanol intake in rats was demonstrated. We studied preference for concentrations of ethanol between 2.2 and 10 percent versus tap water in Brattleboro rats homozygous for diabetes insipidus (di/di), heterozygous (di/+) or normal (+/+). The di/di rats, totally lacking in vasopressin, had greatly reduced preference scores for all concentrations of ethanol. Their intake of ethanol (g/day) was higher than heterozygotes or normals, but only when 2.2 percent ethanol was offered as a choice. Treatment with vasopressin or related peptides restored ethanol drinking to normal but also corrected water balance. In the experiments reported here, Roman High Avoidance (RHA) rats of three genotypes (+/+, di/+, and di/di) were also tested for ethanol intake and preference with similar but not identical results. Thus, the effects of the di gene are independent of the genetic background on which it is placed to at least some extent. Chlorothiazide, a drug unrelated to vasopressin, also normalized ethanol drinking and corrected water balance in di/di rats. In nephrogenic diabetes insipidus mice, there was a strong negative correlation between severity of polydipsia and preference for ethanol. Thus, no paradigm tested was effective in dissociating polydipsia from reduced ethanol preference and increased ethanol intake. While these results cannot exclude a possible regulatory role for endogenous vasopressin in ethanol preference drinking, they more strongly suggest that reduced preference for ethanol and increased ethanol intake are epiphenomena secondary to a polydipsic state.

Alcohol Drinking↗
PubMed1995

Compulsive water drinking in the setting of anticholinergic drug use: an unrecognized cause of chronic renal failure.

Compulsive water drinking (psychogenic polydipsia) is a well-recognized clinical entity that is often seen in individuals with psychiatric disorders, especially schizophrenia. Although urinary tract abnormalities including enlarged bladders and hydronephrosis have been reported, the presence of chronic renal failure is rarely reported in this disorder. We report four patients with psychogenic polydipsia who presented with chronic renal failure due to obstructive uropathy in the absence of demonstrable anatomic causes of obstruction. The likely mechanism of functional obstructive uropathy is bladder failure due to a combination of excessive water ingestion, enlarged bladder volumes, and use of anticholinergic medications.

Adult↗
PubMed1994

Naloxone attenuates drinking behavior in psychiatric patients displaying self-induced water intoxication.

1. The present study was performed to examine the effect of naloxone on drinking behavior in three schizophrenic inpatients with psychosis, intermittent hyponatremia, and polydipsia. 2. Their body weight were checked five times daily and the maximum weight gain during a day was chosen as an index of their polydipsia. 3. After control recording for six weeks, a daily naloxone (0.6 mg) injection series was performed once every two weeks for three series (six weeks). Withdrawal of this drug for six weeks resulted in weight gain recovering to control level. 4. The present study showed that naloxone seems to be a potential treatment for psychiatric patients displaying self-induced water intoxication and that endogenous opioid systems are involved in the compulsive drinking behavior of this syndrome.

Drinking Behavior↗
PubMed1995

Heat stress causes excessive drinking in fed and food deprived pregnant goats.

Water intake was studied in six goats during late pregnancy to investigate if heat stress induces primary polydipsia. The goats were fed twice daily or deprived of food for 24 hr to avoid postprandial drinking and induce hyponatremia. Signs of stress was evaluated by determination of plasma cortisol concentration. Ambient temperature was increased from 20 degrees C to 38.0-39.5 degrees C for 5.15 hr. Water temperature was 35 +/- 1 degree C during heat stress. Fed goats started to drink 13 +/- 3 min after the heaters were turned on and water diuresis developed in five of them. The body weight increased simultaneously with decreased plasma Na concentration and osmolality showing that the goats also stored water. During food deprivation, plasma Na concentration and osmolality fell, and plasma aldosterone concentration increased. Despite hyponatremia, food deprived goats started to drink 44 +/- 15 min after the heaters were turned on and then they drank repeatedly. Three of them underwent water diuresis. Hemodilution was observed both in fed and food-deprived goats during heat stress. These results show that heat stress induced primary polydipsia in pregnant goats. It is suggested that stimulating signals from warmth receptors overrode inhibiting influences from receptors signalling hyponatremia and hypoosmolality at the "thirst center" in the hypothalamus. Heat stress did not increase plasma cortisol concentration, but catching sight of food caused an abrupt, short-lasting elevation.

Aldosterone↗
PubMed1993

Lateral preoptic neurons inhibit thirst in the rat.

Kainic acid (KA) and muscimol were injected into the lateral preoptic area (LPO) of the rat to study their effects on drinking behavior. A low dose (5 ng) of KA, which stimulates neurons, decreased the amount of water intake induced by hypertonic saline (IP) and angiotensin II (SC). Injection of 2 ng muscimol, a potent GABAA receptor agonist that suppresses neurons, facilitated drinking responses induced by hypertonic saline, but did not affect angiotensin II-induced drinking. Rats injected with a high dose (150 ng) of KA, which destroys neurons, showed marked polydipsia accompanied by increased urination. One week after the KA lesion, drinking and urine output recovered to normal. During the polydipsia, a small volume of concentrated urine could be excreted if water intake was restricted. After recovery, excessive drinking responses followed water deprivation and hypertonic saline load. The rats normally drank water in response to angiotensin II and to polyethylene glycol solution. The results show that activation of LPO neurons inhibits water intake, and that suppression of LPO neurons facilitates osmotically induced water intake. Therefore, LPO neurons are probably involved in the inhibition of thirst.

Animals↗
PubMed1993

Vasopressin- and oxytocin-immunoreactive hypothalamic neurones of inbred polydipsic mice.

In the late 1950s the inbred polydipsic mice, STR/N, was discovered. The early studies indicated that the extreme polydipsia was not due to a lack of vasopressin but probably due to innate thirst of unknown origin. Because the recent investigation has revealed the presence of some functional abnormality in the brain of the STR/N mouse, we now investigated, using immunohistochemical techniques, distribution of vasopressin (AVP)- and oxytocin (OXT)-containing neurones in the hypothalamus of polydipsic strain of mouse and compared with that of the control. The pattern of distribution of AVP- and OXT-immunoreactive neurones in the paraventricular (PV), supraoptic (SO), and suprachiasmatic nuclei (SCN) of the STR/N polydipsic mouse was similar to that of the control, but the number of AVP-immunoreactive neurones was more numerous in the PVN and SON and less in the SCN in the polydipsic mouse than in the control. In addition, a discrete group of AVP- and OXT-containing neurones that was not clearly seen in the control was discovered in the STR/N. These results implicate that abnormal distribution in the brain AVP and OXT contribute to the mechanism responsible for the polydipsia shown by the strain STR/N.

Animals↗
PubMed1985

Midazolam oral self-administration.

The technique of chronic schedule-induced drug solution intake was used to determine the possible addiction liability of the short-acting benzodiazepine midazolam. Schedule-induction produces polydipsia over a wide range of fluids as a function of the imposed schedule of food availability. The inducing schedule used presented food pellets automatically once per minute, fixed time (FT) 1-min, for 3 h daily. Two groups of rats, drinking either water or 0.05 mg/ml midazolam solution, were exposed to schedule-induction sessions for approx. 2 months. Then, other FT-values (0, 0.5, 3 and 5 min) were instituted on occasion for single sessions. Each of these 'probe' session determinations was done twice. Although midazolam concentration had been adjusted so that the mean group intakes were equal at FT 1-min, probe values greater than 1 min revealed a greater acceptance of midazolam compared to water. This technique produced session midazolam intakes as great as 25 mg/kg. In the next phase, the entire experiment was repeated except both groups were offered a choice between water and midazolam solution during sessions. Only at FT 0 and FT 5-min was there an indication that midazolam was preferred over water. Two additional groups of animals were exposed to the same schedule-induced polydipsia regimen, drinking water and midazolam solution, respectively. Pre-session administration of doses of Ro 15-1788, CGS 8216 (benzodiazepine antagonists) or midazolam had no effects on either water or midazolam intakes, although the higher dose of midazolam (2 mg/kg, s.c) had a moderately suppressive effect on the non-tolerant water-polydipsic group. All groups were tested on occasion for physical dependence on midazolam with an auditory stimulus as the precipitator and midazolam polydipsic groups were found to have a mild to moderate dependence (clonic seizures, running fits).

Administration, Oral↗
PubMed1995

Carbamazepine and PIP-syndrome in temporal lobe epilepsy.

We describe four patients with left temporal lobe epilepsy who developed psychosis, intermittent polydipsia and hyponatremia (PIP-syndrome) while being treated with carbamazepine. These cases illustrate the close links between dysfunction of the limbic system causing epileptic seizures and psychosis on the one hand and dysregulation in hypothalamic centers manifestating in polydipsia and osmodysregulation on the other.

Anticonvulsants↗
PubMed1996

Repetitive behaviors in schizophrenia: a single disturbance or discrete symptoms?

Schizophrenia patients often display multiple repetitive behaviors. We investigated relations among nine repetitive behaviors and evaluated the hypothesis that these behaviors are varied manifestations of a single underlying biobehavioral disturbance. Nine repetitive behaviors from the Elgin Behavioral Rating Scale were assessed in 400 schizophrenia patients residing at a state hospital. A majority of patients were smokers (76.3%) and very few had pica (3%). Several other repetitive behaviors showed substantial frequency. A principal components analysis revealed eight of nine behaviors shared at least 10% of their variance with a single, common component. However, a principal factor analysis suggested a five-factor model best represented the data. The five factors and items identifying them were: (1) 'oral consumption' behaviors-polydipsia and smoking; (2) 'Kluver-Bucy' behaviors-bulimia and hypersexuality; (3) 'movement' behaviors-mannerisms/postures and pacing; (4) 'bizarre use of objects'-bizarre grooming and hoarding; (5) 'Pica'. Associations among repetitive behaviors varied. Symptoms such as smoking and polydipsia appeared reliably related, and others such as pica appeared discrete and independent. Overall, the data did not support the 'single disturbance' hypothesis and suggested a multifactorial model is needed to characterize repetitive behavior disturbances in schizophrenia.

Adult↗
PubMed2005

Fatal water intoxication in a schizophrenic patient--an autopsy case.

We report a case of fatal water intoxication due to polydipsia. A 69-year-old schizophrenic male was found dead at his room of the hospital in which he had been admitted. Medico-legal autopsy was carried out to determine the cause of his death. The autopsy revealed no severe trauma leading him to the death. Internally, it was noticed that the stomach was vigorously expanded, including fluid contents. Intracardiac blood, being dark-red in color, seemed to be diluted. The both lungs ballooned aqueously, showing apparently edema. However, there was neither macroscopic nor histopathological lesion, being responsible for his death. Postmortem biochemical analyses revealed severe hyponatremia of 92 mEq/ml. In cases with short postmortem interval, serum sodium level almost similarly reflected antemortem level. According to his psychiatric doctor, he had been diagnosed as water intoxication due to polydipsia. Moreover, at 2 h before the discovery of his body, he had been found to drink much running water. It was concluded the cause of his death as fatal water intoxication.

Aged↗
PubMed2004

Physiological and pathophysiological influences on thirst.

Thirst motivates animals to seek fluid and drink it. It is regulated by the central nervous system and arises from neural and chemical signals from the periphery interacting in the brain to stimulate a drive to drink. Our research has focussed on the lamina terminalis and the manner in which osmotic and hormonal stimuli from the circulation are detected by neurons in this region and how that information is integrated with other neural signals to generate thirst. Our studies of osmoregulatory drinking in the sheep and rat have produced evidence that osmoreceptors for thirst exist in the dorsal cap of the organum vasculosum of the lamina terminalis (OVLT) and in the periphery of the subfornical organ, and possibly also in the median preoptic nucleus. In the rat, the hormones angiotensin II and relaxin act on neurons in the periphery of the subfornical organ to stimulate drinking. Studies of human thirst using functional magnetic resonance imaging (fMRI) techniques show that systemic hypertonicity activates the lamina terminalis and the anterior cingulate cortex, but the neural circuitry that connects sensors in the lamina terminalis to cortical regions subserving thirst remains to be determined. Regarding pathophysiological influences on thirst mechanisms, both excessive (polydipsia) and inadequate (hypodisia) water intake may have dire consequences. One of the most common primary polydipsias is that observed in some cases of schizophrenia. The neural mechanisms causing the excessive water intake in this disorder are unknown, so too are the factors that result in impaired thirst and inadequate fluid intake in some elderly humans.

Animals↗