Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Water Intoxication”

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 1,675 records · Page 93Linked to original sources
PubMed1995

Progression of alcohol consumption across the drinking career in alcoholics and social drinkers.

OBJECTIVE: To document and compare the changes in alcohol intake over the drinking career in alcoholic (n = 273) and social (n = 152) drinkers and to relate the changes to age and to the prevalence of morning drinking. METHOD: Lifetime alcohol intake was assessed in face-to-face interviews by asking subjects to report drinking patterns during different "phases" of their drinking careers, beginning with the onset of regular drinking and continuing up to the present. RESULTS: Alcohol consumption began at higher quantities and higher frequencies in alcoholics (prealcoholics) and rapidly escalated within a few years to values well out of the range of moderation. The alcohol intake of social drinkers at the beginning phase was only about 70% that of alcoholics. In contrast to alcoholics, the alcohol intake of social drinkers remained relatively constant across subsequent drinking phases at about three to four drinks per drinking occasion, with only a slight increase in the frequency of drinking over sequential drinking phases. The relationship of total alcohol consumption to age in alcoholics was described best by a curvilinear function, with alcohol consumption peaking near age 40. CONCLUSIONS: Gender differences in consumption were decreased with adjustment for body water content. The higher initial alcohol intakes in alcoholics may reflect a lower sensitivity to the intoxicating effects of alcohol, or, alternatively, a greater ability of alcoholics to develop tolerance. The high prevalence of morning drinking in alcoholics compared to social drinkers reinforces the usefulness of morning drinking as a diagnostic tool, particularly for female alcoholism.

Adult↗
PubMedDate not supplied

[Principles of pharmacotherapy in geriatrics].

This article examines the pharmacokinetics and pharmacodynamics of drugs under the aspects of senile changes in organs and systems in the neurohumoral regulation and in metabolism. It gives reasons for the inadequacy of polypharmacy in the treatment of elderly and old people and for the need of a strict individualization. The retarded reactivity of the organism of old people, their increased susceptibility and reduced tolerance of the effects of drugs necessitate smaller dosages of drugs in geriatrics in comparison with the generally usual dosages, especially at the beginning of treatment. The multitude of exogenous and endogenous changes in the organism, that go hand in hand with the process of aging, leads in old people to an increased susceptibility to more frequent and pronounced secondary effects caused by drugs. Of special importance in the prevention of a possible intoxication by drugs are, in the case of elderly people, the proper composition of food, the water balance and the electrolyte metabolism.

Aged↗
PubMedDate not supplied

Cholestyramine improves tropical-related diarrhea.

Patients exposed to the toxic dinoflagellate Pfiesteria develop an illness characterized by secretory diarrhea, conjunctival irritation, skin lesions, and varying degrees of neurologic manifestations. The anion-exchange resin, cholestyramine has been reported in one small case series to be an effective treatment of severe diarrhea associated with Pfiesteria intoxication. A 54-year-old man traveled to the Dominican Republic where he went swimming in what he describes as "dirty ocean water". Within an hour, he noted a generalized burning and itching of his skin. Later on, he noted pruritic vesicular skin lesions, intense frontal headache, and conjunctivitis. A few days later, he complained of abdominal cramping, nausea, and hourly episodes of watery, non-bloody diarrhea. Due to the constellation of symptoms, Pfiesteria intoxication was suspected. On arrival in the United States, he sought medical care for continued symptoms. Physical examination was remarkable for conjunctival injection, linear vesicular lesions (5 cm in length) over his right ankle and left orbit as well as erythema over foreskin of his penis. Mental status and memory were normal. Laboratory studies revealed an elevated serum creatinine, which eventually normalized, and stool studies were negative for leukocytes, blood, and enteric pathogens. Intense diarrhea persisted until he was started on cholestyramine (4 g PO tid). The diarrhea resolved within 2 hours of starting treatment. The headache was initially treated with narcotic agents but only resolved with IV diphenhydramine (25 mg q 4 h). Cholestyramine and diphenhydramine appear to be effective therapeutic agents for tropical-related diarrhea and headache, respectively.

Anion Exchange Resins↗
PubMed1989

Dose-response relationship in intoxication by the pyrrolizidine alkaloid monocrotaline.

Rats develop pulmonary hypertension over a 2-wk period of continuous ingestion of monocrotaline dissolved in drinking water (20 mg/l). The relationship between monocrotaline concentration and duration of exposure was investigated by giving male rats (initial body weight 100 g) monocrotaline in drinking water (5, 10, 20, 40, or 60 mg/l) for 0, 1, 2, 4, 6, 10, or 20 d. Rats were killed 20 d after initiating treatment, and increased lung and right ventricular to body weight ratios were measured as indices of pulmonary hypertension. The accumulative dose of monocrotaline delivered over a 10-d period using a drinking water concentration of 10 mg/l (18 mg/kg) produced the same degree of right ventricular hypertrophy and lung weight increases as the doses ingested over a 4-d period by rats consuming 20 or 40 mg/l monocrotaline water (14 and 29 mg/kg). Phenobarbital pretreatment did not substantially alter the time course of toxicity induced with 20 mg/l monocrotaline water. Ingestion of 60 mg/l monocrotaline water for 1 d (11 mg/kg) resulted in right ventricular hypertrophy at 20 d. Since accumulative doses of less than 11 mg/kg did not produce toxicity and all doses greater than 14 mg/kg did, this range may be considered a threshold for inducing toxicity. However, organ weight increases following threshold exposures reversed over a 4-wk period. Increases in the wall thickness of pulmonary arteries correlated with the development of right ventricular hypertrophy. Pulmonary inflammation was not an early response to monocrotaline administration, since there was no change in the proportion of cell types recovered in lung lavage fluid during the first 6 d of monocrotaline treatment.

Administration, Oral↗
PubMed1993

Effect of cadmium on enzymatic digestion and sugar transport in the small intestine of rabbit.

Cadmium compounds are found widely in our environment: for example, in food, water, soil, and ambient air. The most important exposure route of animals to cadmium in the general environment is via oral exposure. In oral cadmium intoxication, the immediate target organ is the gastrointestinal tract. The aim of the present work was to determine how cadmium acts on the intestinal absorption of sugars and on the sucrase activity through rabbit jejunum, after in vitro administration and/or oral administration of CdCl2 in drinking water. Results obtained show that cadmium decreases D-galactose accumulation in the jejunum tissue. This effect seems to be the results of an action mainly located on Na(+)-dependent sugar transport of the mucosal border of the intestinal epithelium, because cadmium seems not to modify the sugar diffusion across the intestinal epithelium. Cadmium has also been shown to inhibit the (Na(+)-K+)-ATPase activity of the enterocyte, which might explain the inhibition of the D-galactose Na(+)-dependent transport. Nevertheless, a direct action of the cadmium molecule on the Na(+)-dependent carrier cannot be discarded. Cadmium altered the sucrose activity when it was administered in the drinking water for 4 d.

Adenosine Triphosphatases↗
PubMed2000

Increased production of proinflammatory cytokines by murine macrophages following oral exposure to sodium selenite but not to seleno-L-methionine.

Selenium (Se) is an essential as well as a toxic trace element in animal and human nutrition. The immune system is a known target of Se intoxication. The objectives of the present study were to determine the effects of oral exposure to inorganic and organic forms of Se on the murine immune system and to compare the relative toxicity of the different chemical forms. Male BALB/c mice, 6-7 weeks of age, were exposed continuously to 0, 1, 3 or 9 ppm of Se as sodium selenite or seleno-L-methionine in the drinking water for 14 days. Following the treatment period mice were euthanized; trunk blood, spleen, thymus, liver and kidney were aseptically collected and organs weighed. Single-cell splenocyte cultures were made from the spleens and used to determine the effects of Se treatment on mitogen-induced lymphocyte blastogenesis and cytokine production. There were no changes in the 0 and 1 ppm Se groups as selenite. The thymus/body weight ratio was significantly reduced at 3 ppm Se as sodium selenite, and all other parameters remained unaffected. Exposure to 9 ppm of Se as sodium selenite resulted in marked decrease in body weight gain and relative organ weights. Treatment of mice with 9 ppm Se as sodium selenite increased erythrocyte counts in peripheral blood, reduced splenic cellularity, but increased the basal rate of splenocyte proliferation and induced a dose-dependent increase in phytohemagglutinin-P-induced lymphocyte proliferation. Sodium selenite at this dose increased the production of proinflammatory cytokines, tumor necrosis factor alpha and interleukin-1 beta, in lipopolysaccharide-stimulated splenic macrophages. Mice exposed to Se as seleno-L-methionine in the drinking water did not display any effects on the parameters examined at the dose range in this study. Results indicated that splenic macrophages and lymphocytes are sensitive to Se intoxication and there is a disparity in the immune system toxicity of inorganic and organic forms of Se administered via the drinking water, inorganic Se being more toxic.

Administration, Oral↗
PubMed2002

Neonatal activation of alcohol-related prenatal memories: impact on the first suckling response.

BACKGROUND: Rat fetuses seem to be capable of associative learning mediated through alcohol's unconditioned properties. The newborn's suckling response immediately after birth is dependent on olfactory stimuli present in the fetal milieu and/or odorants perceived immediately after birth. The present study analyzed the impact of olfactory fetal learning supported by maternal-fetal alcohol intoxication on the newborn's first postnatal suckling response, in the presence or absence of chemosensory cues originally associated with alcohol during prenatal life. METHODS: During gestational days 17 to 20, fetuses experienced a salient novel cue (cineole) explicitly paired or not with the induction of alcohol intoxication resulting from maternal intragastric intubation of a 2 g/kg ethanol dose. A separate set of dams were intubated with only water. In experiment 1, cesarean-delivered pups were tested shortly after birth for their response to a surrogate nutritive nipple scented with cineole or with no explicit odor. In experiment 2, pups were similarly evaluated after the prenatal treatment when cineole, a novel odorant (lemon), or no explicit odor was presented either in conjunction with the nipple or before being tested with the nipple. RESULTS: In both experiments, fetal olfactory conditioning supported by alcohol intoxication had a significant effect on the newborn's first suckling episode, depending on the olfactory cues presented before or during suckling. Presence of cineole but not of novel odorants seemed to activate the associative memory acquired in utero. Once the memory was activated, pups that were subjected to fetal odor-alcohol pairings were found to attach significantly more to surrogate nutritive nipples than did fetal control animals. CONCLUSIONS: Prenatal experience with alcohol intoxication can result in chemosensory associative learning mediated by the drug's postabsorptive effects. This learning determines attachment patterns of newborns when they reexperience olfactory cues that had signaled onset of the state of acute alcohol intoxication when they were fetuses. Considered in view of previous experiments, the present results generate two alternative hypotheses relative to the affective component of the memory established in utero: (1) alcohol intoxication is an appetitive reinforcer during fetal life, or (2) the calming effects of postnatal suckling behavior counteract negative hedonic components of the memory accrued in utero.

Alcohol Drinking↗
PubMed2000

Enhanced intake of ethanol in preweanling rats following interactions with intoxicated siblings.

Recently Hunt, Holloway, & Scordalakes (1999) described a novel procedure for examining how social interactions with an intoxicated sibling can enhance periadolescent rats' voluntary intake of ethanol. In the present series of experiments we extend these findings to preweanlings. In Experiment 1, same-sex sibling 16-day-olds were assigned to be either (a) a demonstrator that was administered 1.5 g/kg ethanol or water control or (b) an observer that was tested for ethanol intake following a brief interaction with the demonstrator. Observers interacting with EtOH demonstrators exhibited increased intake of ethanol relative to observers interacting with water demonstrators. In Experiment 2, subjects were 8, 12, or 16 days of age and at all ages, ethanol intakes increased following exposure to an intoxicated sibling. In Experiment 3, repeated exposures to ethanol demonstrators on days 12, 14, and 16 was found to promote ethanol intake after weaning (on postnatal day 22). Collectively these data indicate that exposure to ethanol cues in the context of home/social cues can lead to modifications in ethanol acceptance, and that repeated exposures to such cues during infancy can impact ethanol ingestion after weaning.

Alcohol Drinking↗
PubMed1976

Toxic and gonadotropic effects of cadmium and boron relative to standards for these substances in drinking water.

Experimental research was conducted on the study of the relationship of the general toxic and gonadotoxic effects of cadmium and boron under conditions of subacute and chronic oral intoxication on white random-bred rats, by use of biochemical, physiological, cytological, and pathomorphological methods. It is shown that the gonadotoxic effect of cadmium is manifested on the same level (3 mg/kg of body weight) as the general toxic effect. The gonadotoxic effect of boron is dominant and is manifested at a lower level (6 mg/kg of body weight) than the general toxic effect (20 mg/kg). On the basis of the results of chronic experiments, 0.001 mg/l. is recommended as the hygienic standard for cadmium in water and 0.5 mg/l. for boron.

Animals↗
PubMed2005

Pathology of domoic acid toxicity in California sea lions (Zalophus californianus).

Over 100 free-ranging adult California sea lions (Zalophus californianus) and one Northern fur seal (Callorhinus ursinus), predominantly adult females, were intoxicated by domoic acid (DA) during three harmful algal blooms between 1998 and 2000 in central and northern California coastal waters. The vector prey item was Northern anchovy (Engraulis mordax) and the primary DA-producing algal diatom was Psuedonitzschia australis. Postmortem examination revealed gross and histologic findings that were distinctive and aided in diagnosis. A total of 109 sea lions were examined, dying between 1 day and 10 months after admission to a marine mammal rehabilitation center. Persistent seizures with obtundation were the main clinical findings. Frequent gross findings in animals dying acutely consisted of piriform lobe malacia, myocardial pallor, bronchopneumonia, and complications related to pregnancy. Gross findings in animals dying months after intoxication included bilateral hippocampal atrophy. Histologic observations implicated limbic system seizure injury consistent with excitotoxin exposure. Peracutely, there was microvesicular hydropic degeneration within the neuropil of the hippocampus, amygdala, pyriform lobe, and other limbic structures. Acutely, there was ischemic neuronal necrosis, particularly apparent in the granular cells of the dentate gyrus and the pyramidal cells within the hippocampus cornu ammonis (CA) sectors CA4, CA3, and CA1. Dentate granular cell necrosis has not been reported in human or experimental animal DA toxicity and may be unique to sea lions. Chronically, there was gliosis, mild nonsuppurative inflammation, and loss of laminar organization in affected areas.

Animals↗
PubMedDate not supplied

Biochemical correlations between some organs and the liver after acute ethanol intoxication in rats.

The influence of different doses of ethanol on the phospholipid metabolism in rat was investigated with 32P. Male rats received by oral intubation a single intoxicating dose of ethanol (3.5 or 5.8 g/kg body wt) as a 45% solution. The corresponding control rats received an equal volume of water. The rats were killed at 2, 4, 6, 24, 48 and 72 hours. The liver, brain, kidney and spleen responses depend on the administered dose and vary with time.

Alcoholic Intoxication↗
PubMed1986

Membrane fluidity and alcohol dependence.

Rats were chronically intoxicated with alcohol by exposing them to increasing concentrations of ethanol vapor over a 4-week period. They were tested for alcohol consumption in a free choice situation of water and 10% (v/v) alcohol. On the basis of their intakes they were divided into alcohol-dependent and nondependent groups. Synaptosome membrane fluidity evaluated by fluorescence polarization was compared between the two groups and against nonintoxicated controls. The intoxicated animals had a lower membrane fluidity than controls, mainly because of a highly significant increase of rigidity in the alcohol-dependent group. Furthermore, membrane fluidity was found to be correlated with the degree of behavioral dependence (i.e., alcohol intake during the free choice period).

Alcohol Drinking↗
PubMed1982

[Nuclear magnetic resonance studies of effects of glycerol on brain edema].

Effects of glycerol on the state of water in edematous brain tissues were studied by the pulse FT NMR technique. Brain edemas were induced experimentally by cold injury and triethyl tin (TET) intoxication in Wistar rats. Ten percent w/v glycerol (1 g/kg body weight) were injected intravenously at 30 minutes before decapitation for the NMR measurements. Transverse relaxation times (T2) in the cerebral gray and white matter were measured by Meiboom-Gill pulse sequence at the resonant frequency of 100 MHz. Water content was calculated from the difference between wet and dry weight after heating in an oven at 95-100 degrees C for 72 hours after the NMR measurements. In the normal brain T2 value was 76.4 msec and 75.4 msec in the gray and white matter respectively. In the edematous brain, T2 separated into two components, one slow and one fast, corresponding with the increase of water content. Values of the slow component (slow T2) were characteristic of both types of brain edema. In the cold injury edema, slow T2 values became 105 msec in the gray matter and 96 msec in the white matter, while in the TET induced edema, it became 450 msec in the white matter. After glycerol infusion, slow T2 became faster in these regions in both types of brain edema, showing 92.1 msec in the gray matter and 88.1 msec in the white matter of the cold injury edema, and 388 msec in the white matter of TET induced edema. The degree of the changes of slow T2 values per unit change of water content was greater in the cold injury edema than in the TET induced edema. Serum osmolality elevated 23.8 mOsmol greater than the control value after glycerol infusion in this experiment. It is concluded from these findings that glycerol retracts free mobile water molecules from the edema fluid by osmotic pressure gradient.

Animals↗
PubMedDate not supplied

[Aluminum poisoning].

Aluminum intoxication is common in patients with chronic renal failure because of absorption of aluminum during dialysis from aluminum-containing dyalysate water and ingestion of phosphate binders containing aluminum. Aluminum accumulation in the body is followed by bone disease, encephalopathy and anemia. Bone diseases can be recorded in 44% of the patients treated with long-term dialysis. Two early histologic types of retarded bone turnover can be seen, i.e. osteomalacia and aplastic bone disease. In dialyzed patients, osteomalacia is usually followed by low PTH level in human serum. On the contrary, studies on uremic rats have shown that previous parathyroidectomy can prevent aluminum intoxication, because hyperparathyroidism in an early phase of chronic renal failure increases aluminum absorption from the gut and its accumulation in the body. As the pathogenesis of aluminum-induced alterations is unclear, the prevention of bone disease should be provided through lowering the aluminum intake in dialyzed patients. Bone biopsy is unavoidable for the early detection and diagnosis of the disease. Promising results in the treatment of aluminum intoxication have been obtained using deferoxamine, a chelating agent.

Aluminum↗
PubMed1978

Effect of ethanol on glucose and water absorption in hamster jejunum in vivo. Methodological problems: anesthesia, nonabsorbable markers, and osmotic effect.

We studied the effect of ethanol on glucose and water absorption in vivo. In preliminary experiments, using sodium amytal anesthesia, we found that control animals, whose jejunal segment was perfused without ethanol, required more anesthetic agent than those perfused with ethanol. Thus, to allow for unbiased comparison of the absorption data between the two groups of animals, all absorption studies were carried out on conscious restrained hamsters. We found that ethanol did not influence the permeability of the jejunum to polyethylene glycol (PEG) and meglumine diatrizoate. In addition, ethanol did not influence the time required for the onset of steady-state absorption. Using both the gravimetric and the electrical methods, we were unable to show any measurable osmotic pressure exerted by ethanol (150-1050 mM) on the hamster jejunum. In the absorption studies we found that perfusion of the hamster jejunum with five increasing concentration of ethanol (450-1050 mM) appeared to cause a concentration-dependent depression in steady-state glucose transport. Water transport was depressed only when 4.8% (1050 mM) ethanol was perfused.

Alcoholic Intoxication↗
PubMed2004

Biochemical changes in the kidneys after perinatal intoxication with lead and/or cadmium and their antagonistic effects when coadministered.

Lead acetate (300 mg/L) and/or cadmium acetate (10 mg/L) were administered as drinking water to pregnant Wistar rats from day 1 of pregnancy to parturition (day 0) or until weaning (day 21) to investigate the possible nephrotoxic effects of these metals. We also studied the possibility of toxicological interactions between both metals. Kidneys were used to determine the activity of several enzymes considered key to correct renal function: alkaline and acid phosphatases, Mg(2+)/Ca(2+)-dependent ATPase, and Na(+)/K(+)-dependent ATPase. The results showed a general decrease in the activity of these enzymes after treatment with the heavy metals; this fact suggests that lead and cadmium are able to impair renal function due to biochemical alterations, since ATPases are essential for reabsorption and secretion processes and phosphatases are involved in the differentiation of the proximal tubules. On the other hand, simultaneous perinatal administration of both metals seems to protect against the toxicity produced by cadmium or lead separately. It is not clear whether this is due to decreased absorption or increased sequestration or excretion.

Animals↗
PubMed2004

Bioflavonoids and glutamine in diet and the Mg, Ca, Cu, Zn concentrations in heavy metals intoxicated rats' skins.

The effect of bioflavonoids on the Mg, Ca, Cu and Zn concentration in rats' skin intoxicated with heavy metals Pb or Cd. The animals were divided at random into nine groups, each of 6 rats. Group I obtained in drinking water the solution of plumbum nitrate, Pb(NO3)2 in concentration of 500 mg Pb/dm3, group II solution of lead ions--500 mg Pb/dm3 and quercetin--200 mg/dm3 and glutamine 4 g/dm3, group III--lead ions solution (500 mg Pb/dm3), catechin--200 mg/dm3 and glutamine 4 g/dm3, group IV received water solution of Pb(NO3)2--500mg Pb/dm3, naringenin--200 mg/dm3 and glutamine 4 g/dm3, V-VII groups obtained the same that groups I-IV, but instead of lead cadmium chloride (CdCl2) in the amount of 500 mg Cd/dm3 was used. Group IX was a control group, and these animals received redistilled water to drink. All the groups of rats were on a normal diet (LSM dry food) and they got solutions and food ad libitum. After the experiment, the animals were sacrificed under ketamine narcosis and while collecting tissues, the skins (together with furs) used for further studies were also obtained. Heavy metals intoxication caused a significant decrease of magnesium and calcium concentrations in the examined rats' skins, and bioflavonoids with glutamine dietary addition did not improve or improve to a small degree the levels of those elements. Lead, in opposition to cadmium, decreased zinc and copper levels in skins, and bioflavonoids with glutamine caused the return of those elements' concentrations to the values of control group.

Animal Feed↗