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 1,729 records · Page 96Linked to original sources

Lead as an inductor of changes in the citrate transport to rat brain synaptic mitochondria.

The aim of the experiments presented here was to discern whether prolonged consumption of leaden water, that imitates environmental exposure, affects citrate transport to synaptic mitochondria. Our results indicate that during chronic lead intoxication both the velocity and the affinity of citrate transport to synaptic mitochondria decreased affecting the operation of Krebs cycle and consequently energetic processes in these mitochondria.

Animals↗

Mitochondrial oxidative damage and myocardial fibrosis in rats chronically intoxicated with moderate doses of ethanol.

Mitochondrial oxidative balance and myocardial fibrosis were investigated in pair-fed rats received ethanol (3%) or saccharose in drinking water for 8 weeks. The concentrations of glutathione, malondialdehyde, protein carbonyls and sulfhydrils were determined. The presence and distribution of fibronectin were detected by immunohistochemistry. The myocardial concentrations of reduced glutathione and protein sulfhydrils were lower in ethanol treated rats. The oxidised/reduced glutathione ratio, the levels of malondialdehyde and protein carbonyls were higher in ethanol-treated rats. The mitochondrial amount of proteins, glutathione and protein sulfhydrils were lower in ethanol treated rats, whereas the content of protein carbonyls and malondialdehyde were higher. Accumulation of fibronectin was detected at subepicardial and subendocardial districts in ethanol-treated rats, with moderate degree of fibrosis in 20% of the cases. In conclusion, moderate ethanol consumption is associated with oxidative damage to heart mitochondria and fibronectin deposition. These oxidative and ultrastuctural changes may be assumed as basic alterations in the development of alcoholic cardiomyopathy.

Administration, Oral↗

Avocado (Persea americana) intoxication in caged birds.

Avocados of 2 varieties were mashed and administered via feeding cannula to 8 canaries and 8 budgerigars. Two control budgerigars were given water via feeding cannula. Six budgerigars and 1 canary died within 24 to 47 hours after the first administration of avocado. Deaths were associated with administration of both varieties of avocado. Higher dose was associated with greater mortality. The 2 budgerigars given water were normal throughout the observation period. Results indicated that avocados are highly toxic to budgerigars and less toxic to canaries. Postmortem findings observed in some birds included subcutaneous edema in the pectoral area and hydropericardium.

Animals↗

[The application of in vivo diffusion weighted magnetic resonance imaging to intracranial disorders].

We have developed a magnetic resonance (MR) spin echo method to obtain diffusion weighted imaging using motion-probing gradient (MPG) pulses in one or three orthogonal directions before and after a 180 degree pulse. Phantom models containing water and acetone, normal volunteers and patients with brain tumors, brain edema and infarction were examined. Experimental models of brain edema including triethyltin intoxication and cold injuries were also examined in Wistar rats. MRI was performed at a 1.0-T clinical machine or a 4.7-T experimental machine using spin echo pulse sequences with or without additional MPGs on one or three orthogonal axes. The one direction method was useful to define diffusion anisotropy of myelinated axonal fibers in white matter. Faster diffusion was detected in the white matter parallel to the direction of MPGs. On the other hand, slower diffusion was detected perpendicular to the direction of MPGs because the myelin sheath restricted water diffusion. The three orthogonal gradients method was useful to demonstrate the difference in the diffusion coefficients in various diseases due to its larger total gradient strength. The clear distinction between the cytotoxic edema, which revealed slower diffusion, and the vasogenic edema, which revealed faster diffusion, was demonstrated in the experimental models using diffusion weighted image. In the clinical cases, faster diffusion was demonstrated in the brain tumor and perifocal vasogenic edema, which was in agreement with the results in the experimental models of rats. Brain tumors such as low grade astrocytoma with microcysts and perifocal vasogenic edema have very wide extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Recovery of cyclic antidepressants with gastric lavage.

The role of lavage fluid volume in recovery of cyclic antidepressant with gastric lavage was determined in 13 patients treated for moderate to severe cyclic antidepressant intoxication. An orogastric tube was placed, gastric contents aspirated, and gastric lavage performed with 60 to 180 mL aliquots of tap water or 0.9% NaCl for irrigation. A volume of 12.8 +/- 4.4 liters of lavage fluid was instilled, and 97.6 +/- 6.9% of this volume was recovered. The recovered aspirate and lavage fluid were inspected for the presence of particulate matter and saved in 4 to 5 liter collections. Determination of cyclic antidepressant and metabolite concentrations was performed using gas chromatography-mass spectrometry, and the amount of cyclic antidepressant recovered was calculated. The mean total amount recovered was 110 mg and ranged from 2.4 mg to 342 mg. Of the total amount recovered, 88% +/- 13% was recovered in the first 4 to 5 liters of lavage fluid. An estimate of the dose ingested was available in 7 patients, with 8.7% (0.4% to 21.7%) of the estimated dose recovered by lavage. There were no cases of significant drug recovery in clear lavage fluid. We conclude that if gastric lavage is undertaken in cyclic antidepressant intoxications, it should utilize 5 liters initially and then continue only if particulate matter is seen.

Adolescent↗

Hyperammonemia, brain edema and blood-brain barrier alterations in prehepatic portal hypertensive rats and paracetamol intoxication.

AIM: To study the blood-brain barrier integrity, brain edema, animal behavior and ammonia plasma levels in prehepatic portal hypertensive rats with and without acute liver intoxication. METHODS: Adults male Wistar rats were divided into four groups. Group I: sham operation; II: Prehepatic portal hypertension, produced by partial portal vein ligation; III: Acetaminophen intoxication and IV: Prehepatic portal hypertension plus acetaminophen. Acetaminophen was administered to produce acute hepatic injury. Portal pressure, liver serum enzymes and ammonia plasma levels were determined. Brain cortex water content was registered and trypan blue was utilized to study blood brain barrier integrity. Reflexes and behavioral tests were recorded. RESULTS: Portal hypertension was significantly elevated in groups II and IV. Liver enzymes and ammonia plasma levels were increased in groups II, III and IV. Prehepatic portal hypertension (group II), acetaminophen intoxication (group III) and both (group IV) had changes in the blood brain-barrier integrity (trypan blue) and hyperammonemia. Cortical edema was present in rats with acute hepatic injury in groups III and IV. Behavioral test (rota rod) was altered in group IV. CONCLUSION: These results suggest the possibility of another pathway for cortical edema production because blood brain barrier was altered (vasogenic) and hyperammonemia was registered (cytotoxic). Group IV, with behavioral altered test, can be considered as a model for study at an early stage of portal-systemic encephalopathy.

Acetaminophen↗

Integrity of blood-brain barrier during ethanol intoxication and withdrawal in the rat: normal glucose transfer and permeability to Na+ and Cl-.

The unidirectional brain uptake of 14-C-D-glucose, 24Na+ and 36Cl- was measured by the Oldendorf tissue uptake method in order to test whether severe ethanol intoxication or withdrawal affected the glucose transfer across the blood-brain barrier (BBB) or the integrity of the BBB to small ions. The Oldendorf technique rests upon the assumption that water is freely diffusible across the BBB, but in the present study a correction was applied, which takes into account the fact that the water extraction actually depends upon the different cerebral blood flow (CBF) in the groups. The 24Na+ and 36Cl- extraction values were about 1% as reported in other studies and this suggests that there was no major effect on the BBB reaction to small ions during severe ethanol intoxication or during withdrawal. The permeability surface area product did not deviate significantly from control values in any group and thus there was no indication that glucose transfer across the BBB differed during ethanol intoxication or withdrawal.

Alcoholic Intoxication↗

Does severe water deprivation affect the inner ear? An experimental study of the gerbilline endolymphatic sac.

Through an ultrastructural study of the endolymphatic duct (ED) and sac (ES) system, the effects of an impaired body fluid metabolism on the inner ear fluid environment in the mongolian gerbil has been evaluated. A dehydrative state has been determined depriving of water for both five and twelve days this desert animal, which is known to withstand long periods of water abstinence. The morphological changes of the ED and ES under these circumstances have been compared with those induced by ethacrynic acid intoxication. Although the cochlear partition did not show signs of damage, the ED and ES system seems to be negatively influenced by the dehydrative state and displays a marked imbibition of the subepithelial tissue, which at places shows accumulation of an organic matrix. A regulating role for the antidiuretic hormone on the inner ear fluids of the mongolian gerbil is also proposed and discussed.

Animals↗

[The effect of acute alcoholic intoxication on the morphofunctional properties of the peripheral blood erythrocytes].

In experiments on rabbits it has been established that the acute alcoholization causes prolonged uncompensated alterations of such physical and chemical properties of erythrocytes as the average volume, the concentration of dry substance and water, the density, the content of endoerythrocytal hemoglobin, as well as the concentration of erythrocytes and hemoglobin in blood.

Alcoholic Intoxication↗

The water extract of Coleus barbatus Benth decreases gastric secretion in rats.

Coleus barbatus (Labiatae) Benth is popularly used in Brazil "for the healing of liver and stomach diseases". The water extract (WE 1 to 10 g/kg, p.o.) of stem and leaves given to rats and mice did not induce signs of intoxication. Previous treatment of mice with WE (1 g/kg, p.o.) shortened the sleeping time induced by pentobarbital (50 mg/kg, i.p.) by 37%, although the extract alone did not increase the spontaneous activity nor did it induce hyperexcitability. In mice WE (2 g/kg, p.o.) increased the intestinal transit of charcoal by 30%, while reduced gastric secretions in rats treated with WE (2 g/kg intraduodenal) (3.9 +/- 1.0 to 0.5 +/- 0.2 ml/4 h, respectively). The treatment also reduced the total acid secretion from 34.4 +/- 11.0 to 2.7 +/- 0.5 mEq/l and raised gastric pH from 2.2 +/- 0.3 to 6.5 +/- 0.8. Treatment with WE (2 g/kg, p.o.) protected against gastric ulcers induced by stress (5.3 +/- 1.6 and 1.5 +/- 0.5 ulcers/cm2), but it did not protect against indomethacin induced ulcers. The results show that the water extract of C. barbatus Benth produces mild stimulation of the central nervous system and increases intestinal movements. The extract also reduces gastric secretion indicating an antidyspeptic activity, and protects against gastric ulcers induced by stress.

Animals↗

Acute alcohol intoxication in socially drinking female and male offspring of alcoholic fathers.

Alcohol pharmacokinetics, mood-state alterations and psychomotor performance were investigated in women and men at risk for developing alcoholism. Estimated body water was used to calculate the alcohol dose in an effort to eliminate differences in alcohol pharmacokinetics between women and men due to differences in body composition. Differences were not detected between women and men or family history groups (family history positive, FH +, and family history negative, FH-) on absorption time, peak blood alcohol level (BAL), elimination time, or area under the blood alcohol curve (AUC). FH + men reported no central stimulant effects at peak BAL on the Sensation Scale, whereas FH- men and women all reported central stimulant effects. Further, FH + men reported a decrease in anxiety after the ingestion of alcohol. Acute intoxication did not affect performance in the FH + group on a finger-tapping task. In the FH - group, the dominant hand was significantly impaired during the ascending limb of the blood alcohol curve and recovered during the descending limb. Differences between family history groups or sex were not detected on a grooved-pegboard task. Results indicated that FH + men may experience alcohol differently from the FH - group and FH + women. FH + women also showed different reactions to acute alcohol than the FH - group. However, these differences were not as consistent across tasks.

Adult↗

Evaluation of oral exposure to Polnoks R for female rats in developmental toxicity studies.

This study was performed to evaluate the effects of prenatal development of rats exposed to Polnoks R, an antioxidant in elastomer processing. Pregnant female rats were exposed to Polnoks R by gavage every day on days 6-15 of gestation at doses of 170, 340, and 670 mg/kg body weight (b,w) (6%, 13%, and 25% LD50). Clinical observations, maternal body weights, and food and water consumption were recorded throughout gestation. At scheduled necropsy on 20 day of gestation maternal animals were evaluated for body weight, liver, spleen, ovarjan kidney, and adrenal weights, number of ovarian corpora lutea, and status of uterine implantation sites. Fetuses were counted, weighed, and examined for external, skeletal, and visceral alterations. Maternal weight gain was reduced in the group receiving Polnoks R at the 670 mg/ kg dose. In all groups the daily food and water consumptions were similar to controls. The relative weights of the adrenals, ovaries, spleen, and liver of the females intoxicated with the highest dose of Polnoks R were significantly higher than control organs. Polnoks R is an embryotoxic and fetotoxic agent. It produced a significant increase in the average number of postimplantation losses and a decrease in both the weight and body length of the fetuses from the pregnant female rats exposed to the highest dose. This chemical also produced birth defects-absent or short tail, cleft palate, and internal hydrocephalus-but only at doses toxic to the mother.

Abnormalities, Drug-Induced↗

Mitochondrial DNA deletion of proximal tubules is the result of itai-itai disease.

BACKGROUND: The pathogenesis of itai-itai disease continues to be controversial, although cadmium (Cd) poisoning which arises via polluted water and rice in Japan is likely involved. Until recently, however, a well-defined animal model for Cd intoxication was not available. An animal model for itai-itai disease was produced in rats by low-dose Cd treatment, intraperitoneally for a period of 70-80 weeks. Osteomalacia followed the renal damage. RESULTS: A gene deletion in the mitochondrial DNA was found in the mitochondria of the proximal tubule cells of rats with chronic Cd intoxication, as was shown by the increased smaller PCR product seen by gel electrophoresis in one DNA region, where ATPase and cytochrome oxidase genes are located. However, the PCR product was different from that seen with a gene deletion associated with aging: del4834bp. Renal damage from Cd intoxication initially caused mitochondrial dysfunction indicated by the disturbance in reabsorption in the proximal tubules and decreased amounts of ATP, ATPase, and cytochrome oxidase with gradually progressing tubular proteinuria, and, finally, chronic renal failure with tubulointerstitial damage throughout the renal cortex. These gave rise to osteomalacia, subsequently. CONCLUSION: We concluded that in Cd poisoning, a mitochondrial gene deletion in the mitochondria of the proximal tubule cells was the primary event for the pathogenesis of osteomalacia in itai-itai disease.

Absorption↗

SR147778, a CB1 cannabinoid receptor antagonist, suppresses ethanol preference in chronically alcoholized Wistar rats.

This study investigated the effect of the new CB1 cannabinoid receptor antagonist, SR147778, on ethanol preference in chronically alcoholized Wistar rats. In study 1, SR147778, at doses of 0.3, 1, or 10 mg/kg/day (mg/kg/d) intraperitonealy (ip), was administered during chronic pulmonary ethanol intoxication for 30 days. The rats were then exposed to a two-bottle choice (ethanol 10% v/v vs. water) for at least 30 days. Neither 0.3 nor 1 mg/kg/d had any effect on ethanol preference. In contrast, the high dose induced a significant transient increase in ethanol intake between days 6 and 10. In study 2, SR147778, at doses of 0.3, 1, or 10 mg/kg/d ip, was administered during the free-choice period after chronic alcoholization. Both ethanol preference and intake were significantly reduced only for 1 and 10 mg/kg/d. These results reinforce the hypothesis that the cannabinoid CB1 receptor is part of the neural substrate mediating alcohol intake and the motivational properties of alcohol. When these results are compared with those obtained with SR141716 (Rimonabant) on ethanol preference, we observed that (1) coadministration of 10 mg/kg/d SR147778 during chronic alcoholization induced a shorter transient increase of ethanol intake than Rimonabant and (2) SR147778 treatment during the free-choice period at doses of 1 and 10 mg/kg/d decreased ethanol intake more dramatically than SR141716 which, furthermore, continued for the duration of the free choice.

Alcoholism↗

Fluoride concentrations in three types of commercially packed tea drinks in Taiwan.

Tea is a popular drink around the world. It is also one of the major sources of fluoride intake. The objectives of this study were to assess fluoride concentrations in popular non-, semi-, and full-fermented tea drinks sold on the Taiwan market. Concentration differences among three types of commercially available tea drinks (tea leaf, tea bag, and packaged tea beverage) were explored. Several influential factors in intake concentrations were evaluated. The acute threshold intake (ATI) and allowable daily intake (ADI) of those tea drinks were also estimated. For each commercial type, samples from the most popular tea in one particular fermentation degree (non, semi, and full) were randomly purchased and analyzed for fluoride concentrations. Fluoride levels in different rounds of tea, in different containers, and with different ratios of water and tea leaf were also assessed. In total, 132 tea samples were analyzed. The mean fluoride concentrations in leaf tea without the first round, leaf tea with the first round, bagged tea, and packaged tea were 7.04, 7.79, 5.37, and 25.7 mg/l, respectively. Most of the intake concentrations in those samples exceeded 4 mg/l F, the lower bound of fluoride levels reported in the literatures to be associated with a lower IQ in children and a higher risk of bone fracture. Fluoride concentrations in packaged tea were the highest among the three types of commercially available tea. For studied leaf and bagged tea, almost a constant amount of fluoride was infused from the same amount of tea leaf regardless of the water volume. Besides this, making tea with glass or pottery tea makers would not affect fluoride intake concentrations. Acute intoxication is unlikely to occur. However, tea lovers in high fluoride content areas shall consider limit their consumption of tea drinks to avoid potential chronic effects.

Administration, Oral↗

[Biosafety: phicotoxins (part 3)].

DSP toxins group and its classification are discussed. Optimal environment conditions for synthesis and source organisms are pointed. Its occurrence in food web and mollusks reaction on toxic algae presence in water are described. Mechanism of action, toxicity, tolerable contaminant levels in food, cases of poisoning and clinical presentation of intoxication are presented.

Animals↗

[Evaluation of the combined effect of copper chloride and sodium nitrate on blood methemoglobin and tryptophan level in rats (subchronic exposure)].

The study was performed on 4 groups of male Wistar rats, receiving p.o. through 3 months every day: 1) sodium nitrite in dose 30 mg/kg b.w. x day (0.2 LD50); 2) copper chloride in dose 4.67 mg/kg b.w. x day (0.03 LD50); 3) copper chloride and sodium nitrite in amounts as above, and 4 - control group - received distilled water. The methemoglobin and hemoglobin were determined in whole blood and tryptophan in plasma 24 hours after the last intoxication. There was showed, that every day intoxication of rats with sodium nitrite cause the increase of methemoglobin concentration and decrease the free tryptophan level in the blood. There was also observed, that copper chloride, administrated together with sodium nitrite, decreases significantly his methemoglobin creating action.

Animals↗

Acute alcohol intoxication increases interleukin-18-mediated neutrophil infiltration and lung inflammation following burn injury in rats.

In this study, we examined whether IL-18 plays a role in lung inflammation following alcohol (EtOH) and burn injury. Male rats ( approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dl before burn or sham injury ( approximately 12.5% total body surface area). Immediately after injury, rats were treated with vehicle, caspase-1 inhibitor AC-YVAD-CHO to block IL-18 production or with IL-18 neutralizing anti-IL-18 antibodies. In another group, rats were treated with anti-neutrophil antiserum approximately 16 h before injury to deplete neutrophils. On day 1 after injury, lung tissue IL-18, neutrophil chemokines (CINC-1/CINC-3), ICAM-1, neutrophil infiltration, MPO activity, and water content (i.e., edema) were significantly increased in rats receiving a combined insult of EtOH and burn injury compared with rats receiving either EtOH intoxication or burn injury alone. Treatment of rats with caspase-1 inhibitor prevented the increase in lung tissue IL-18, CINC-1, CINC-3, ICAM-1, MPO activity, and edema following EtOH and burn injury. The increase in lung IL-18, MPO, and edema was also prevented in rats treated with anti-IL-18 antibodies. Furthermore, administration of anti-neutrophil antiserum also attenuated the increase in lung MPO activity and edema, but did not prevent the increase in IL-18 levels following EtOH and burn injury. These findings suggest that acute EtOH intoxication before burn injury upregulates IL-18, which in turn contributes to increased neutrophil infiltration. Furthermore, the presence of neutrophils appears to be critical for IL-18-meditaed increased lung tissue edema following a combined insult of EtOH and burn injury.

Alcoholic Intoxication↗