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Oxytocin is a peptide hormone that plays a key role in regulating the female reproductive system, including during labor and lactation. It is produced primarily in the hypothalamus and secreted by the posterior pituitary gland. Oxytocin can also be administered as a medication to initiate or augment uterine contractions. To study the effectiveness and safety of oxytocin, previous studies have randomized patients to low- and high-dose oxytocin infusion protocols either alone or as part of an active management of labor strategy along with other interventions. These randomized trials demonstrated that active management of labor and high-dose oxytocin regimens can shorten the length of labor and reduce the incidence of clinical chorioamnionitis. The safety of high-dose oxytocin regimens is also supported by no associated differences in fetal heart rate abnormalities, postpartum hemorrhage, low Apgar scores, neonatal intensive care unit admissions, and umbilical artery acidemia. Most studies reported no differences in the cesarean delivery rates with active management of labor or high-dose oxytocin regimens, thereby further validating its safety. Oxytocin does not have a predictable dose response, thus the pharmacologic effects and the amplitude and frequency of uterine contractions are used as physiological parameters for oxytocin infusion titration to achieve adequate contractions at appropriate intervals. Used in error, oxytocin can cause patient harm, highlighting the importance of precise administration using infusion pumps, institutional safety checklists, and trained nursing staff to closely monitor uterine activity and fetal heart rate changes. In this review, we summarize the physiology, pharmacology, infusion regimens, and associated risks of oxytocin. [ABSTRACT FROM AUTHOR]

Brain edema – a frequently fatal pathological state in which brain volume increases resulting in intracranial pressure elevation – can result from almost any insult to the brain, including traumatic brain injury. For many years, the objective of experimental studies was to find a method to prevent the development of brain edema at the onset. From this perspective, the use of methylprednisolone (MP) appears promising. High molecular MP (MW>50 kDa) can be incorporated into the brain – in the conditions of the experimental model – either by osmotic bloodbrain barrier disruption (BBBd) or during the induction of cellular edema by water intoxication (WI) – a condition that increases the BBB permeability. The time window for administration of the MP should be at the earliest stages of edema. The neuroprotective effect of MP on the permeability of cytoplasmatic membranes of neuronal populations was proved. MP was administrated in three alternative ways: intraperitoneally during the induction of cytotoxic edema or immediately after finishing cytotoxic edema induction in a dose of 100 mg/kg b.w.; into the internal carotid artery within 2 h after finishing cytotoxic edema induction in a dose of 50 mg/kg b.w.; into internal carotid artery 10 min after edema induction by BBBd in a dose of 50 mg/kg b.w. [ABSTRACT FROM AUTHOR]

Magnetic resonance imaging has been used for evaluating of a brain edema in experimental animals to assess cytotoxic and vasogenic edema by the apparent diffusion coefficient (ADC) and T2 imaging. This paper brings information about the effectiveness of methylprednisolone (MP) on experimental brain edema. A total of 24 rats were divided into three groups of 8 animals each. Rats with cytotoxic/intracellular brain edema induced by water intoxication were assigned to the group WI. These rats also served as the additional control group CG when measured before the induction of edema. A third group (WIMP) was intraperitoneally administered with methylprednisolone 100 mg/kg during water intoxication treatment. The group WI+MP was injected with methylprednisolone 50 mg/kg into the carotid artery within two hours after the water intoxication treatment. We evaluated the results in four groups. Two control groups (CG, WI) and two experimental groups (WIMP, WI+MP). Rats were subjected to MR scanning 24 h after edema induction. We observed significantly increased ADC values in group WI in both evaluated areas - cortex and hippocampus, which proved the occurrence of experimental vasogenic edema, while ADC values in groups WIMP and WI+MP were not increased, indicating that the experimental edema was not developed and thus confirming the protective effect of MP. [ABSTRACT FROM AUTHOR]

Copyright of Zentralblatt fuer Arbeitsmedizin, Arbeitsschutz und Ergonomie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Induction of cellular cerebral edema (CE) was achieved by a standard method of water intoxication which consisted of fractionated intraperitoneal administration of distilled water (DW) together with the injection of desmopressin (DP). Using metabolic cage, fluid and food balance was studied in two groups of eight animals: group C - control; group CE - cellular edema induced by water intoxication. For each rat the intake (food pellets and water) and excretion (solid excrements and urine) were recorded for 48 h together with the initial and final body weight. CE animals consumed significantly less food, drank less water and eliminated the smallest amount of excrements. The induction of cellular cerebral edema was accompanied with a significant loss of body weight (representing on average 13 % of the initial values) mainly due to a reduction of food intake. This phenomenon has not yet been reported. [ABSTRACT FROM AUTHOR]

Abstract Nitrate pollution has emerged as a problem of great importance because in recent years, the levels of nitrate in soil and groundwater have increased, mainly through anthropogenic activities, such as the use of fertilizers in agriculture, domestic wastewater and septic tanks, industrial waste and deforestation. In animals, nitrate reduction to nitrite (NO 2) and nitric oxide (NO) promote the formation of methemoglobin in the blood and the generation of highly reactive intermediates that induce oxidative stress in target organs. Exposition to nitrates has been associated with methemoglobinemia, reproductive toxicity, metabolic and endocrine alterations and cancer. This study analyzed acute intoxication with sodium nitrate (NaNO 3) in male Wistar rats, aged 12–16 weeks. Four groups with n = 10 rats each were formed: group 1 was the control, and group 2, group 3 and group 4 were treated for 10 days with intragastric doses of 19, 66 and 150 mg/kg/d NaNO 3 , respectively. Hematological, metabolic and histological biomarkers in the liver were analyzed. The results showed high percentages of methemoglobin, an increase in NO 2 in the plasma and an accumulation in the liver. Moreover, there were high counts of white blood cells and platelets in all treated groups. Additionally, there was an increase in the spleen weight in group 4. High levels of glucose, triglycerides, lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed and were significantly increased in groups 3 and 4. For oxidative stress biomarkers, there were increases in Thiobarbituric Acid Reactive Substances (TBARS), total GSH and SOD activity, mainly in group 4. Changes in mitochondrial activity were not significant. Histopathological analyses of the liver showed inflammation, infiltration of mononuclear cells, steatosis, ischemia and necrosis, and these findings were more evident at high doses of NaNO 3 in which high of S-nitrosylation were found. In conclusion, NaNO 3 was reduced to NO 2 , thereby inducing methemoglobinemia, whereas other reactive species generated oxidative stress, causing hematological and metabolic alterations and injury to the liver. Graphical abstract fx1 Highlights • Subacute intoxication with NaNO 3 increases the level of NO 2 in the plasma and the percentage of methemoglobin in Wistar rats. • Short term exposition to NaNO 3 causes alterations in white blood cell and platelet counts. • An increase in the dose of NaNO 3 also increases the TBARS and S-nitrosylation levels and triggers the antioxidant response. • Inflammation, steatosis, ischemia and necrosis in the liver were found at a high dose, namely, 150 m/kg/d NaNO 3. [ABSTRACT FROM AUTHOR]

Blooms of Ostreopsis cf. ovata , causing health incidence and mass human intoxications in the Mediterranean, gained special attention over the past decades. To study the potential effects of temperature and nutrient enrichment on this benthic dinoflagellate and other associated microalgae in situ, a multifactorial experiment was set up along a temperature gradient of a heat pump system in Monaco. Microalgae were quantified in experimental units, in the natural biofilm and in the water column. No significant interaction was observed between temperature and nutrients. A species- and bloom phase-dependent effect of the increased temperature was recorded, while the nutrient enrichment had a significant effect only at the end of the experiment (when cell abundances were low). Temperature effects were also visible in the biofilm and the surrounding water. The observed assemblages were mainly driven by changes in abundances of Ostreopsis cf. ovata and Actinocyclus sp., affected in different ways. [ABSTRACT FROM AUTHOR]

Continuous monitoring of the intracranial pressure (ICP) detects impending intracranial hypertension resulting from the impaired intracranial volume homeostasis, when expanding volume generates pressure increase. In this study, cellular brain edema (CE) was induced in rats by water intoxication (WI). Methylprednisolone (MP) was administered intraperitoneally (i.p.) before the start of CE induction, during the induction and after the induction. ICP was monitored for 60 min within 20 h after the completion of the CE induction by fibreoptic pressure transmitter. In rats with induced CE, ICP was increased (Mean±SEM: 14.25±2.12) as well as in rats with MP administration before the start of CE induction (10.55±1.27). In control rats without CE induction (4.62±0.24) as well as in rats with MP applied during CE induction (5.52±1.32) and in rats with MP applied after the end of CE induction (6.23±0.73) ICP was normal. In the last two groups of rats, though the CE was induced, intracranial volume homeostasis was not impaired, intracranial volume as well as ICP were not increased. It is possible to conclude that methylprednisolone significantly influenced intracranial homeostasis and thus also the ICP values in the model of cellular brain edema. [ABSTRACT FROM AUTHOR]

Our previous experiments revealed that water intoxication and osmotic BBB disruption in the rat allow penetration of highmolecular substances into the brain and that resulting changes in the internal environment of the CNS lead to pathological development, such as the loss of integrity of myelin. The aim of the present study was to determine whether the previously described phenomena are associated with increased water content in the brain. To answer the question following methods were used: a) water intoxication: intraperitoneal administration of distilled water, b) osmotic BBB disruption: application of mannitol (20 %) selectively into the internal carotid artery, c) brain wet weight was measured after decapitation, and subsequently (after six days in thermostat set at 86 °C) the dry weight were estimated d) in animals with 20 % and 30 % hyperhydration the degree of myelin deterioration was estimated e) animal locomotor activity was tested by continuous behavior tracking and analysis. Brain water content after water intoxication and following the administration of mannitol was higher than in the control group. Different degrees of hyperhydration led to different levels of brain water content and to different degrees of myelin impairment. Hyperhydration corresponding to 20 % of the body weight brought about lower locomotor activity. Increased water content in the brain after the BBB osmotic disruption is surprising because this method is frequently used in the clinical practice. [ABSTRACT FROM AUTHOR]

Summary: Soon after their introduction in 1957, thiazide diuretics became a recognized cause of hyponatremia. Thiazides may be the sole cause and they may exacerbate hyponatremia in patients with disorders that cause the syndrome of inappropriate antidiuretic hormone secretion. Although thiazides do not inhibit the ability to concentrate the urine, they impair diluting ability in several ways: inhibition of sodium and chloride transport at cortical diluting sites; stimulation of vasopressin release; reduction of glomerular filtration and enhanced proximal water reabsorption, which reduce delivery to the distal diluting sites; and, possibly, a direct effect on water flow in the collecting duct. Water retention caused by impaired water excretion combined with cation depletion may result in severe hyponatremia. Thiazides should be avoided in frail elderly patients with chronically high water intake or in others who depend on the excretion of maximally dilute urine to maintain fluid balance, such as patients with psychogenic polydipsia or heavy beer drinking. Inadvertent rapid correction of hyponatremia is common in thiazide-induced hyponatremia because the ability to dilute the urine is restored when the diuretic is discontinued and volume deficits are repaired. Hypokalemia, which often is present, increases the susceptibility to osmotic demyelination syndrome and replacement of potassium deficits contributes to the increase in serum sodium concentration. [ABSTRACT FROM AUTHOR]

Abstract: Psychogenic polydipsia (PPD) or water intoxication with polyuria and polydipsia is common among patients with psychiatric disorders. Although the underlying pathology is unclear, PPD or drinking more than 3 liters of fluid daily can be a highly disabling and life-threatening condition. In half of the cases, it can lead to mortality because of cerebral edema and central nervous system dysfunction with delirium, seizures, coma, and death. Excessive drinking can accompany other repetitive behaviors in schizophrenic, bipolar, or psychotic patients. A screening program can detect cases early to minimize morbidity and mortality. This article describes the evidence-based screening, evaluation, and management of water intoxication or polydipsia and includes a case study to illustrate evaluation and management. [Copyright &y& Elsevier]

Copyright of Revista Ciência & Saúde Coletiva is the property of Associacao Brasileira de Pos-Graduacao em Saude Coletiva and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Summary: Virtually all investigators now agree that self-induced water intoxication, symptomatic hospital-acquired hyponatremia, and hyponatremia associated with intracranial pathology are true emergencies that demand prompt and definitive intervention with hypertonic saline. A 4- to 6-mmol/L increase in serum sodium concentration is adequate in the most seriously ill patients and this is best achieved with bolus infusions of 3% saline. Virtually all investigators now agree that overcorrection of hyponatremia (which we define as 10 mmol/L in 24 hours, 18 mmol/L in 48 hours, and 20 mmol/L in 72 hours) risks iatrogenic brain damage. Appropriate therapy should keep the patient safe from serious complications of hyponatremia while staying well clear of correction rates that risk iatrogenic injury. Accordingly, we suggest therapeutic goals of 6 to 8 mmol/L in 24 hours, 12 to 14 mmol/L in 48 hours, and 14 to 16 mmol/L in 72 hours. Inadvertent overcorrection owing to a water diuresis may complicate any form of therapy, including the newly available vasopressin antagonists. Frequent monitoring of the serum sodium concentration and urine output are mandatory. Administration of desmopressin to terminate an unwanted water diuresis is an effective strategy to avoid or reverse overcorrection. [ABSTRACT FROM AUTHOR]

In Latin America and the Caribbean (LAC), human intoxication to lead is considered as an important public health issue. In Port-au-Prince, concentrations of lead ranging from 40 μg/L to 90 μg/L, greater than the threshold value (10 μg/L) for drinking water, were measured in groundwater and drinking water. This study aims to assess human health risks generated by exposure to lead in the Port-au-Prince water supply. Two sampling campaigns were performed between April 2004 and December 2004 on different structures of the public water supply. A significant lead concentration of 250 μg/L, greater than the threshold value, had been detected in a water tank. Risk of deterioration of the psychological development of children exposed to these waters was calculated. These results require monitoring in order to control the human health risk by lead in Port-au-Prince's drinking water. [ABSTRACT FROM AUTHOR]

Abstract: Lead acetate (300mg Pb/L) and/or cadmium acetate (10mg Cd/L) in blood and liver were administrated as drinking water to pregnant Wistar rats from day 1 of pregnancy to parturition (day 0) or until weaning (day 21), to investigate the toxic effects in blood and in the liver. Both metals produced mycrocitic anaemia in the pups as well as oxidative damage in the liver, as suggested by the significant increase in TBARS production and the high catalase activity. Moreover, intense alkaline and acid phosphatase activity, used as biomarkers of liver adaptation to damaging factors, was observed. In addition, the toxikinetics are different for Pb and Cd: while Cd is a hepatotoxic from day 0, Pb is not until day 21. Finally, simultaneous perinatal administration of both metals seems to protect, at least, in the liver TBARS production against the toxicity produced by Cd or Pb separately. [Copyright &y& Elsevier]

• Acute Water Intoxication (AWI) can manifest with nausea, headache, seizure, coma and death. • AWI should be in the differential for diffuse cerebral edema. • Reversal of cerebral edema due to AWI can be accomplished with appropriate management of hyponatremia. Acute water intoxication (AWI) is a disorder of excess water intake that can manifest in neurological injury and death. We describe a case of a 54-year-old man that presents to the emergency department with a generalized toxic-clonic seizure due to AWI. Initial computed tomography of the brain demonstrated diffuse cerebral edema. However, with correction of serum sodium over the one hospital day, the patient's neurological symptoms and imaging completely resolved. Clinicians should recognize of reversibility of this entity with management of hyponatremia. [ABSTRACT FROM AUTHOR]

Thirst and resultant water drinking can arise in response to deficits in both the intracellular and extracellular fluid compartments. Inhibitory influences mediating the satiation of thirst also are necessary to prevent overhydration. The brain regions that underpin the generation or inhibition of thirst in these circumstances can be categorized as sensory, integrative, or cortical effector sites. The anterior cingulate cortex and insula are activated in thirsty human beings as shown by functional brain-imaging techniques. It is postulated that these sites may be cortical effector regions for thirst. A major sensory site for generating thirst is the lamina terminalis in the forebrain. Osmoreceptors within the organum vasculosum of the lamina terminalis and subfornical organ detect systemic hypertonicity. The subfornical organ mediates the dipsogenic actions of circulating angiotensin II and relaxin. Major integrative sites are the nucleus of the tractus solitarius, the lateral parabrachial nucleus, the midbrain raphé nuclei, the median preoptic nucleus, and the septum. Despite these advances, most of the neural pathways and neurochemical mechanisms subserving the genesis of thirst remain to be elucidated. [ABSTRACT FROM AUTHOR]

A 41-year-old female suffering from water intoxication showing consciousness disturbance with a serum sodium level of 104mEq/l followed by repeated seizures is reported. She had been treated for 16 years with the drug, chlorpromazine. The computed tomography (CT) showed a bilateral hemispheric swelling. This swelling improved after spontaneous urination with an amount of 6700ml within the first 12h. We postulate that severe hyponatremia is possibly life-threatening, moreover, it is hardly recognized if the past history or previous prescription record was not known, because the CT appearance is sometimes misinterpreted. [Copyright &y& Elsevier]

This case study observed the effect of glycerol hyperhydration (GH) in a highly trained male triathlete on endurance performance and cardiovascular and thermoregulatory responses. For this purpose, the subject ingested, in a double-blind random fashion, either a glycerol solution (1.2 g/kg body weight [BW] with 26 mL/kg BW of fluid) or a placebo (26 mL/kg BW of fluid). The subject then performed 2 hr of cycling at 65% VO2max and 25 C, which was followed by an endurance performance test to exhaustion. During exercise, the subject drank 830 mL of sports drink. Compared to placebo hyperhydration (PH), GH increased total body water (TBW) by 1,033 mL before exercise. After 2 hr of cycling, sweat rate, heart rate and perceived exertion were similar between trials, but GH reduced urine production by 300 mL, prevented hypohydration, and decreased rectal temperature by 0.42 C. Compared to PH, GH increased endurance performance by 24%, which was associated with a reduced rectal temperature of the order of 0.3 C. Thus, in this highly trained triathlete, GH better maintained hydration during a 2 hr cycling exercise at 65% VO2max, which reduced core temperature and improved endurance performance. [ABSTRACT FROM AUTHOR]

Six subjects randomly completed four experimental trials consisting of 2 hours of controlled fluid ingestion at rest, followed by 110min of cycle ergometry exercise at 44±11 %VO2max. Fluid was also ingested during exercise, and the trials differed in either the pre-exercise or during exercise fluid ingestion. The control trial consisted of the pre-exercise ingestion of 26 mL/kg of flavored water, and 5 mL/kg every 20 min of 5% glucose during exercise (WC). For the remaining trials the solutions ingested were 1.2 g/kg glycerol in a total of 26 mL/kg (GH) pre-exercise, and either 5% glucose (GC), 0.5% glycerol in 5% glucose (GCGA), or 1.5% glycerol in 5% glucose (GCGB) during exercise. Compared to WC, GH decreased urine flow (4.7±2.2 vs 7.6±3.7 mL.min, P<0.001) and free water clearance (-1.4±1.3 vs 2.5±1.3 mL/min, p=<0.001). Consequently, pre-exercise hydration was largest with GH(0.9±0.4 vs 0.3±0.3 L for the mean of GC, GCGA and GCGB vs WC). Compared to WC, GH also increased serum osmolality (283.3±3.3 to 281.0±2.6 vs 284.3±0.2 to 291.0±2.3 mOsmol/kg, p<0.01) despite no difference in serum antidiuretic hormone (ADH)(2.3±2.0 vs 2.4±1.0 pg/mL at 120 min). When comparing WC to GCGA and GCGB, continued glycerol ingestion during exercise increased cardiac stroke volume (163.3±27.9 vs 174.4±22.8 mL, p<0.01), and decreased heart rate (128.2±19.0 vs 122.0±14.5 b/min,p<0.01). GH increases body hydration by decreasing renal free water clearance via a non-ADH mediated mechanism. Continued glycerol and water ingestion during exercise increases the cardiovascular benefits of pre-exercise GH, and prolongs the state of hyperhydration. [ABSTRACT FROM AUTHOR]

Pelvic ultrasonography (US) is a simple and non-invasive radiologic test to evaluate the pelvic organs. It requires a full bladder for better visualization. Our case is a 14-year-old female with diabetes insipidus (DI) who admitted to . the pediatric emergency service with the complaints of seizure and agitation after drinking 4 liters of water in one hour for a pelvic US examination due to work-up for delayed puberty. Her biochemical and clinical evaluation revealed water intoxication (WI). To our knowledge, this is the first WI case developed in a patient with DI. Here, we discuss the underlying factors leading to this complication and recommended an approach to obtain a better sonographic image without necessitating oral water intake to fill the urinary bladder. [ABSTRACT FROM AUTHOR]

Abstract: Related to severe hyponatremia, various symptoms, such as confusion, vomiting, changes in mental state, status epilepticus, and a variety of conscious disturbances are sometimes seen in the emergency department (ED) but seldom recognized as water intoxication in the early stages. Status epilepticus is an emergent and life-threatening condition if not diagnosed and managed promptly and efficiently. The authors reported a case of a 31-year-old woman with history of schizophrenia with poor drug compliance. The compulsive drinking of more than 15,000mL of water per day for 4 days resulted in intermittent episodes of vomiting and seizures and she was sent to our ED by ambulance. Water intoxication with severe hyponatremia ([Na+]=112mEq/L) was diagnosed and hypertonic sodium supplements and airway protection were then offered. Detailed history taking and early detection of hyponatremia is crucial to prevent fatal complications of water intoxication. Emergency physicians should be suspicious of hyponatremia from water intoxication in psychiatric patients with neurologic symptoms during the observation period in the ED. [Copyright &y& Elsevier]

The article discusses the authors' use of the Ultimatum Game to evaluate the reciprocal fairness feeling in 5 patients with polydipsic schizophrenia. The game involved a medical staff member and a patient where the former first made a proposal about how to split 3,000 mL of water between the 2 of them and the latter could accept or reject the proposal. It suggests that patients with polydipsic schizophrenia seemed to act more rationally in the Ultimatum Game than other groups of responders.

The article provides information about the benefits of drinking enough water. Water is the second most important life-sustaining element. There should be water equilibrium in a human's system because lack of water causes malfunctioning of the body while too much of it will lead to water intoxication which can lead to life-threatening conditions.

This report includes cases of hyponatremia in preeclampsia. Two patients were identified with preeclampsia complicated by hyponatremia, one with and the other without nephrotic syndrome. Together with 3 cases of hyponatremia recently reported, these additional cases from the same geographic area suggest that hyponatremia is not a rare complication of preeclampsia. (Am J Obstet Gynecol 2001;184:231-2.) [ABSTRACT FROM AUTHOR]