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PubMed1985

Incidence of seizures that follow rehydration of hypernatremic rabbits with intravenous glucose or fructose solutions.

Hypernatremic dehydration was induced in rabbits during a 3- to 5-day period resulting in mean plasma sodium concentrations of 187 meq/liter. The animals were then rehydrated during a 4-h period by intravenous administration of a 2.5% glucose or fructose solution. The water content of four regions of brain sample showed a significant (P less than 0.05) increase in brain water content above normal in the rehydrated groups. Brain water content was significantly (P less than 0.01) greater in those animals with seizures compared with those without seizures, suggesting the importance of water intoxication in the pathogenesis of seizure activity. Changes in muscle Na, K, Cl, and water content were not similar to those of brain, indicating that muscle content of these substances was not an accurate reflection of the brain content specific time. The incidence of seizures was significantly (P less than 0.05) greater when glucose solution was used for rehydration (49%) compared with the use of fructose solution (25%). The mechanism(s) by which fructose resulted in a lower incidence of seizures is not known. The frequency of seizure activity was directly proportional to the rate of administration of intravenous solutions utilized to correct hypernatremia. In addition, the specific carbohydrate of the solution appeared to play an important role in the pathophysiology of the development of seizures.

Animals↗
PubMed1989

Muscle cell potassium, RNA and hydration in pregnancy and pre-eclampsia.

Thirty four pregnant women from 26 to 38 weeks gestation and 24 pregnant women with pre-eclampsia gave samples of muscle (rectus abdominis) at caesarean section. Muscle samples were analysed for H2O, K+, Mg2+ and Na+. Cell extracellular H2O was partitioned by the use of the Cl- space. Also protein, nucleic acids and Zn2+ were determined. From 26 to 38 weeks gestation the concentration of K+ per litre of cell water ([Ki]) slowly declined. The slope was significant. Points for patients with pre-eclampsia fell below the line and analysis of covariance showed that the two populations were different (P less than 0.001). Patients A-J were regarded clinically as severe pre-eclamptics. Points for these patients, in general, fell between 1 and 2 SDs below the normal line. Since other cations per litre of muscle cell water did not change, questions are raised. is the cation gap filled by amino acids or does vascular spasm cause a leakage of K+ from muscle cells? Does hypotonicity eventually develop leading to water intoxication? The low oncotic pressure in pre-eclampsia (shown here), the negative free water clearance could all favour increased cell hydration (some evidence for this is presented here towards term). Assessment of available information concerning creatinine excretion during normal pregnancy and K40, K42 studies together with our own rodent studies leads us to believe that a significant increase in muscle mass occurs, but such may not be the case in pre-eclampsia since the reduction in RNA and Zn2+ concentrations in muscle would suggest excessive protein degradation.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Muscles↗
PubMed1976

Inappropriate secretion of antidiuretic hormone after cerebral injury.

A case has been presented in which a patient sustained a closed head injury with concomitant maxillofacial injuries; early signs of water intoxication and ISADH developed six days after injury. This disorder was corrected by restricting free water intake for six days until equilibration occurred. Successful reduction of the facial fractures was accomplished after stabilization of the patient's neurological condition and correction of her metabolic disorder. The ISADH and resulting hyponatremia have been documented in a variety of disease states including trauma to the central nervous system. Disruption or irritation to the hypothalamic-neurohypophyseal system has been proposed as the mechanism of dysfunction after cerebral injury. The results of the secretion of inappropriate amounts of ADH relative to renal function and homeostatis have been discussed. Clinical and laboratory diagnosis as well as the elective and emergency management of ISADH have been reviewed. The fact that the sequelae of this abnormal metabolic state may mimic or mask the neurological deterioration which may follow cerebral injury is significant. This may contribute to the difficulty in making a correct diagnosis and designing proper therapy. The problem is basically one of differentiating a correctable metabolic disorder from a lesion that can be fatal unless surgically removed.

Adult↗
PubMed1976

The sink action of cerebrospinal fluid volume flow. Effect on brain water content.

Effects of changes in serum osmolarity on volume flow of fluid into the cerebral ventricles of cats were measured by ventriculocisternal perfusion with mock cerebrospinal fluid (CSF), mock CSF containing acetazolamide, or a 30 mOsm/liter sucrose solution. Serum osmolarity was altered by intravenous infusion of a sucrose solution ranging between 10 and 650 mOsm/liter changing volume flow. For all perfusion fluids, regression lines relating volume flow to infused solution osmolarity were parallel. After infusion of a 10 mOsm/liter solution, brain water content increased. One hour after infusion, volume flow returned to normal, although serum was still hypotonic. Gray matter water content was still elevated; white matter returned to normal. The results suggest that the source of increased volume flow is the brain, and that the CSF acts as a sink, limiting excess water accumulation during water intoxication.

Animals↗
PubMed1980

Carbamazepine intoxication due to triacetyloleandomycin administration in epileptic patients.

In 17 epileptics receiving carbamazepine (CBZ) alone or in combination with other anticonvulsant drugs, administration of triacetyloleandomycin (Tri A) led to an acute and unexpected intoxication (drowsiness, nausea, vomiting, and dizziness). Similar symptoms occurred again in 3 patients after Tri A was administered a second time. The same toxic manifestations were observed in two patients receiving CBZ and erythromycin. A rapid increase in plasma levels of CBZ occurred after institution of Tri A therapy in 6 patients, the CBZ levels quickly returning to normal after withdrawal of Tri A. Thus, it is suggested that the observed intoxication is due to the simultaneous administration of CBZ and Tri A (or erythromycin). The possible role of hepatic dysfunction in this syndrome of intoxication is discussed. Furthermore, the intoxication may be at least partially related to serum electrolyte disturbances, as suggested by one case in which obvious signs of water intoxication were detected. The severity and frequency of intoxication should lead to proscribing Tri A or other macrolide antibiotics in patients receiving CBZ.

Adolescent↗
PubMed1977

Inappropriate secretion of antidiuretic hormone. An overview of the syndrome.

The syndrome of inappropriate secretion of antidiuretic hormone is characterized by production of less than maximally dilute urine in the presence of hypotonic plasma. It may be secondary to malignant disease, central nervous system disorders, or pulmonary disease, among other conditions, or it may be idiopathic. Manifestations are those of water intoxication, eg, confusion, fatigue, nausea, headache, and neurologic signs. The pathogenesis is not completely understood. Restriction of fluid intake to obtain a negative water balance is effective treatment.

Drug-Related Side Effects and Adverse Reactions↗
PubMed2003

Hyponatraemic coma induced by desmopressin and ibuprofen in a woman with von Willebrand's disease.

A middle-aged woman was admitted to the hospital after being found unconscious at home. A brain CT scan excluded an intracranial bleed or other focal abnormality. Laboratory analysis showed hyponatraemia (sodium: 121 mmol L(-1)) and a low plasma osmolality, with normal sodium excretion and urine osmolality. A diagnosis of hyponatraemic coma was made. The patient was treated with water restriction; 24 h later the sodium was 135 mmol L(-1) and the patient was neurologically fully recovered. The patient, who suffered from von Willebrand's disease, had received desmopressin and ibuprofen for analgesia 2 days before after a dental intervention. She had received desmopressin several times in the past without any complications. A few patients treated with desmopressin for coagulation abnormalities have been reported to develop water intoxication and severe hyponatraemia resulting in seizures and coma. By inhibiting prostaglandin synthesis, non-steroid anti-inflammatory agents (NSAIDs) potentiate the effect of water reabsorption in the renal tubules of vasopressin, therefore enhancing water retention. Desmopressin and NSAIDs should not be used in combination in patients with bleeding disorders, but it is often followed in clinical practice. In addition, this is probably not an unusual situation in patients treated with desmopressin for other 'non-haemorrhagic' indications. This report emphasizes the need for practitioners to be aware of this rare but severe complication.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1988

Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia.

Water intoxication is a serious problem in many patients with chronic psychiatric illness. In an effort to determine the mechanism of this disorder, we investigated the osmoregulation of water intake and antidiuretic function in psychiatric patients with polydipsia and hyponatremia and in matched controls with psychiatric illness but neither polydipsia nor hyponatremia. We found that a water load suppressed plasma osmolality and vasopressin and urine osmolality in both groups, but that urinary dilution and free water clearance were impaired in the patients with hyponatremia, even though plasma levels of vasopressin and solute clearance were similar in the two groups. Moreover, during water loading and infusion of hypertonic saline, the plasma level of vasopressin was higher at any given plasma osmolality in the test patients than in the controls, indicating a downward resetting of the osmostat. Patients' estimates of the amount of water they desired were shown to correlate significantly with the amount of water consumed and, at any given level of plasma osmolality, appeared to be higher in the test patients than in the controls. We conclude that psychiatric patients with polydipsia and hyponatremia have unexplained defects in urinary dilution, the osmoregulation of water intake, and the secretion of vasopressin.

Adult↗
PubMed2004

Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain edema.

Aquaporin-4 (AQP4) is the major water channel in the brain, expressed predominantly in astroglial cell membranes. Initial studies in AQP4-deficient mice showed reduced cellular brain edema following water intoxication and ischemic stroke. We hypothesized that AQP4 deletion would have the opposite effect (increased brain swelling) in vasogenic (noncellular) edema because of impaired removal of excess brain water through glial limitans and ependymal barriers. In support of this hypothesis, we found higher intracranial pressure (ICP, 52+/-6 vs. 26+/-3 cm H2O) and brain water content (81.2+/-0.1 vs. 80.4+/-0.1%) in AQP4-deficient mice after continuous intraparenchymal fluid infusion. In a freeze-injury model of vasogenic brain edema, AQP4-deficient mice had remarkably worse clinical outcome, higher ICP (22+/-4 vs. 9+/-1 cm H2O), and greater brain water content (80.9+/-0.1 vs. 79.4+/-0.1%). In a brain tumor edema model involving stereotactic implantation of melanoma cells, tumor growth was comparable in wild-type and AQP4-deficient mice. However, AQP4-deficient mice had higher ICP (39+/-4 vs. 19+/-5 cm H2O at seven days postimplantation) and corresponding accelerated neurological deterioration. Thus, AQP4-mediated transcellular water movement is crucial for fluid clearance in vasogenic brain edema, suggesting AQP4 activation and/or up-regulation as a novel therapeutic option in vasogenic brain edema.

Animals↗
PubMed1984

Effects of long-term carbamazepine treatment on water metabolism and plasma vasopressin concentration.

Plasma osmolality, sodium and vasopressin were measured in 7 patients before and during long-term treatment with carbamazepine, under resting conditions, and following an oral water load of 20 ml/kg body weight. During carbamazepine treatment, the ability to excrete the oral water load was decreased, the urine/plasma osmolality ratio was higher, and the free water clearance was lower. In two patients, the ability to excrete the oral water load was severely impaired, and the free water clearance remained negative following water loading. Plasma osmolality and sodium concentration were significantly lower during carbamazepine administration, but despite this the plasma vasopressin concentration remained unchanged or was even slightly increased. Four patients showed inappropriately high vasopressin concentrations in relation to the corresponding plasma osmolality when taking carbamazepine. The findings suggest a decrease in plasma osmolality during carbamazepine treatment, which might account for the inappropriate secretion of vasopressin. The latter might cause clinical symptoms of water intoxication, as has previously been reported in a few patients on carbamazepine therapy.

Adult↗
PubMed2000

Role of water channels in fluid transport studied by phenotype analysis of aquaporin knockout mice.

Aquaporin-type water channels are expressed widely in mammalian tissues, particularly in the kidney, lung, eye and gastrointestinal tract. To define the role of aquaporins in organ physiology, we have generated and analysed transgenic mice lacking aquaporins (AQP) 1, 3, 4 and 5. Multiple phenotype abnormalities were found in the null mice. For example, in kidney, deletion of AQP1 or AQP3 produced marked polyuria whereas AQP4 deletion produced only a mild concentrating defect. Deletion of AQP5, the apical membrane water channel in the salivary gland, caused defective saliva production. Deletion of AQP1 or AQP5, water channels in lung endothelia and epithelia, resulted in a 90% decrease in airspace-capillary water permeability. In the brain, deletion of AQP4 conferred marked protection from brain swelling induced by acute water intoxication and ischaemic stroke. The general paradigm that has emerged from these phenotype studies is that aquaporins facilitate rapid near-isosmolar transepithelial fluid absorption/secretion, as well as rapid vectorial water movement driven by osmotic gradients. However, we have found many examples in which the tissue-specific expression of an aquaporin is not associated with any apparent phenotypic abnormality. The physiological data on aquaporin null mice suggest the utility of aquaporin blockers and aquaporin gene replacement in selected human diseases.

Animals↗
PubMed2004

Vasopressin and desmopressin in central diabetes insipidus: adverse effects and clinical considerations.

The management of central diabetes insipidus has been greatly simplified by the introduction of desmopressin (DDAVP). Its ease of administration, safety and tolerability make DDAVP the first line agent for outpatient treatment of central diabetes insipidus. The major complication of DDAVP therapy is water intoxication and hyponatremia. The risk of hyponatremia can be reduced by careful dose titration when initiating therapy and by close monitoring of serum osmolality when DDAVP is used with other medications affecting water balance. Herein we review the adverse effects of DDAVP and its predecessor, vasopressin, as well as discuss important clinical considerations when using these agents to treat central diabetes insipidus.

Antidiuretic Agents↗
PubMed1989

Beer potomania syndrome in an alcoholic.

To summarize, patients with the "beer potomania" syndrome are characterized by 1) a history of chronic alcohol ingestion (in a hypotonic form); 2) protein malnutrition; 3) signs, symptoms and laboratory values consistent with water intoxication, including hyponatraemia, hypochloraemia and, usually, hypokalaemia; 4) no evidence of another cause of hyponatraemia such as steroid use, diuretic use, hyperlipidaemia, etc. The pathophysiology involves the inability to excrete sufficient free water, based on a loss of normal renal urea gradients. Patients may actually be total-body sodium depleted, yet have elevated urinary sodium and fractional sodium excretion due to this disorder of water metabolism. Attention to proper nutrition during the acute illness may obviate the need for potentially hazardous administration of hypertonic saline.

Alcoholism↗
PubMed2004

Alpha-syntrophin deletion removes the perivascular but not endothelial pool of aquaporin-4 at the blood-brain barrier and delays the development of brain edema in an experimental model of acute hyponatremia.

The formation of brain edema, commonly occurring as a potentially lethal complication of acute hyponatremia, is delayed following knockout of the water channel aquaporin-4 (AQP4). Here we show by high-resolution immunogold analysis of the blood-brain-barrier that AQP4 is expressed in brain endothelial cells as well as in the perivascular membranes of astrocyte endfeet. A selective removal of perivascular AQP4 by alpha-syntrophin deletion delays the buildup of brain edema (assessed by Diffusion-weighted MRI) following water intoxication, despite the presence of a normal complement of endothelial AQP4. This indicates that the perivascular membrane domain, which is peripheral to the endothelial blood-brain barrier, may control the rate of osmotically driven water entry. This study is also the first to demonstrate that the time course of edema development differs among brain regions, probably reflecting differences in aquaporin-4 distribution. The resolution of the molecular basis and subcellular site of osmotically driven brain water uptake should help design new therapies for acute brain edema.

Animals↗
PubMed1995

Water electrolyte homeostasis in acute bronchiolitis.

Children with acute bronchiolitis frequently require hospitalization and parenteral fluid therapy. Water retention due to impaired renal water excretion has been described in several pulmonary conditions in children. We studied 20 infants (3.6 +/- 2.9 months), hospitalized consecutively for acute bronchiolitis for water and electrolyte changes during the acute stage and compared them to those on recovery. Serum sodium and plasma osmolality, urinary sodium and osmolality were measured in all infants. Ten infants each were assigned alternatively to study body water compartment or renal water handling (water load excretion and free water excretion capacity) on the day of hospitalization and after recovery. Mean ( +/- SD) value of serum sodium of the infants at admission was 132.7 +/- 7.2 mEq/L which increased to 137.1 +/- 5.4 mEq/L on recovery (p < 0.05). Plasma osmolality changed from 284 +/- 14 mOsm/kg at admission to 294 +/- 10 mOsm/kg at recovery (p < 0.05). There was a significant decrease in urinary sodium from 54 +/- 39 mEq/L to 20 +/- 18 mEq/L and urinary osmolality from 415 +/- 213 mOsm/kg to 252 +/- 204 mOsm/kg at admission and at recovery, respectively. All 10 infants showed significant increase in total body water (mean +/- SD; 22.8 +/- 7.5 ml/kg) at admission as compared to that at recovery. The total body water (TBW) excess was mainly in extracellular water compartment (16.3 +/- 3.6 ml/kg). Seven of 10 infants had significant impairment in renal water excretion. Increase in maximum free water clearance of these 7 infants on recovery was 0.69 +/- 0.27 ml/min, i.e., 15 times more than that at admission. It is concluded that bronchiolitis of infancy is characterized by water retention which is caused by impaired renal water excretion. In the management of severe bronchiolitis careful attention to fluid therapy is mandatory; liberal fluid therapy may lead to water intoxication.

Bronchiolitis↗
PubMed1979

Idiopathic, sustained, inappropriate secretion of ADH with associated hypertension and thirst.

A 15 year old girl presented with excessive thirst and hypertension (170/110 mm Hg). Biochemical investigations revealed serum sodium 118 meq/liter, serum osmolality 238 mosmol/liter, urine sodium 90 meq/liter, urine osmolality 700 mosmol/liter, persistenly elevated serum antidiuretic hormone (ADH) levels (5.8 to 11.9 pg/ml) and no obvious cause for the hypertension. The hypertension is, at least in part, volume-related, diminishing with fluid restriction. Features of gross water intoxication (e.g., confusion, coma) have not occurred. The etiology of the inappropriate secretion of ADH is not obvious but is not thought to be due to "resetting of osmoreceptors" as evidenced by failure to maximally dilute urine following a water load test and persistently elevated serum ADH levels. A similar patient described by Epstein and associates in 1962 is presently well with persistent features of inappropriate secretion of ADH.

Adolescent↗
PubMed1999

Severe hyponatraemia in an amiloride/hydrochlorothiazide-treated patient.

A 85-year-old woman treated with, among other drugs, a thiazide diuretic presented with a severe hyponatraemia. She met several of the criteria for SIADH and, besides drugs, no cause for SIADH was found. After stopping the thiazide diuretic and restricting fluid intake the patient recovered fully. It was later proved that the thiazide was the cause of the water intoxication by rechallenging the patient with a single dose of amiloride/hydrochlorothiazide 5/50 mg. This "thiazide provocation test" showed its usefulness in the differential diagnosis of suspected SIADH. Moreover, the test demonstrated the paradoxal effect of thiazide diuretics to cause water retention in susceptible patients.

Aged↗
PubMed2000

Skeletal muscle function and water permeability in aquaporin-4 deficient mice.

It has been proposed that aquaporin-4 (AQP4), a water channel expressed at the plasmalemma of skeletal muscle cells, is important in normal muscle physiology and in the pathophysiology of Duchenne's muscular dystrophy. To test this hypothesis, muscle water permeability and function were compared in wild-type and AQP4 knockout mice. Immunofluorescence and freeze-fracture electron microscopy showed AQP4 protein expression in plasmalemma of fast-twitch skeletal muscle fibers of wild-type mice. Osmotic water permeability was measured in microdissected muscle fibers from the extensor digitorum longus (EDL) and fractionated membrane vesicles from EDL homogenates. With the use of spatial-filtering microscopy to measure osmotically induced volume changes in EDL fibers, half times (t(1/2)) for osmotic equilibration (7.5-8.5 s) were not affected by AQP4 deletion. Stopped-flow light-scattering measurements of osmotically induced volume changes in plasmalemma vesicles also showed no significant differences in water permeability. Similar water permeability, yet approximately 90% decreased AQP4 protein expression was found in EDL from mdx mice that lack dystrophin. Skeletal muscle function was measured by force generation in isolated EDL, treadmill performance time, and in vivo muscle swelling in response to water intoxication. No differences were found in EDL force generation after electrical stimulation [42 +/- 2 (wild-type) vs. 41 +/- 2 (knockout) g/s], treadmill performance time (22 vs. 26 min; 29 m/min, 13 degrees incline), or muscle swelling (2.8 vs. 2.9% increased water content at 90 min after intraperitoneal water infusion). Together these results provide evidence against a significant role of AQP4 in skeletal muscle physiology in mice.

Animals↗