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At least 919 records · Page 51Linked to original sources
PubMed2000

4.0 T water proton T1 relaxation times in normal human brain and during acute ethanol intoxication.

BACKGROUND: It has been reported that acute ethanol intoxication decreases the brain water proton magnetic resonance T1 values, an effect that has been interpreted to indicate brain dehydration during this condition. Because water macromolecular interactions largely determine tissue water T1, another possible explanation for reduced brain water proton T1 values is that the interaction between water and brain macromolecules is altered by ethanol. METHODS: A 4.0 T magnetic resonance imaging (MRI) instrument was used to measure brain water proton T1 relaxation times before, during, and after ethanol intoxication (dose, 0.75 mg/kg) in healthy controls. RESULTS: The T1 relaxation times as assessed with MRI were highly reproducible. The mean, paired ethanol-induced differences in T1 were -0.004 +/- 0.007 sec (mean +/- standard deviation) for white matter and 0.010 +/- 0.015 sec for internal gray matter structures, neither of which was significant. CONCLUSIONS: This reasonably sensitive measurement does not support the view that tissue water content or water macromolecule interactions are significantly altered in the brain during acute alcohol intoxication in otherwise healthy subjects.

Adult↗
PubMed1980

Effect of cold water immersion and its combination with alcohol intoxication on urine flow rate of man.

Urine flow rate was determined for man before and after immersion in either thermoneutral (33 degrees C) or cold (10 degrees C) water. The effect of alcohol intoxication of a level of approximately 80 mg dL-1 was also evaluated for the cold water immersion. Immersion and cold were additive in their effect, resulting in a mean urine flow rate of 4.25 mL min-1, approximately 3.5 times the preimmersion level. Alcohol intoxication in conjunction with cold water immersion caused a further large increase in urine flow to 8.03 mL min-1. These results permit better evaluation of the importance of volume diuresis as it relates to the reduction of insulative performance of dry-type immersion suits for cold water survival, and to the possible enhancement of "rewarming shock" during therapy for hypothermia victims. The increased urine production observed when alcohol treatment was added to cold immersion provides information for speculation on mechanisms of volume diuresis.

Adult↗
PubMed1989

Increased lung water and ascites after massive cocaine overdosage in mice and improved survival related to beta-adrenergic blockage.

STUDY OBJECTIVE: To determine the effect of massive cocaine intoxication on lung water and ascites accumulation and the effect of beta- and alpha-adrenergic blockade on survival in massive cocaine intoxication in the mouse. DESIGN: The effect of massive cocaine intoxication on lung water, ascitic fluid accumulation, and survival following LD 100 doses of intravenous cocaine with and without alpha- and beta-adrenergic blockade was determined. INTERVENTIONS: Cocaine hydrochloride (0.15 mg/g body weight) was administered intravenously with no other interventions; with propranolol hydrochloride intravenously (0.5 mg per mouse) before and after cocaine; and with phentolamine intravenously (10.5 micrograms per mouse) before cocaine. MEASUREMENTS AND MAIN RESULTS: Intravenous cocaine hydrochloride resulted in an increase in lung water (saline controls, 4.17 +/- 1.3 [standard deviation] mg water per g mouse; cocaine hydrochloride, 5.94 +/- 0.9 mg water per g mouse; P less than 0.002). Cocaine hydrochloride always resulted in the accumulation of transudative ascitic fluid (saline controls, no measurable ascitic fluid; cocaine administration, 20.2 +/- 12.9 micrograms per mouse; ascitic fluid protein concentration, 23.5 +/- 8.5 g/L). Propranolol hydrochloride administered before or after intravenous cocaine hydrochloride resulted in a striking reduction in mortality (84 of 84 mice without propranolol died [mortality = 100%]; 7 of 39 mice with propranolol died [mortality = 18%]; P less than 0.001). CONCLUSIONS: Massive cocaine intoxication is associated with increased lung water and transudative ascites. Fluid accumulation is not prevented by either alpha- or beta-adrenergic blockers. Propranolol, administered either before or after cocaine, sharply reduces mortality. The results should be extrapolated to treatment in humans with caution.

Animals↗
PubMed1976

Hysterical polydipsia (compulsive water drinking) in children.

Two patients had entirely different clinical presentations of hysterical polydipsia: convulsions and coma in a 5-year-old boy with intrinsic renal disease and a single kidney, and abnormal behavior in a 3-year-old girl with normal kidneys. In neither case was the correct diagnosis made on initial evaluation. Physiological studies demonstrated primary polydipsia to be responsible for both clinical presentations. The differential diagnosis of polydipsia and polyuria is reviewed, and the nonuniform presentation of hysterical polydipsia is emphasized. In children with intrinsic renal disease, hysterical polydipsia may be life-threatening.

Child, Preschool↗
PubMed1981

Serious hyponatremia in patients with cancer: management with demeclocycline.

Seventeen patients with cancer or aplastic anemia received demeclocycline as treatment for hyponatremia. Prior to demeclocycline therapy no patients showed clinical signs of fluid overload or saline depletion. In all patients inappropriately concentrated urine (mean urine osmolality = 548 mOSM/kg H2O) or increased urine content of sodium (mean urine sodium = 91 mEq/L) were documented prior to demeclocycline therapy. No patient had developed hyponatremia in association with antineoplastic drug therapy. The average serum sodium (NaS) at the time of initiation of therapy was 121 mEq/L. NaS increased in all patients despite the simultaneous administration of generous volumes of fluid. NaS exceeded 130 mEq/L and average of 3.5 days following institution of demeclocycline. Patients lost an average of 2.3 kg during demeclocycline. The toxicity noted following demeclocycline was azotemia and increased serum creatinine. Eight patients developed serum urea nitrogen (SUN) in excess of 25 mg/dl; average maximum creatinine in these eight patients was 1.9 mg/dl. Average peak creatinine in eight patients who did not develop azotemia was 0.87 mg/dl. Azotemia seemed to be correlated with simultaneous administration of other nephrotoxic agents and with administration of higher doses (1200 mg/day) of demeclocycline.

Creatinine↗
PubMed1992

Evaluation of acute brain edema using quantitative magnetic resonance imaging: effects of pretreatment with dexamethasone.

We developed a quantitative magnetic resonance imaging method to permit a rapid assessment of brain water content during osmotic brain edema produced by intraperitoneal (ip) injection of distilled water. Fifteen minutes after water injection, the normalized mean image intensity (MIn) from a spin-echo pulse sequence (TE = 80 ms, TR = 1085 ms) was the same as that measured from control animals not injected with water. Sixty minutes after the water injection, the mean +/- SEM brain image MIn had increased by 10.8 +/- 2.4% compared to 3.4 +/- 0.7% in control animals (P less than 0.05). Blood plasma osmolality decreased by 6-10% during this time interval. A subsequent ip injection of hypertonic NaCl solution (100 gm/liter) caused the blood plasma osmolality and brain image MIn to return toward their initial values. MIn of cerebral gray matter correlated with tissue water content measured in parallel studies. Animals pretreated with 0.25 mg/(kg day) dexamethasone had cerebral gray matter MIn values during osmotic edema which were lower than those of untreated animals.

Acute Disease↗
PubMed1980

[Evaluation and treatment of hyponatremia (author's transl)].

In all patients with hyponatremia, an etiologic diagnosis must be made. A diagnostic classification of hyponatremic states is proposed, which is based on extracellular fluid volume status. A spot urinary sodium concentration will be helpful in confirming the diagnosis. Treatment should concentrate on correction of etiologic factors and fluid restriction after any extracellular fluid volume depletion is treated. A regimen of rapid correction of hyponatremia is outlined for serious, symptomatic cases. It consists of diuretic induced diuresis, accompanied by hypertonic sodium replacement of urinary losses. Finally, the usefulness of demeclocycline hydrochloride is characterized.

Furosemide↗