Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A disturbed water and electrolyte homeostasis is not generally held to be a primary mechanism in the pathogenesis of acute mountain sickness (AMS) and high altitude pulmonary edema (HAPE), but the association of oliguria and weight gain with AMS and HAPE has led to the hypothesis that water retention may be a facilitative mechanism, possibly caused by an effect of hypoxia to release antidiuretic hormone (ADH). To examine the problem, normal Long-Evans rats (N) and the strain with congenital diabetes insipidus (DI) were exposed to hypobaric hypoxia (0.5 atm) for 4 days, and fluid balance in the whole animals and in their lungs was studied. Both strains reduced water intake and were oliguric on acute exposure, but the N rats gained body weight and increased lung water, while the DI rats increased neither body weight nor lung water. Neither strain increased lung blood at high altitude. The oliguria in the DI rats could not have been due to a release of antidiuretic hormone, and was attributed to the diminished water intake in both strains. The protection against HAPE in the DI rats was probably due to their more severe dehydration that exists already in normoxia, and its further increase in hypoxia, compared with N rats.
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PMID:Water balance and lung fluids in rats at high altitude. 160 61

In exploratory studies aimed at elucidating CNS effects due to heavy metal toxicity, signs of compromised renal function were seen in rats. The studies reported here describe the sequential steps of the development of nephrotoxicity by trimethyltin chloride (TMT) in rats. Single doses of 12.25 mg/kg TMT administered orally to 150- to 175-g Long-Evans rats elicited overt signs of toxicity including behavioral abnormalities and marked weight loss. Concurrent with the development of these signs, nephrotoxicity was manifested as functional kidney compromise and associated histopathologic evidence of tubular damage. Pathological changes in the kidneys from treated rats were hyaline droplet inclusions, attenuated brush border, basolateral vacuolization, and eosinophilic granular casts in the proximal tubule cells. These lesions were detected as early as 2 days post-treatment and progressed with time in an orderly and sequential fashion. Renal lesions between 5 and 8 days were mild to severe cortical tubular dilatation, hydropic degeneration, and diffuse hyaline droplet deposition in the lower nephron tubules. Medullary edema and exfoliation of degenerated tubular epithelial cells with cast formation followed from 8 to 11 days. The morphological changes were accompanied by marked elevation of blood urea nitrogen, parallel with polyuria at Day 2 and oliguria by Day 14. Behavioral abnormalities as well as weight loss correlated well with the time course and severity of renal dysfunction and progression of morphological changes. A second experiment compared the effects of TMT in rats of different weights. Heavier rats were more sensitive than lighter rats to the nephrotoxic effects of TMT. These effects were independent of recognizable neurotoxic effects of TMT in the hippocampus.
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PMID:The pathogenesis of trimethyltin chloride-induced nephrotoxicity. 355 27

1. Intake and output of water, Na+ and K+ were measured in Long Evans and Brattleboro rats (deficient in hypothalamic and pituitary vasopressin) before and after subcutaneous injection of polyethylene glycol (PEG) sufficient to cause a substantial hypovolaemia. 2. In the Long Evans rats an initial fluid retention (due to oliguria and polydipsia) was accompanied by Na+ retention and K+ loss. On the second day there was a diuresis but Na+ retention persisted until days 3 and 4 when there was a natriuresis. 3. Brattleboro rats initially also showed fluid retention but this was achieved by hypodipsia with a greater oliguria; there was an accompanying retention of Na+ and K+. On the second day, a reduced fluid balance was still accompanied by Na+ retention but associated with kaliuresis. Diuresis and natriuresis occurred on the third day after PEG injection. 4. Thus, rats deficient in vasopressin respond to hypovolaemia by retaining fluid. The renal actions of aldosterone do not explain fully the changes in renal electrolyte handling.
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PMID:Fluid and electrolyte handling in Long Evans and Brattleboro rats following injection of polyethylene glycol. 362 39

Fluid deficits should be divided into two categories (dehydration and volume depletion) according to pathophysiology and into 3 categories (hyponatremic, hypernatremic, and isotonic) according to the plasma sodium concentration. Dehydration (total water deficit especially intracellular) is always hypernatremic, while volume depletion (intravascular water and sodium deficit) is either hyponatremic, hypernatremic, or isotonic. There are no clear clinical differences among the various categories, but a delay of capillary refill, tachycardia, and orthostatic hypotension are more common with early volume depletion. An Evans blue and mannitol test can be used to distinguish between hypernatremic volume depletion and dehydration. Careful clinical assessment and laboratory tests (especially serum sodium) are the key to diagnosis and effective management. According to the type (hypernatremic, hyponatremic, or isotonic), severity of fluid deficit, and associated symptoms, oral or parenteral fluid should be given along with treatment of the underlying cause. In hemodynamically compromised individuals with orthostatic hypotension and oliguria, replacement with isotonic saline until hemodynamic stabilization is crucial. Terminal hydration is still controversial. Important ethical principles govern clinical decision-making about hydration at the end of life.
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PMID:Evaluation and treatment of cancer-related fluid deficits: volume depletion and dehydration. 1158 67