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Urea and amphibian water economy.

Accumulation of urea in the body fluids enables some amphibians to tolerate high ambient salinities (Bufo viridis, Xenopus laevis, Rana cancrivora, Ambystoma tigrinum, Batrachoseps spp.) or to estivate in soil with low water potentials (Scaphiopus spp.). These species are assumed not only to accumulate urea produced in the normal metabolism, but to synthesize urea in response to water shortage. Re-examination of the data did not support the view of an osmoregulatory urea synthesis. Increased urea synthesis on exposure to high salinities in X. laevis, R. cancrivora and Batrachoseps spp. seemed to reflect reactions to an adverse environment. It is suggested that in amphibians, solute concentration in the plasma and rate of excretion of urea are coordinated so that at a certain plasma concentration, urea is excreted at the same rate at which it is produced. The higher the level of urea in the body fluids at balance between production and excretion, the higher the tolerance of the species of low external water potentials. The mechanisms that integrate the relationship between plasma solute concentration and handling of urea by the kidneys are not known.

Adaptation, Physiological↗

Coffee consumption and total body water homeostasis as measured by fluid balance and bioelectrical impedance analysis.

To investigate the impact of coffee consumption on fluid balance, 12 healthy volunteers were supplied with a standardized diet for 2 days after having abstained from consumption of methylxanthines for 5 days. During the first day, fluid requirement was met by mineral water. On the following day the same amount of fluid was supplied and the mineral water was in part replaced by 6 cups of coffee containing 642 mg of caffeine. This led to an increase in 24-hour urine excretion of 753 +/- 532 ml (p < 0.001), a corresponding negative fluid balance and a concomitant decrease in body weight of 0.7 +/- 0.4 kg (p < 0.001). Total body water as measured with bioelectrical impedance analysis decreased by 1.1 +/- 1.2 kg or 2.7% (p < 0.01). Urinary excretion of sodium and potassium was elevated by 80 +/- 62 mmol or 66% (p < 0.01) and 14 +/- 12 mmol or 28% (p < 0.01), respectively.

Adult↗

Electrolyte balance in gastrointestinal disease.

Even small losses of gastrointestinal secretions when combined with reduced intake of electrolytes may seriously disturb electrolyte balance. Knowledge of the ionic composition of secretions lost is essential in planning therapy. Loss of gastric contents usually results in excessive loss of chloride; in achlorhydria this is not the case. Loss of sodium and potassium may be large in either case and is often underestimated. Small bowel obstruction results in a more balanced loss of electrolyte which may not affect acidbase balance greatly. In diarrhea loss of base predominates, and may result in a large potassium deficit. Steatorrhea due to nontropical sprue results in large fecal losses of sodium, potassium and chloride, in addition to the large calcium and phosphorus loss. In chronic peptic ulcer excessive ingestion of milk and absorbable alkalies may result in hypercalcemia, azotemia and alkalosis, without hypercalciuria. Since renal function is usually adequate in the milder gastrointestinal disturbances, electrolyte and fluid replacement should be started early, and can be guided by generally available laboratory tests, the carbon dioxide combining power and serum chloride levels, provided the predominate ionic loss is known and potassium deficiency remedied. If this is done, development of serious fluid and electrolyte deficits can usually be prevented.

Alkalosis↗