Nitrogen excretion Subject

The nitrogen excretion In the feces, urine, and the balance throughout the experimental study period In the second pair of subjects (Patients 3 and 4) showed no remarkable changes. The balance data were apparent balances. Inasmuch as the nitrogen excretion In the sweat was not considered In calculating these balances. 

Numerous studies have been carried out in animals in which total adrenalectomy has been performed and subsequent injury has not been accompanied by replacement therapy. The 2 acute phase globulins rise after repeated injurious stimuli in rats adrenalectomized animals retain the globulin response and serum mucoid response to tissue damage although it is reduced. Replacement therapy with cortisol in adrenalectomized animals restores the response to normal (W3). Adrenalectomy suppresses the breakdown of liver polypeptides and urinary nitrogen excretion in rats subjected to whole-body irradiation (Nl). 

Fig. 38.16. Nitrogen excretion during fasting. Human subjects were initially given intravenous (IV) glucose as indicated, then fasted. Total nitrogen excretion was measured as well as the nitrogen in urea (dark area). Based on Ruderman NB, et al. Gluconeogenesis and its disorders in man. In Hanson RW, Mehknan MA, eds. Gluconeogenesis Its Regulation in Mammalian Species. New York John Wiley, 1976 518.

In human subjects, the metabolic effects did not differ appreciably from those of prednisolone. Its activities with respect to nitrogen excretion, ACTH suppression, and reduction of circulating eosinophils were similar to those of prednisolone. The sodium retention and potassium loss were slightly less than with prednisolone (49). 

NONGOUTY SUBJECTS, NONE EXCEEDED kO YEARS OF AGE. ALL HAD RELATIVELY LOWER URINE PH. THE CREATININE AND TOTAL NITROGEN EXCRETIONS WERE also quite COMPARABLE FOR BOTH GROUPS. In 19 NONGOUTY SUBJECTS, THE MEAN PLASMA URATE WAS 5 5 0.8 MGJ, AND THE MEAN URINE PH WAS 5 + 0.2, TITRATABLE ACID WAS 24.8 + 6.1 A E q/ MIN, NHh WAS 35 0 + 7 3 N, URINARY URIC ACID WAS 0 5 MG +... 

None of the exposures produced changes in clinical chemistry values (blood count, blood nitrate, blood urea nitrogen, serum enzymes, and serum electrolytes or urinalysis and nitrate and nitrite urinary excretion), spontaneous electrical activity of the cortex of the brain (detected by EEG), pulse rate and sinus rhythm, or pulmonary function. Visual and auditory acuity, exercise EKG, and time estimation tests did not differ from control values for any of the exposures. Only one of several cognitive tests was affected by exposure and the change occurred only in the four subjects exposed at 1.5 ppm. The test was taken during the time the subjects were experiencing severe headaches. 

When absorbed into the systemic circulation, ammonia is primarily excreted by the kidney as urea and urinary ammonium compounds (Gay et al. 1969 Pitts 1971). Absorbed ammonia also can be excreted as urea in feces (Richards et al. 1975) and as a perspiration constituent (Guyton 1981 Wands 1981). In a study of male subjects exposed to ammonia at concentrations up to 500 ppm for 30 min, Silverman et al. (1949) found that 70-80% of inhaled ammonia was excreted in expired air. Ammonia in expired air returned to normal concentrations within 3 to 8 min after exposure was stopped. The investigators calculated that if all the retained ammonia were absorbed into the blood, there would be no significant change in blood or urine urea, ammonia, or nonprotein nitrogen. 

The fact that relatively large amounts of urea can be produced by subjects in whom an enzyme defect of the urea cycle has been proved has perplexed many investigators. Despite the fact that the activity of the rate-limiting enzyme has been reduced even to zero as measured by a sophisticated method, urea production still continues. It must therefore be concluded that, in all these cases, urea production is only impaired, not abolished. In all normal circumstances, all but a small fraction of the nitrogen in excess of tissue protein requirements is still excreted as urea and/or as the amino acid whose further metabolism is blocked. The impairment shows itself in the elevated levels of blood ammonia and consequently of glutamine, which vary according to the stress placed upon the urea cycle by varying the rates of protein intake. 

M26. Mitchell, H. H., and Hamilton, T. S., Dermal excretion under controlled environmental conditions of nitrogen and minerals in human subjects with particular reference to calcium and iron. J. Biol. Chem. 178, 345-361 (1949). 

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