Increase In Ammonia Levels Research Articles

Ammonia metabolism in Reye syndrome and the effect of citrulline

Ammonia metabolism in Reye syndrome was studied by quantitative analysis of the time course of hyperammonemia and the urinary excretion of ammonia, urea, and total nitrogen. These measures were then utilized to assess the effect of citrulline administration in 8 patients compared to results in 22 patients managed without citrulline. Two indices of the severity and duration of hyperammonemia correlated strongly with mortality: the half-time for decline of hyperammonemia and the area under the hyperammonemia curve (an index of the total burden of ammonia presented to the brain). These results suggest that the total amount of ammonia delivered to brain may be important to the pathogenesis of encephalopathy. Citrulline-treated patients had more severe disease at admission and greater abnormalities in indices of nitrogen and ammonia metabolism, though the latter did not reach significance. The urine ammonia/urea nitrogen excretion ratio, an index of the efficiency of ammonia conversion to urea, normalized more rapidly in the citrulline-treated group, evidence that citrulline may have improved urea cycle function. Overall mortality did not differ in the two groups. The deaths of 2 citrulline-treated patients in this small group were attributable to factors unrelated to treatment, however, so the possible effect of citrulline on mortality was not definitively tested. No indication was found that citrulline was harmful, nor that it increased ammonia levels.

Letters to the Editor

Dr. Larkin is correct in noting that hyperammonemia is a complication of parenteral aumentation. When the note of caution was prepared by the Committee on Nutrition, little published information was available concerning hyperammonemia as a pediatric problem due to the administration of protein hydrolysates, although the presence of high ammonium concentration in protein hydrolysate preparations had been known for at least 15 years.1,2 Webster and Davidson1 and Finkbiner and coworkers2 demonstrated that normal subjects tolerated infusion of protein hydrolysates, while subjects with hepatic disease showed markedly increased ammonia levels during infusion.

Tolerance and Initial Metabolic Response to Ammonia Intoxication in Selected Bats and Rodents

Metabolic rates, as measured by oxygen consumption, and tolerances of three bats, Tadarida brasiliensis, Myotis lucifugus , and Eptesicus fuscus , and the laboratory rat, Rattus , and mouse, Mus , were determined in increasingly concentrated ammonia in air mixtures. Rats and mice exhibited increased oxygen consumption when exposed to increased ammonia levels. Oxygen consumption in rats ranged from 0.8 to 1.2 cc/g/hr in environmental gradients ranging from normal air to 5000 parts per million ammonia (ppm ammonia), while mice exhibited a rise in oxygen consumption from 3.7 to 4.7 cc/g/hr in concentrations of 0–3000 ppm ammonia. Myotis lucifugus exhibited erratic responses in mixtures of 0–5000 ppm ammonia, and oxygen consumption fluctuated between 4.9 and 10.6 cc/g/hr. Similarly, in E. fuscus consumption fluctuated from 3.3 to 7.2 cc/g/hr in 0–7000 ppm ammonia. In neither species was oxygen consumption correlated to the change in ammonia concentration. Tadarida brasiliensis exhibited decreased oxygen consumption ranging from 8.8 cc/g/hr to 2.3 cc/g/hr in air containing 0–7000 ppm ammonia. Tadarida brasiliensis and E. fuscus lived for 2½ and 1½ hrs, respectively, when exposed to 7000 ppm ammonia, but for only 10–20 min at 10,000 ppm ammonia. Myotis lucifugus and laboratory rats lived for 30–45 min in 5000 ppm ammonia. Laboratory mice lived for 2½ hrs at 3000 ppm and 10–20 min at 5000 ppm ammonia.

Changes in the interoceptive reflexes at an increased ammonia level in the blood

Changes in the interoceptive reflexes at an increased ammonia level in the blood