The Contribution of Various Organs to Ammonia Formation. Factors Determining the Arterial Concentration

Recently in your Journal Huizenga et al. described the arterio-venous difference of ammonia in various organs of the body including skeletal muscle where a positive arterio-venous difference is always present. I In 1994 we reported that in uraemic patients under regular haemodialysis (HD) the high serum concentration of ammonia in arterialized blood (fistula) decreases after HD.2 The review article by Huizenga et al. and our previous report prompted us to evaluate the difference ?f ammonia levels in arterial and venous blood in the muscle of uraemic patients treated by haemodialysis (HD) and in normal subjects. Arterial (fistula, P02 > 88 mmHg) and venous (forearm without fistula) blood sample~ were collected in the morning before the session of HD in 20 uraemic patients free of liver disease who were treated by HD three times a week. In 16 healthy controls, arterial and venous blood samples were collected in the morning from. the forearm. Whole blood ammonia was determined by a colorometric method (Wako Chemicals GmbH). Health control values ranged from 300 to 860 iJ.g/L. Mean (SD) ammonia concentration in uraemic patients under HD was 990 (31) arterial and 690 (22) venous while in control subjects the values were 76·9 (18'9) and 79·9 (\8-4) iJ.g/L, respectively. Pre HD uraemic patients have higher ammonia levels in the arterial blood, than in venous blood whilst no difference was observed in the control group (Fig. I). The digestive tract is the main site for production of ammonia from hydrolysed urea and an increase in blood urea is accompanied by increased production of ammonia in the gastrointestinal tract which gives rise to high concentrations in the portal circulation. The principal mechanism of ammonia detoxification in normal individuals is the formation of urea in the liver:

[1]  B. Keevil,et al.  Measurement of Sweat Sodium Using a Modified Enzymatic Assay , 1996, Annals of clinical biochemistry.

[2]  E. Worthy,et al.  Is the Sweat Test Safe? Some Instances of Burns Received during Pilocarpine Iontophoresis , 1996, Annals of clinical biochemistry.

[3]  T. James,et al.  Enzymatic determination of sodium and chloride in sweat. , 1996, Clinical biochemistry.

[4]  C. Gips,et al.  The Contribution of Various Organs to Ammonia Formation: A Review of Factors Determining the Arterial Ammonia Concentration , 1996, Annals of clinical biochemistry.

[5]  B. Agroyannis,et al.  Evaluation of Blood Ammonia Alterations in Uremic Patients under Hemodialysis and Capd , 1994, The International journal of artificial organs.

[6]  V. Felipo,et al.  Control of urea synthesis and ammonia utilization in protein deprivation and refeeding. , 1991, Archives of biochemistry and biophysics.

[7]  T. Nakamura,et al.  Decreased carnitine and increased ammonia—Which comes first? , 1990 .

[8]  V. Felipo,et al.  Paradoxical protection of both protein-free and high protein diets against acute ammonium intoxication. , 1988, Biochemical and biophysical research communications.

[9]  A. Green.  When and How Should We Measure Plasma Ammonia? , 1988, Annals of clinical biochemistry.

[10]  T. Ono,et al.  A new enzymatic assay of chloride in serum. , 1988, Clinical chemistry.

[11]  D. Häussinger,et al.  Hepatic urea synthesis and pH regulation , 1985 .

[12]  G. Deferrari,et al.  Leg metabolism of amino acids and ammonia in patients with chronic renal failure. , 1985, Clinical science.

[13]  A Green,et al.  A Study of Sweat Sodium and Chloride; Criteria for the Diagnosis of Cystic Fibrosis , 1985, Annals of clinical biochemistry.

[14]  J. Schlienger,et al.  The effect of chronic uremia on portal and systemic ammonemia in normal and portal-strictured rats. , 1979, The Journal of laboratory and clinical medicine.

[15]  N. Ruderman,et al.  Muscle nitrogen metabolism in chronic hepatic insufficiency. , 1976, Metabolism: clinical and experimental.