The Role of Ammonia in the Metabolic Effects of Hydrazine.
AEROSPACE MEDICAL RESEARCH LAB WRIGHT-PATTERSON AFB OHIO
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The acute effects of administration of hydrazine on plasma ammonia, blood urea nitrogen, pH, pCO2, and respiratory rate were studied in dogs. In various experiments, various doses of hydrazine were given. The dogs given high doses developed hyperammonemia, respiratory alkalosis, coma and convulsions. Relatively little change in blood urea nitrogen was found. Since brain function is adversely affected by hyperammonemia and alkalosis, it is concluded that ammonia plays an important role in the toxicity of hydrazine. Observations would suggest that hydrazine could competitively inhibit the formation of urea by competitively combining with carbamyl phosphate and or glutamic acid and in turn releasing a stoichometric amount of ammonia. Hydrazine and ammonia could compete with the citric acid cycle for alpha ketoglutaric acid via the conversion to glutamic acid. This could disrupt oxidative metabolism, manifested by coma and convulsions. Author