Abstract
Current hypotheses of the pathogenesis of ammonia intoxication postulate an intracerebral adenosine triphosphate (ATP) depletion as a result of: 1) decreased ATP synthesis due to inhibitory effect of ammonia on cerebral oxidative metabolism; and 2) increased ATP utilization during ammonia detoxication. In this investigation net cerebral cortical ATP concentration of ammonium acetate-injected precomatose and comatose, as well as control rats, was determined using the luciferin-luciferase-luminescence assay. The normal mean cerebral cortical ATP level was 2.43 ± .50 µm/g of brain. No alteration from normal of cerebral cortical ATP was found in rats with ammonium acetate-induced precomatose and comatose states. These findings, which do not exclude ATP deficiency in some circumscribed vital cerebral site(s), indicate absence of generalized cerebral ATP depletion in experimental ammonia intoxication.
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