Metabolic and Acid-Base Changes Following Acute Cholinesterase Inhibition

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Abstract
Dogs acutely intoxicated with the cholinesterase inhibitors, Parathion or Sarin, develop both respiratory and metabolic acidosis. The former results from respiratory failure and the latter probably from tissue oxygen deprivation secondary to circulatory failure aggravated by an accelerated oxygen demand due to cholinergic stimulation. Accumulation of lactic acid accounts for about half of the metabolic acidosis. Plasma inorganic phosphorus, potassium and glucose become elevated but only the phosphorus rise persists during concomitant artificial respiration. Hypoxia resulting from circulatory insufficiency appears to be a major factor in the shift of phosphorus and potassium from the cells. Excessive release of adrenaline is probably primarily responsible for hyperglycemia.

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