Some Effects of Dehydroascorbic Acid on the Central Nervous System

Abstract

The intraven. injn. of dehydroascorbic acid (DHA) in rats produces salivation and lacrimation. Lacrimation is prevented by atropine. Salivation is prevented by atropine and by the destruction of the chorda tympani nerve. The intraven. injn. of DHA produces a rise in blood pressure similar to that following epinephrine. The response is prevented by Dibenamine, atropine, sympathectomy with right splanchnicotomy and by low cervical cordotomy. It is not influenced by adrenalectomy. When repeated injns. of a given dose of DHA are given to a rat, the blood pressure response increases progressively to a max. and then falls off. A max. blood pressure rise of 40 mm. of Hg is obtained with a single dose of 40 mg./kg. With repeated injns., a max. response of 70 mm. is obtained with a dose of 60 mg./kg. The toxicity of DHA is markedly decreased by artificial respiration. Dibenamine and atropine increase the toxicity. The ascorbic acid level of the brain is more than doubled by the intraven. injn. of 200 mg./kg. of DHA. A similar dose of ascorbic acid has no effect. With repeated doses of DHA the brain ascorbic acid level continues to rise, but the rate of increase becomes less as ascorbic acid accumulates in the brain. It is postulated that the central nervous system stimulation which follows the intraven. injn. of DHA is the result of the production of acid by the reduction of neutral DHA to ascorbic acid.