Abstract
While investigating the peripheral action of barbiturates it was observed that in all experimental animals where the cardiac vagus response to weak faradic stimulation had been abolished by large doses of most barbiturates, and by moderate doses of amytal and pernoston, the administration of physostigmine salicylate in doses from 0.2 to 0.35 mg. per kilo by vein, caused usually no detectable spontaneous effect upon the heart rate or blood pressure. The injection of comparable doses of acetylcholine and pilocarpine produced in the same animals a marked fall in blood pressure which in many cases was accompanied by a slowing of the heart. 1 If 2 or 3 minutes were allowed to elapse after the intravenous administration of physostigmine and then the peripheral vagus was stimulated electrically, profound cardiac slowing and fall in blood pressure was produced in 6 dogs, 4 cats and 6 rabbits. In 7 experiments these vagus effects outlasted for several minutes the actual stimulation of the nerve. This physostigmine sensitization of the vagus to stimulation of the preganglionic fibers lasted for about a half hour and was antagonized in ten animals by further doses of barbiturates. Since barbiturates abolished the cardiac vagus response to faradic stimulation but not to pilocarpine, it was postulated that their vagus-impairing effects are due to ganglionic depression (see also Kobacker and Rigler, 2 and Garry. 3 ) We have, therefore, employed nicotine and curare, drugs known to produce ganglionic paralysis. After sufficient doses of nicotine (2 to 10 mg. per kilo) or curare (3 to 6 mg. per kilo) had been given intravenously to abolish the peripheral vagus effects in 2 dogs, 3 rabbits and 3 cats, 0.2 to 0.3 mg. of physostigmine salicylate per kilo was injected intravenously.
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