THE ACTION OF PHYSOSTIGMINE WITH SPECIAL REFERENCE TO THE CIRCULATORY SYSTEM AND THE INTESTINE

¹ From the Department of Pharmacology, Egyptian University, Cairo, Egypt

In the literature, the effects of physostigmine on involuntary muscle, including the heart, are, broadly speaking, ascribed to two different actions: (a) a stimulation of parasympathetic nerve ends and (b) a direct stimulation of the muscle.

Considering first the effect on the heart of small doses, the experiments described above show: (a) no action on the heart of the rabbit, (b) slowing and weakening of the heart of the frog and toad, not affected by atropine, (c) no evidence of stimulation of the muscle with any dose in these animals, and (d) marked slowing of the heart of the dog, attributed to stimulation of the vagus nerve ends, as it is abolished by atropine.

With larger doses, the effects are more pronounced. In the rabbit heart, there is slowing and weakening, not due to vagus stimulation as it is not removed by atropine. Similarly, in the frog and toad, there is more marked slowing and weakening, even diastolic arrest; this is not affected by atropine. In these 3 cases the cause of the depression must be direct action on the cardiac muscle. In the intact dog, more marked slowing of the beat occurs.

The only animal, in which slowing of the heart due to action on the vagus has been found, is, therefore, the dog. There is some slight evidence that this may occur in man (12), but the author has not attempted to obtain any confirmation of this.

In the toad, rabbit and dog, there is evidence of paralysis of the ganglion cells on the course of the cardiac vagus, after large doses.

Physostigmine causes a large rise of tone in isolated rabbit intestine, which is abolished by atropine and so attributed to stimulation of the parasympathetic nerve ends. With larger amounts, the ganglion cells of the parasympathetic are paralyzed and with excessive doses the muscle is itself depressed. In the case of the dog, evidence was obtained of a direct stimulant action on the unstriated muscle of the blood vessels.