FURTHER STUDIES ON THE PRODUCTION OF CYCLOPROPANE–EPINEPHRINE TACHYCARDIA

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Abstract
0.005 to 0.01 mg./kg. epinephrine was injected intraven. in dogs under cyclopropane anesthesia. By various surgical interventions, carried out under nembutal anesthesia, different parts of the body of the dogs could be exposed to cyclopropane or epinephrine alone, or to both agents. In 6 dogs, the brachio-cephalic and left subclavian arteries and the superior vena cava were clamped. The occlusion of cerebral circulation was limited to 5 mins., so that the reflex meditation by the hypothalamus was not disturbed. With this arrangement, both cyclopropane and epinephrine were excluded from the head circulation. All 6 animals developed ventricular tachycardia, and 3 of 6 developed ventricular fibrillation. In 3 expts., cross circulation was established between dogs; the donors received 100 mg./kg. pontamine fast pink BL to prevent coagulation. The peripheral end of the brachio-cephalic artery of the recipient was connected to the central end of the left common carotid artery of the donor. The superior vena cava of the recipient was joined to the left external jugular vein of the donor. The isolation of the cerebral circulation was verified experimentally.. Cyclopropane and epinephrine were likewise restricted to the body circulation of 2 recipients, and ventricular tachycardia was produced in both cases. In 3 dogs, cyclopropane was allowed to reach the entire animal while epinephrine was restricted to the body circulation; ventricular tachycardia was produced in all cases. Ventricular tachycardia could not be produced in 6 animals after anemic decerebration, with the cyclopropane and epinephrine restricted to the body circulation. Similarly no ventricular tachycardia could be produced after epinephrine when the cyclopropane was restricted to the cerebral circulation. Cord section between T 6 and T 7 prevented cyclopropane-epinephrine tachycardia in 4 dogs. Bilateral supradiaphragmatic splanchnicotomy and removal of the sympathetic chain from T 9 to L 1 prevented ventricular tachycardias in 13 of 15 dogs. In the remaining two, cord section of T 11 afforded protection. Bilateral adrenalectomy had no effect on ventricular tachycardia. Occlusion of the visceral circulation in 6 nembutalized animals protected from ventricular tachycardia. Partial eviscerations indicated that the receptors of the reflex cyclopropane-epinephrine tachycardia are located in the peripheral 3 cm. of the mesentery. Above expts. indicate that cyclopropane reflexly sensitizes the dog heart to epinephrine. The afferent pathway of this reflex goes from the mesenteric plexuses, splanchnics, and spinal cord to a brain center above the pons. Efferent im- pulses reach the heart by the way of the cardiac sympathetics.

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