On the Mechanism of Spastic Vascular Disease. ∗

Abstract

Two opposing views exist as to the mechanism of spastic disease of blood vessels. Some regard it as an expression of dysfunction of the vaso-motor nerve supply to the vessels. Chief support for this conception is found in the symmetrical nature of the lesion and the paroxysms which characterize it. Others, especially Lewis and his coworkers, regard it as a local fault not primarily associated with abnormal innervation. This local defect as studied in Raynaud's disease of extremities expresses itself in an abnormal response to cold, in the spatial order of development and disappearance of the vascular constriction, and in the failure of local anesthetization of the nerve supply to prevent or release completely an attack. Our own observations on these aspects of the disease lead us to support the contention of Lewis and others.

Evidence is herein presented that the fault is a local one, and represents not a hyper function of a sympathetic innervation, but a change in the blood vessels, namely that they respond to epinephrine in a manner similar to tissues deprived of their sympathetic nerve supply (paradoxical response) while the nerve supply can be demonstrated to be functional.

The evidence is derived from the study of 3 patients with vascular abnormalities of the upper extremities, 2 cases of Raynaud's disease and one case of acro-asphyxia. The first 2 were subjected to the following tests: (1) 1 cc. or less (graded doses) of epinephrine hydrochloride (1-1000) was given hypodermically and the effect on the diseased and control extremities noted. An attack was invariably induced in the diseased extremities. Then the effect of intravenous glucose or of a meal rich in carbohydrate was noted. (2) Ten to IS units of insulin were administered to produce a physiological secretion of epinephrine. The effect on the diseased and control extremities was noted and again the effect of carbohydrate on the attack determined.