Since the general biologic action of epinephrine became known, numerous investigations have been carried out in order to determine its influence on the cerebral blood vessels. This interest is probably due to the conception, first advanced by Brodie,1 that in any given vascular area a definite response to epinephrine is an expression of sympathetic vasomotor innervation. Conversely, the lack of constrictor response to epinephrine provides evidence that the sympathetic system has no influence on the arteries of the organ in question. Recent investigation of the mode of transmission of sympathetic nerve impulses to organs supports this point of view.
The effect of epinephrine on the cerebral blood vessels has been studied chiefly by four experimental methods: (1) intravascular injection into a living animal; (2) injection into the circulation of an isolated surviving head; (3) immersion of excised arteries in solutions of epinephrine, and (4) irrigation of the surface of