Effect of Arterenol (Norepinephrine) and Epinephrine on Cerebral Hemodynamics and Metabolism

There is considerable uncertainty regarding the role of sympathetic amines in the central nervous system; although some have postulated that they may be concerned with neural transmission, supporting evidence is not entirely conclusive. Nevertheless, Vogt¹ has noted the presence of relatively high concentrations of sympathin in the hypothalamus and in the area postrema, with less in the midbrain and in the aqueduct, and has further demonstrated that their local concentrations may be reduced by drugs which stimulate these centers. It has long been recognized that the administration of epinephrine stimulates the waking state and increases spontaneous motor activity. It has been suggested that these effects of circulating epinephrine may in part be due to direct stimulation of ascending and descending reticular systems (Bonvallet, Dell, and Hiebel²; Dell, Bonvallet, and Hugelin³). Sensenbach et al.⁴ were unable to demonstrate significant alteration of cerebral oxygen consumption by the administration