Effects of prolonged hemorrhagic hypotensive stress on catecholamine concentration of mesenteric blood vessels.

Norepinephrine (NE) and epinephrine (E) concentrations were determined fluorometrically as an index of functional adrenergic innervation in small mesenteric arteries, veins, and superior mesenteric arteries of dogs and rats subjected to a period of prolonged hemorrhage at a constant mean arterial pressure of 35 mm Hg. In nonhemorrhaged animals, highest catecholamine concentrations were found in the small principal arteries, next highest in the small veins, and least in superior mesenteric arteries. A significant decrease occurred in the NE and E concentrations of all three vessel types in the dog during the decompensatory phase of the hypotensive stress (defined as the hypotensive period beyond the time at which maximum bleedout volume occurred). In the rat significant decreases were detectable only in the NE concentrations of the small arteries and veins during this phase. It is concluded that the increase in neurogenic vascular tone accompanying severe hemorrhagic stress is lost simultaneously on the arterial and venous sides of compensatory vascular beds. Such loss is closely related to transmitter depletion at the adrenergic neuromuscular junction and, if allowed to continue uncorrected, can contribute significantly to irreversible cardiovascular collapse.