To the Editor:—
I enjoyed reading the review by Gelman and Mushlin1of catecholamine actions on the splanchnic vasculature. Nevertheless, I am confused by an unreferenced statement they made regarding the actions of α-agonists on venous return. They state, “Generally, α- agonists increase venous return under normovolemic conditions, but they decrease it when used at high doses or in the presence of severe hypovolemia.”
The animal data do not support the statement by Gelman and Mushlin. Yamazaki et al. 2studied dogs that had received spinal anesthesia and ganglionic blockers (surely analogous to hypovolemia) and found that methoxamine and clonidine increased venous return. Similarly, Supple et al. 3found that α2-agonists increased the venous return of dogs on constant-flow cardiopulmonary bypass. However, Imai et al. 4showed that α-agonists decrease venous return and β-agonists increase venous return. Similarly, we found that phenylephrine administered to dogs after spinal anesthesia decreased venous return, whereas isoproterenol and ephedrine increased venous return.5Of note, in our study, the animals underwent splenectomy. The canine splenic capsule contracts with α-agonists, and the canine spleen contains a much larger fraction of total blood volume than the human spleen does.
The human data do not support the statement by Gelman and Mushlin. Bell et al. 6found that volunteers receiving a 20-min infusion of phenylephrine (20–120 μg/min—certainly not a “high” dose) showed an increase in splanchnic intravascular volume and a decrease in venous return. Leenen et al. 7infused epinephrine in healthy subjects with and without β-blockers. Using measured changes in left ventricular end-diastolic dimensions, these authors concluded that selective α-stimulation decreased venous return. Brooker et al. 8compared phenylephrine and epinephrine in patients with mild hypotension after spinal anesthesia. There was an increase in stroke volume and cardiac output with epinephrine, with no change or a decrease in cardiac output in those receiving phenylephrine. However, in a group of patients receiving a morphine-based anesthetic during constant-flow cardiopulmonary bypass, Müller-Ruchholtz et al. 9observed α-agonist–induced increase in venous reservoir volume.
In sum, animal and human studies do not provide convincing evidence that α-agonists generally increase venous return under any condition. Finally, the inappropriate use of α-agonists to increase venous return could have disastrous complications during resuscitation.
Wake Forest University School of Medicine, Winston-Salem, North Carolina. email@example.com