Barbiturates and aortic and venous smooth muscle function

Abstract

Using isolated rat aortic strips (AS) and portal veins (PV), it was found that all of the barbiturates studied (thiopental, secobarbital, pentobarbital, amobarbital, phenobarbital, and barbital): (a) inhibit development of spontaneous mechanical activity (vasomotion) in AS and PV in concentrations used to induce surgical anesthesia or concentrations used for anticonvulsive therapy; (b) dose dependently attenuate contractions induced by epinephrine and potassium (K+); (c) cause noncompetitive displacement of the dose response curves of these vasoactive compounds; (d) attenuate calcium (Ca++) induced contractions of K+ depolarized AS and PV; (e) rapidly relax drug induced, as well as Ca++ induced, contractions of AS and PV. In addition, the data indicate that: (a) rat portal venous smooth muscle is more sensitive to the inhibitory actions of barbiturates than is rat aortic smooth muscle, and (b) thiopental, but none of the other barbiturates, can elicit dose dependent contractions of AS. Concentrations of barbiturates known to be present during induction of surgical anesthesia can exert depressant effects on at least 2 types of vascular smooth muscle that may be related to actions on movement and/or translocation of Ca++.