Histamine's effect on pulmonary vascular resistance and compliance at elevated tone.

Histamine's effect on the longitudinal resistance and compliance distribution in the canine pulmonary circulation was determined under control and elevated vascular tone using the thromboxane analogue U46619. The arterial-, venous-, and double-occlusion techniques were used in isolated blood-perfused dog lungs at both constant flow and constant pressure. Large and small blood vessel resistances and compliances were studied in lungs given the following treatments: 1) histamine; 2) histamine in lungs pretreated with the H1-receptor antagonist diphenhydramine, and 3) histamine in lungs pretreated with the H2-receptor antagonist cimetidine. The results of this study indicate that histamine constricts small and large veins through H1-receptor mediation at both normal and elevated vascular tone. When vascular tone was elevated, H2-receptor vasodilatation was also apparent in all blood vessel segments. Histamine decreased total, middle compartment, and large vessel vascular compliances by an H1-receptor effect. When vascular tone was elevated, histamine's H1-receptor-mediated vasoconstrictor effect on compliance vessels was less due to the presence of an H2-receptor-mediated vasodilatory system.