Pharmacologic properties of antihistamines in relation to vascular reactivity

Abstract

Experiments were designed to gain further insight into the vasoconstrictor action of antihistamines and to assess further the validity of using antihistamine constrictor action to implicate the presence of "intrinsic" histamine in the terminal vascular bed of normal animals. Experiments with adrenergic blockers eliminate endogenous epinephrine as the sole mechanism responsible for the observed vasoconstriction with antihistamines. Furthermore, experiments with antiserotonin compounds indicate that the constriction cannot be attributed to endogenous 5-HT. In addition, experiments with a cholinergic blocking agent as well as with a local anesthetic eliminate cholinergic or local anesthetic mechanisms as being responsible for the observed antihistamine constriction. The local action of antihistamines likewise clearly rules out a central nervous system pathway which might operate in animals given antihistamines systemically. Experiments with bilateral adrenalectomized animals reveal heightened antihistamine constrictor action which is greatly exacerbated when these animals are given Dibenzyline. These findings are discussed in relation to recent work with antihistamines on ion transport. The present study questions the use of antihistamine constrictor action, to validate the presence and contribution of intrinsic histamine in microcirculatory regulation of normal animals.