Failure of Antihistaminic Drugs to Reduce Reactive Hyperemia in Man.

Abstract

Measurements of volume change and blood flow in the foot-leg were made in 6 subjects by means of a venous occlusion plethysmograph. Reactive hyperemia was produced by the application and release of an inflatable occluding cuff placed about the thigh. Occlusions were maintained to produce manifest hyperemia (5-10 min.) and threshold or minimal responses as well (0.5 to 3 min.). The initial inflow after release of occlusion was considered to reflect the dilatation produced. After a period of 134 control measurements of resting flow and 39 measurements of reactive hyperemia, "benadryl" (beta-dimethylaminoethylbenzhydryl ether HC1) 10-30 mgs. intraven., or "pyribenzamine" (beta-dimethylaminoethyl-2-pyri-dylbenzylammonium chloride), 50 mg. orally, was administered. Observations were repeated at intervals for a period of more than 1 hr., 99 measurements of resting flow and 36 measurements of reactive hyperemia being made after drug. No diminution was detected in the circulatory response to arterial occlusion. There was no essential difference between subjects, or after varying durations of occlusions. In several instances the intradermal injn. of 0.1 to 0.01 microg. of histamine base demonstrated the effectiveness of the antihistaminic drug. The observation that reactive hyperemia could not be reduced by these antihistaminic drugs, seriously challenges the validity of the concept that hyperemia is primarily due to the accumulation of a histamine-like substance.