Histamine and microcirculation

Recent research of histamine metabolism suggests that microvascular smooth muscle and endothelial cells are under the continuous dilator influence of minute quantities of intrinsically formed histamine, produced by action of an inducible form of histidine decarboxylase. Various autonomous dilator activities of the microcirculation, e.g., vasomotion, reactive and post- exercise hyperemia and autoregulation, may all involve interplay of this intrinsic dilator with an intrinsic constictor mechanism. Drastic stimuli which cause a marked increase in histamine output locally or systemically, may lead to the early, slowly-developing microvascular changes in inflammation and shock, respectively.     

IN VIVO FORMATION AND CATABOLISM OF [14C]HISTAMINE IN MOUSE BRAIN

Abstract— The formation of histamine in brain was studied in mice injected with l -[¹⁴C]-histidine (ring 2-¹⁴C) intravenously (i.v.) or intracerebrally; [¹⁴C]histamine appeared rapidly and exhibited a rapid rate of turnover. Drugs known to block various pathways of histamine catabolism were tested for effects on brain–[¹⁴C]histamine and [¹⁴C]-methyl-histamine in mice given (1) [¹⁴C]histamine i.v., (2) [¹⁴C]histamine intracerebrally, and (3) l -[¹⁴C]histidine i.v. Blood-borne histamine did not enter brain; brain histamine was formed locally by decarboxylation of histidine Methylhistamine did cross the blood-brain barrier. Methylation was the major route of histamine catabolism in mouse brain and some of the methylhistamine formed was destroyed by monoamine oxidase. No evidence for catabolism by the action of diamine oxidase was found.