Human lung tissue and anaphylaxis: the effects of histamine on the immunologic release of mediators.

The IgE-mediated, antigen-induced release of histamine from human lung tissue causes profound changes in lung cyclic adenosine monophosphate and cyclic guanosine monophosphate. Exogenous histamine similarly induces increases in both cyclic nucleotides; pretreatment with H-1 antihistamines prevents the increase in cyclic guanosine monophosphate, whereas H-2 antihistamines prevent the increase in cyclic adenosine monophosphate. Anaphylaxis of human lung in vitro is unaffected by the presence of 1-100 micron histamine, H-1 antihistamines, H-2 antihistamines, or combinations of these agents despite the production of selective increases in total lung cyclic nucleotides. Futhermore, selective histamine agonists (2-methylhistamine [H-1 agonist] or dimaprit [H-2 agonist]) also fail to significantly influence the immunologic release of mediators. Histamine examined in the presence of ethylenediaminetetra-acetate was no more capable of modulating mediator release than when in the presence of calcium, in contrast to previous studies involving the human basophilic leukocyte. Therefore, the human lung mast cell is unresponsive to histamine with regard to modulating the antigen-induced, IgE-dependent, generation of mediators.