HUMAN LUNG-TISSUE AND ANAPHYLAXIS - EFFECTS OF HISTAMINE ON IMMUNOLOGICAL RELEASE OF MEDIATORS

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Abstract
The Ig[immunoglobulin]E-mediated, antigen[Ag]-induced release of histamine from human lung tissue causes profound changes in lung cyclic[c]AMP and cGMP. Exogenous histamine similarly induces increases in both cyclic nucleotides; pretreatment with H-1 anti-histamines prevents the increase in cGMP, whereas H-2 anti-histamines prevent the increase in cAMP. Anaphylaxis of human lung in vitro is unaffected by the presence of 1-100 .mu.M histamine, H-1 anti-histamines, H-2 anti-histamines, or combinations of these agents despite the production of selective increases in total lung cyclic nucleotides. Selective histamine agonists (2-methylhistamine [H-1 agonist] or dimaprit [H-2 agonist]) fail to significantly influence the immunologic release of mediators. Histamine examined in the presence of EDTA 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. The human lung mast cell is unresponsive to histamine with regard to modulating the Ag-induced, IgE-dependent, generation of mediators.