Response to anti-human IgE in human pulmonary arteries. Regulation by endothelium.

Initial reports concerning anaphylactic reactions in the lung have demonstrated that histamine is released, and this mediator may be responsible for the severe hypotension observed in vivo in sensitized animals. However, those mechanisms involved in the antigen-vascular interactions have not been elucidated. Human isolated pulmonary arterial preparations relaxed when challenged with anti-human IgE (a-IgE). This response was associated with a release of histamine and PGI2. Both the relaxation and the release of PGI2 were attenuated by removal of the endothelium or by prior treatment of the tissues with chlorpheniramine. Indomethacin also significantly reduced the relaxations produced by a-IgE. In addition, L-NOARG in the presence of indomethacin blocked the a-IgE-dependent relaxation. Stimulation of these tissues with histamine also induced relaxations which were endothelium dependent and blocked by chlorpheniramine and L-NOARG in the presence of indomethacin. These results suggest that the relaxations via products of the cyclooxygenase and NO pathways were mediated by histamine release which stimulated the endothelium.