Abstract

Previous findings revealed greater contractile responses of guinea pig lung pleural surface strips to antigen or A23187 challenge than denuded lung parenchymal strips (lung strip devoid of any pleura). Moreover, we have identified a high density of mast cells distributed throughout the lung pleura. The present study examined mediators released from guinea pig lung pleural surface and denuded lung parenchyma fragments in response to immunologie challenge with ovalbumin (OA) or non-immunologic challenge with the ionophore A23187. Histamine levels were measured radioenzymatically; leukotrienes (LTs), prostaglandins (PGs) and thromboxane B 2 (TXB 2), a stable metabolite of thromboxane A 2 (TXA 2), were quantitated using an enzyme immunoassay. Histamine release reached a maximal level 3–5 min after OA challenge, whereas A23187-induced histamine release increased gradually in a timedependent manner. Similar kinetics were observed in the release of LTs, PGs and TXA 2. Pleural surface released a substantially (P < 0.05) greater amount of histamine to both challenges than denuded parenchyma. Moreover, histamine content in pleural surface was significantly (P < 0.05) higher than in denuded parenchyma. Pleural surface also released considerably (P < 0.05) more LTB 4, LTC 4, and LTE 4 in response to OA and A23187 than denuded parenchyma. In contrast, pleural surface and denuded parenchyma released equivalent amounts of PGD 2, PGE 2, PGF 2α, and TXA 2 in response to both challenges. The rank order of leukotriene release was LTC 4 > LTE 4 > LTB 4, whereas that of prostanoid release was TXA 2 « PGD 2 ≥ PGF 2α « PGE 2 . We conclude that pleural surface is the major source of histamine and leukotrienes released from guinea pig lung in vitro in response to OA and A23187, whereas both pleural surface and denuded parenchyma participate to the same extent in prostaglandin and TXA 2 production after such challenges.

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