We studied the generation of arachidonic acid cyclooxygenase metabolites (AACMs) during in vitro anaphylaxis of passively sensitized human lung parenchymal and airway fragments. Prostaglandins E, F2(α), D2, 6-keto-prostaglandin F1(α), and thromboxane B2 (PGE, PGF2(α), PGD2, 6-keto-PGF1(α), TXB2, respectively) were assayed by radioimmunoassay. Results with airway tissue were compared with subpleural parenchymal fragments from the same lungs similarly challenged. Spontaneous generation of prostacyclin (PGI2), as measured by its stable metabolite 6-keto-PGF1(α), exceeded by two- to threefold other spontaneous AACM release in both bronchial and parenchymal fragments. In airway antigen produced variable AACM responses, but in general the rank order was 6-keto-PGF1(α) > PGE is approx. the same as PGF2(α) > PGD2 > TXB2. The rank for antigen-induced AACM release from parenchyma was 6-keto-PGF1(α) is approx. the same as PGD2 > > PGF2(α) > TXB2 is approx. the same as PGE. In airway, as in parenchyma, very little AACM production during anaphylaxis can be attributed to smooth muscle contraction per se. Histamine released from bronchi (0.67 ± 0.30 μg/g lung) was significantly less than from parenchyma (3.7 ± 0.70 μg/g) despite comparable histamine content. At comparable levels of histamine release, the parenchyma produced greater quantities than bronchi of all AACMs except PGE. The comparatively limited bronchial capacity to generate PGF2(α), PGD2, TXB2, and histamine (airway constrictors) along with predominant generation of PGI2 and PGE (airway relaxants) may help preserve airway patency.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Applied Physiology Respiratory Environmental and Exercise Physiology|
|State||Published - Jan 1 1982|
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