1 We have investigated the ability of prostacyclin (PGO2) to contract guinea-pig isolated bronchi and the possible involvement of capsaicin-sensitive primary afferents in the response to PG12 . 2 PGO2 (0.1-100pUM) produced concentration-dependent contractions of the guinea-pig isolated bronchi. In vitro capsaicin desensitization (10pM for 30min followed by washing) significantly reduced the PG12-induced contraction at all concentrations tested. A capsaicin-resistant component of contraction (40-60% of the overall response) was also evident. 3 Ruthenium red (3pM), an inorganic dye which acts as a selective functional antagonist of capsaicin, significantly decreased PG12-induced contractions, without affecting the response to substance P, neurokinin A or acetylcholine.4 MEN 10, 207, (Tyr5, D-Trp6'8'9, Arg10)-neurokinin A (4-10) (3pM), a selective antagonist of NK2-tachykinin receptors, significantly decreased PG12-induced contractions and neurokinin A-induced contractions, without affecting the response to acetylcholine. 5 The effect of ruthenium red and MEN 10,207 on the one hand, and that of ruthenium red and capsaicin on the other was non additive. 6 These results indicate that PGI2-induced contraction of the guinea-pig isolated bronchi involves two distinct mechanisms, one of which involves transmitter (tachykinins) release from peripheral endings of capsaicin-sensitive primary afferents. In as much as PG12-activation of primary afferents is sensitive to ruthenium red, we suggest that PGO2 shares a common mechanism of tachykinin release with that activated by capsaicin.

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Background The loop diuretic frusemide has been shown to inhibit the bronchoconstrictor response to exercise, inhaled allergen, distilled water, adenosine, and sodium metabisulphite. Toluene diisocyanate contracts smooth

Objectives-In a previous study on bronchoalveolar lavage fluid from rats exposed in vivo for seven days to 10 ppm nitrogen dioxide (NO2), it has been shown that there is an influx of macrophages into the airways. The present study investigated the effect of seven day exposure to 10 ppm NO2, on: (a) lung tissue inflammation and morphology; (b) airway microvascular leakage; (c) in vitro contractile response of main bronchi.Methods-Lung tissue was studied by light microscopy, after fixing the lungs by inflation with 4% formalin at a pressure of 20 cm HO. Microvascular leakage was measured by extravasation of Evans blue dye in the larynx, trachea, main bronchi, and intrapulmonary airways. Smooth muscle responsiveness was evaluated by concentration-response curves to acetylcholine (10-9-10-3 M), serotonin (10-9_10-4 M), and voltage-response curves (12-28 V) to electrical field stimulation.