We conclude that a single dose of BDP has an acute protective effect on the bronchial response to hyperpnea in both untrained subjects with asthma and athletes with EIB. This effect was associated with decreased excretion of urinary mediators, suggesting that BDP blunted the mast cell activation.

We have studied the presence of five neuropeptides in knee joint synovial fluid from either patients suffering from rheumatoid arthritis and pain (n = 18) or being subjected to arthroscopy due to meniscal/cruciate ligament injuries (n = 13). Radioimmunoassay technique was used for peptide analysis using antisera SP2 against substance P (SP), K12 against neurokinin A (NKA), CGRPR8 against calcitonin gene-related peptide (CGRP), NPY1 against neuropeptide Y (NPY) and VIP2 against vasoactive intestinal polypeptide (VIP). No SP could be detected, and lower levels of NKA was found in arthritic joints vs controls. CGRP and NPY was found in higher concentrations in arthritic patients vs controls. VIP was found sporadically in both arthritis and control patients. Our data show some quantitative differences between patients suffering rheumatoid arthritis and pain, and patients with non-inflamed joints without pain; indicating an involvement of peptidergic fibers in arthritis in humans.

The results support mast cell activation with release of bronchoconstrictive mediators after hyperpnea in athletes with and without EIB and inhibition by SCG. The degree of airway responsiveness to the specific mediator released is likely to determine whether or not bronchoconstriction will occur after EVH.

No abstract