Nasal Blockage Induced by Oral Administration of Non-steroidal Anti-inflammatory Drugs in a Guinea-Pig Model of Allergic Rhinitis

Abstract

Abstract. To elucidate the mechanisms underlying nasal symptoms in patients with aspirin hypersensitivity, we evaluated the effects of orally administered non-steroidal anti-inflammatory drugs (NSAIDs) on the nasal patency of guinea pigs with cedar pollen-induced chronic allergic rhinitis. Indomethacin (10 mg / kg) administered 1 h before a pollen challenge amplified the antigen-induced nasal blockage. More interestingly, even in the absence of the pollen challenge, indomethacin induced nasal blockage at 30 min at 4 h after administration. However, indomethacin-induced nasal blockage was not provoked in non-sensitized animals. Another NSAID, diclofenac (30 mg / kg), also evoked nasal blockage, but unexpectedly, aspirin (500 mg / kg) did not affect nasal patency. Indomethacin-induced nasal blockage was unaffected by a cysteinyl leukotriene receptor (CysLT 1 receptor) antagonist, pranlukast (30 mg / kg, p.o.), or by prostaglandin E 2 (10 −3 M, intranasal), suggesting that the nasal blockage may not be due to hyperproduction of cysteinyl leukotrienes or inhibition of prostaglandin E 2 production. These results indicate that the indomethacin-induced nasal blockage may not be an identical phenomena to airway symptoms in aspirin hypersensitivity patients. However, because chronic nasal inflammation is indispensable for the development of nasal blockage, indomethacin-induced nasal blockage may become a clue to elucidate new mechanisms underlying hypersensitivity to NSAIDs.

Oxymetazoline Inhibits and Resolves Inflammatory Reactions in Human Neutrophils

“…Since OMZ induces formation of PGE 2 and 15(S)-HETE indicating an activation of 15-LO and reduces LTB 4 production indicating a reduction of 5-LO activity, OMZ is suggested to substantially support this switching of the eicosanoid class from LTB 4 to LXA 4 . The importance of PGE 2 induced by OMZ during the inflammatory response in the nasal tissue is emphasized by the study of Han et al (44), showing that the nasal patency is reduced when the COX activity is inhibited by non-steroidal anti-inflammatory drugs. Moreover, the respiratory burst activity and the oxidative stress induced by UCP and OZ are inhibited by OMZ.…”