Participation of prostaglandins in pathogenesis of aspirin-sensitive asthma.

Recent evidence suggests that the induction of bronchoconstriction in aspirin-sensitive patients by analgesics is due to the inhibition of PG biosynthesis in their respiratory tract. PGEs might play the main defensive role in the bronchi of aspirin-sensitive asthmatics. Removal of this potent bronchodilator by PG synthetase inhibitors leaves the effects of spasmogens unopposed, and possibly promotes the release of histamine from its stores.