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Pathogenesis of Aspirin-Exacerbated Respiratory Disease and Reactions
2013, Immunology and Allergy Clinics of North AmericaCitation Excerpt :Metabolites of TXA2 are present in higher levels in bronchoalveolar lavage fluid from patients with AERD compared with aspirin-tolerant asthmatics at baseline,5 potentially reflecting the presence of platelets in the respiratory tissue (see Fig. 1). Furthermore, TXA2 may be involved in the bronchoconstrictive effects of cysLTs, because the increase in airway resistance induced by either LTC4 or LTD4 in guinea pigs is prevented by a selective TXA2 synthase inhibitor.42 Moreover, the potentiation of histamine reactivity of human and guinea pig bronchi by LTE4 could be blocked by an antagonist of the T prostanoid (TP) receptor, the only high-affinity receptor for TXA2, or by pretreatment of the tissues with indomethacin to block COX function.43
Prostanoids as pharmacological targets in COPD and asthma
2006, European Journal of PharmacologyEffect of combined leukotriene D<inf>4</inf> and thromboxane A<inf>2</inf> receptor antagonist on mediator-controlled resistance in guinea pigs
2000, European Journal of PharmacologyBinding of YM158, a new dual antagonist for leukotriene D<inf>4</inf> and thromboxane A<inf>2</inf> receptors, to guinea pig lung membranes
1998, European Journal of Pharmacology