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Am. J. Respir. Crit. Care Med., Volume 160, Number 6, December 1999, 2100-2103

Effect of Leukotriene and Thromboxane Antagonist on Propranolol-induced Bronchoconstriction

MASAKI FUJIMURA, MIKI ABO, YUMIE KAMIO, SHIGEHARU MYOU, YOSHIHISA ISHIURA, TAKUMA HASHIMOTO, and TAMOTSU MATSUDA

The Third Department of Internal Medicine and Department of Laboratory Medicine, Kanazawa University School of Medicine; The Central Laboratory, Kanazawa University Hospital, Kanazawa, Japan

beta -adrenoreceptor blockers such as propranolol provoke bronchoconstriction only in asthmatic patients. Although cysteinyl leukotrienes (cLTs) and thromboxane A2 (TXA2) have been proposed to be involved in the pathophysiology of asthma, the role of these lipid mediators in propranolol-induced bronchoconstriction (PIB) has not been evaluated in asthmatics. This study was conducted to elucidate it. Nine patients with stable asthma, in whom a 20% or more decrease in FEV1 occurred by inhalation of 20 mg/ml or less propranolol, participated in this study. A cLT antagonist, pranlukast (225 mg twice a day), a TXA2 antagonist, seratrodast (80 mg once a day), and placebo were orally given for 2 wk in a randomized and double-blinded manner. The provocative concentration of propranolol causing a 20% fall in FEV1 (PC20) was determined on the last day of each 2-wk treatment. Pranlukast, but not seratrodast, tented to increase FEV1 compared with placebo (2.14 ± 0.29 versus 1.99 ± 0.34 L, p = 0.0543). Pranlukast or seratrodast did not affect the PC20 in comparison with placebo. We conclude that cLTs or TXA2 are not involved in PIB of asthmatics. Fujimura M, Abo M, Kamio Y, Myou S, Ishiura Y, Hashimoto T, Matsuda T. Effect of leukotriene and thromboxane antagonist on propranolol-induced bronchoconstriction.




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