Inhibition by thromboxane antagonists of airway hyperresponsiveness to histamine induced by 13,14-dihydro-15-keto-PGF2α in guinea-pigs
Article first published online: 27 APR 2006
Clinical & Experimental Allergy
Volume 24, Issue 7, pages 669–675, July 1994
How to Cite
KUROSAWA, M., YODONAWA, S., INAMURA, H. and TSUKAGOSHI, H. (1994), Inhibition by thromboxane antagonists of airway hyperresponsiveness to histamine induced by 13,14-dihydro-15-keto-PGF2α in guinea-pigs. Clinical & Experimental Allergy, 24: 669–675. doi: 10.1111/j.1365-2222.1994.tb00971.x
- Issue published online: 27 APR 2006
- Article first published online: 27 APR 2006
- Submitted 20 September 1993; revised 22 November 1993; accepted 1 March 1994.
Summary. We studied the effect of intravenous administration of 13,14-dihydro-15-keto-prostaglandin (PG) F27alpha; on airway responsiveness to histamine and airway wall thickening in guinea-pigs. Guinea-pigs were killed and the lungs were fixed in formalin. Slides from paraffin-embedded sections of the lungs were stained and the airways that were cut in transverse section were measured by tracing enlarged images using a digitizer. Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyser and we calculated two indices, an index of airway wall thickening and the one of airway hyperresponsiveness to histamine, from changes of baseline-Raw and peak-Raw following intravenous administration of histamine before and after the intravenous administration of 13,14-dihydro-l5-keto-PGF2n. Intravenous administration of 10/μg/kg 13,14-dihydro-15-keto-PGF2α for 1 h did not induce an increase of the relative thickness of the airway wall by the histological examination. In analysis of airway function, intravenous administration of 10μg/kg 13,14-dihydro-15-keto-PGF2α for 1 h induced airway hyperresponsiveness to histamine without airway wall thickening. Thromboxane A2 (TXA2) receptor antagonists ONO-NT-126 and ONO-8809 inhibited the 13,14-dihydro-15-keto-PGF2α-induced airway hyperresponsiveness to histamine, suggesting that the effect of 13,14-dihydro-15-keto-PGF2α on bronchial hyperresponsiveness is likely to be mediated through TXA2.