Akar F, Kanzik I
Department of Pharmacology, Faculty of Pharmacy, Gazi Universitesi Eczacilik Fakültesi, Etiler, Ankara, Turkey.
Prostaglandins Leukot Essent Fatty Acids. 1989 Jul;37(1):25-9. doi: 10.1016/0952-3278(89)90182-8.
The role of prostanoids in the pulmonary actions of histamine(HA) was investigated using various antagonists and assay organs in superfusion cascade. Intraarterial injection of HA to the perfused lung caused contractions of rabbit aorta, rat stomach strips, guinea pig trachea, but contraction followed by relaxation of bovine coronary artery, superfused with lung effluent. Lung effluent produced no significant changes in resting tensions of guinea pig ileum or rat colon. The thromboxane synthetase inhibitor, UK 38485, reduced and the thromboxane/prostaglandin receptor antagonist, SQ 29548 abolished HA-induced contractions of all superfused assay tissues. Both contractile and relaxant responses of bovine coronary artery were completely inhibited by indomethacin. The pulmonary pressor effect of HA was also significantly inhibited by all of these antagonists. Our results indicate that HA releases thromboxane A2, prostaglandin endoperoxides, and prostacyclin but not leukotriene and prostaglandin E2- like substances from the guinea pig lung.
利用多种拮抗剂和超灌注级联中的检测器官，研究了前列腺素类物质在组胺（HA）肺内作用中的作用。向灌注肺内动脉注射HA可引起兔主动脉、大鼠胃条、豚鼠气管收缩，但可使与肺流出液一起超灌注的牛冠状动脉先收缩后舒张。肺流出液对豚鼠回肠或大鼠结肠的静息张力无显著影响。血栓素合成酶抑制剂UK 38485可减轻，血栓素/前列腺素受体拮抗剂SQ 29548可消除HA诱导的所有超灌注检测组织的收缩。吲哚美辛可完全抑制牛冠状动脉的收缩和舒张反应。这些拮抗剂也显著抑制了HA的肺升压作用。我们的结果表明，HA可从豚鼠肺中释放血栓素A2、前列腺素内过氧化物和前列环素，但不释放白三烯和前列腺素E2样物质。
