Tsukagoshi H, Yodonawa S, Kurosawa M
First Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1993 Jun;31(6):707-11.
In this study, we investigated the effects of peroral (p.o.) administration of a thromboxane A2 (TXA2) synthetase inhibitor, OKY-046, on the airway hyperresponsiveness (AHR) in guinea pigs induced by intravenous administration of leukotriene C4 (LTC4). A 3 micrograms/kg/hr LTC4 infusion induced airway wall thickening (AWT) and AHR to 1.8 and 3.6 micrograms/kg histamine bolus shot. OKY-046 100 mg/kg p.o. partially inhibited the AHR induced by LTC4 without inhibition of AWT. Previously, we have reported that LTC4-induced AHR was partially inhibited, to the same exert as by OKY-046, by TXA2 receptor antagonists, ONO-NT-126 and ONO-8809. These data suggest that intravenous administration of LTC4 generates TXA2, and TXA2 augments LTC4-induced AHR partially in guinea pigs.
在本研究中，我们调查了经口（p.o.）给予血栓素A2（TXA2）合成酶抑制剂OKY-046对静脉注射白三烯C4（LTC4）诱导的豚鼠气道高反应性（AHR）的影响。以3微克/千克/小时的速度输注LTC4可诱导气道壁增厚（AWT）以及对1.8微克/千克和3.6微克/千克组胺推注的AHR。经口给予100毫克/千克的OKY-046可部分抑制LTC4诱导的AHR，但不抑制AWT。此前，我们曾报道，TXA2受体拮抗剂ONO-NT-126和ONO-8809对LTC4诱导的AHR的抑制程度与OKY-046相同。这些数据表明，静脉注射LTC4会生成TXA2，并且TXA2可部分增强豚鼠中LTC4诱导的AHR。
