Hirose T, Aoki E, Domae M, Ishibashi M, Ikeda T, Tanaka K
Prostaglandins Leukot Med. 1983 Feb;10(2):187-96. doi: 10.1016/s0262-1746(83)80009-2.
To evaluate the potential beneficial effect of a thromboxane synthetase inhibitor, OKY-1581, on increased pulmonary vascular permeability in pulmonary microembolization, we have measured the filtration coefficient in the nonembolized lung after unilateral microembolization in dogs. The unilateral microembolization caused marked elevations in pulmonary artery pressure and blood flow to the nonembolized lung, while pulmonary venous pressure in nonembolized lung did not change. The pulmonary vascular resistance in nonembolized lung did not increase significantly. The filtration coefficient (Kf) in nonembolized lung increased to 0.14 +/- 0.02 from the baseline value of 0.07 +/- 0.01 ml/min/mmHg/100g at 30 min after microembolization when the initial hemodynamic changes reduced toward the baseline value. In OKY-1581 treated dogs, similar hemodynamic changes did not result in the increase in the filtration coefficient in nonembolized lung. Platelet aggregation was also inhibited after microembolization in OKY-1581 treated dogs. Based on these results, we could conclude that OKY-1581 could prevent the increase in pulmonary vascular permeability following pulmonary microembolization by inhibiting platelet aggregation and possibly by preventing the release of thromboxane A2.
为评估血栓素合成酶抑制剂OKY - 1581对肺微栓塞中肺血管通透性增加的潜在有益作用，我们测量了犬单侧微栓塞后未栓塞肺的滤过系数。单侧微栓塞导致肺动脉压和未栓塞肺的血流显著升高，而未栓塞肺的肺静脉压未改变。未栓塞肺的肺血管阻力没有显著增加。微栓塞后30分钟，当初始血流动力学变化向基线值恢复时，未栓塞肺的滤过系数（Kf）从基线值0.07±0.01ml/min/mmHg/100g增加到0.14±0.02。在接受OKY - 1581治疗的犬中，类似的血流动力学变化并未导致未栓塞肺滤过系数增加。在接受OKY - 1581治疗的犬中，微栓塞后血小板聚集也受到抑制。基于这些结果，我们可以得出结论，OKY - 1581可通过抑制血小板聚集以及可能通过阻止血栓素A2的释放来预防肺微栓塞后肺血管通透性的增加。
