Hirose T, Aoki E, Aizawa H, Ishibashi M, Domae M, Ikeda T, Tanaka K
Jpn J Med. 1982 Jul;21(3):180-6. doi: 10.2169/internalmedicine1962.21.180.
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 te base line value of 0.07 +/- 0.01 ml/min/mmHg/100 g at 30 min after microembolization when the initial hemodynamic changes reduced toward the base line value. In OKY-1581 treated dogs, similar hemodynamic changes did not result in the filtration coefficient in nonembolized lung. Platelet aggregagation was also inhibited after microembolization in OKY-1581 treated dogs. Based on these results, we could conclude that OKY-1581 will serve as a potent beneficial protective drug against pulmonary edema by inhibiting the release of thromboxane A2 following microembolization in the pulmonary vascular bed.
为评估血栓素合成酶抑制剂OKY - 1581对肺微栓塞时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非栓塞肺的滤过系数。单侧微栓塞导致肺动脉压和非栓塞肺血流量显著升高，而非栓塞肺的肺静脉压未改变。非栓塞肺的肺血管阻力未显著增加。微栓塞后30分钟，当初始血流动力学变化向基线值恢复时，非栓塞肺的滤过系数（kf）从基线值0.07±0.01 ml/min/mmHg/100 g增加至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非栓塞肺的滤过系数升高。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通过抑制肺血管床微栓塞后血栓素A2的释放，将作为一种有效的有益保护药物来预防肺水肿。
