Protective effect of a thromboxane synthetase inhibitor, OKY-1581, on increased lung vascular permeability in pulmonary microembolization in dogs
| Autor: | Takahito Hirose, Masayoshi Ishibashi, Togo Ikeda, Mariko Domae, Kenzo Tanaka, Emiko Aoki |
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| Rok vydání: | 1983 |
| Předmět: |
Male
Pulmonary Circulation medicine.medical_specialty Time Factors Physiology Thromboxane Hemodynamics Vascular permeability Thromboxane Synthetase Biochemistry Capillary Permeability Dogs Endocrinology Internal medicine medicine.artery medicine Animals Lung business.industry Blood flow Blood Cell Count medicine.anatomical_structure Acrylates Pulmonary artery Vascular resistance Cardiology Methacrylates Female Thromboxane-A Synthase Oxidoreductases Pulmonary Embolism business |
| Zdroj: | Prostaglandins, Leukotrienes and Medicine. 10:187-196 |
| ISSN: | 0262-1746 |
| Popis: | 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 (K f ) 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 A 2 . |
| Databáze: | OpenAIRE |
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