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目的 :观察急性缺氧动物再缺氧损伤现象及探讨其发生机理。方法 :采用右心漂浮导管检测法 ,及放免法测定了血浆ET1 含量的变化。结果 :急性缺氧动物肺动脉平均压在吸入 10 0 %氧气后即明显下降 ,在突然停止吸氧而改吸室内空气后 ,下降的肺动脉压逐渐回升 ,5min后恢复到吸氧前水平 ,但随着时间的延长 ,肺动脉压继续攀升 ,10min后肺动脉压已明显高于吸氧前水平 ,15min后 ,肺动脉压达最高值 ,与此同时 ,缺氧动物心率、肺血管阻力、血浆ET1 水平均显著高于吸氧前水平 ,而血氧分压反较吸氧前低。结论 :急性缺氧动物存在着再缺氧损伤 ,而血浆ET1 升高引起的肺动脉压异常升高在其发生中起重要作用。
Objective: To observe the phenomenon of reoxygenation injury in acute hypoxia and its mechanism. Methods: The right heart floating catheter detection method, and radioimmunoassay determination of plasma ET1 content changes. Results: The average pulmonary arterial pressure of acute hypoxic animals decreased significantly after inhaling 100% oxygen. The pulmonary pressure decreased gradually after inhaling oxygen in the acute phase of inhalation, and returned to the pre-oxygen level after 5 minutes With prolongation of time, pulmonary pressure continued to rise. Pulmonary arterial pressure tended to be significantly higher than that before oxygen inhalation. Pulmonary arterial pressure reached its maximum after 15 minutes. At the same time, heart rate, pulmonary vascular resistance and plasma endothelin Higher than before the level of oxygen, while the partial pressure of oxygen compared to oxygen before low. CONCLUSION: Hypoxia is found in acute hypoxia animals. The abnormal increase of pulmonary arterial pressure caused by elevated plasma ET1 plays an important role in the pathogenesis.