PGI_2与TXA_2在不同模型的肺水肿中的作用并不清楚,意见不一。我们用肾上腺素(0.1mg/kg)造成大鼠剧烈的致死性肺水肿,其机理类似于中枢性肺水肿,具有动力性与非动力性双重机制,既有肺毛细血管压力升高,又有肺毛细血管通透增高,我们先后取了颈动脉血及支气管-肺泡洗涤液,测定了肺水肿时动脉血浆及支气管-肺泡洗涤液中PG-6K-F_(1α)与TXB_2的含量,以探讨在PGI_2及TXA_2在发病机理中的作用。 The role of PGI_2 and TXA_2 in different models of pulmonary edema is unclear and disagree. We use epinephrine (0.1mg / kg) to cause severe fatal pulmonary edema in rats, its mechanism is similar to the central pulmonary edema, with both dynamic and non-motor mechanisms, both pulmonary capillary pressure, and Pulmonary capillary permeability increased, we have taken the carotid artery and bronchoalveolar lavage fluid, determination of pulmonary edema in the arterial plasma and bronchoalveolar lavage fluid PG-6K-F_ (1α) and TXB_2 content to explore Role of PGI_2 and TXA_2 in pathogenesis.