RT期刊文章SR电子T1高海拔肺水肿的发病机制：肺毛细血管应激失败的直接证据JF欧洲呼吸杂志Jo Eur呼吸J FD欧洲呼吸学会SP 523 OP 529 vo 8 IS 4 A1 West，JB A1 West，JB A1 Colice，JB A1 Colice，GL GL188bet官网地址A1 Lee，YJ A1 Namba，Y A1 Kurdak，SS A1 Fu，Z A1 OU，LC A1 Mathieu-Costello，O YR 1995 ul //www.qdcxjkg.com/content/8/4/4/4/523.abstract abstract。高海拔肺水肿（HAPE）的发病机理有争议。最近的报道表明，HAPE和肺动脉压的发生之间存在很强的相关性，并且众所周知，水肿是高渗透性类型的。因此，我们提出HAPE是由于其壁的压力故障而导致的肺毛细血管的超微结构损害。但是，HAPE患者没有可满足的电子显微镜研究，并且很难找到动物模型。麦迪逊菌株Sprague-Dawley大鼠对急性缺氧的肺部压力反应轻快，并且容易受到HAPE的影响。我们将13只麦迪逊大鼠的压力暴露于294个TORR的压力长达12.5小时，或4只大鼠至236托尔，直至8小时。用导管测量的肺动脉或右心室收缩压从对照组（n = 4）中的30.5 +/- 0.5（SEM）增加到48 +/- 2 TORR（n = 11）。用血管内戊二醛将肺固定用于电子显微镜。 Frothy bloodstained fluid was seen in the trachea of three animals. Ultrastructural examination showed evidence of stress failure of pulmonary capillaries, including disruption of the capillary endothelial layer, or all layers of the wall, swelling of the alveolar epithelial layer, red blood cells (RBCs) and oedematous fluid in the alveolar wall interstitium, proteinaceous fluid and RBCs in the alveolar spaces, and fluid-filled protrusions of the endothelium into the capillary lumen.(ABSTRACT TRUNCATED AT 250 WORDS)