Craddock P R, Fehr J, Brigham K L, Kronenberg R S, Jacob H S
N Engl J Med. 1977 Apr 7;296(14):769-74. doi: 10.1056/NEJM197704072961401.
During hemodialysis, cardiopulmonary decompensation may appear in uremic patients, possibly caused by plugging of pulmonary vessels by leukocytes. In 34 patients we noted leukopenia (20% of initial levels) during hemodialysis that in 15 was associated with impaired pulmonary function. When we infused autologous plasma, incubated with dialyzer cellophane, into rabbits and sheep, sudden leukopenia and hypoxia occurred, with doubling of pulmonary-artery pressures and quintupling of pulmonary-lymph effluent. Histologic examination showed severe pulmonary-vessel-leukostasis and interstitial edema. The syndrome was prevented by preinactivation of complement but was reproduced by infusions of plasma in which complement was activated by zymosan. Thus, acute pulmonary dysfunction from complement-mediated leukostasis may play a major part in the acute cardiopulmonary complications of cellophane-membrane hemodialysis.
在血液透析过程中，尿毒症患者可能会出现心肺失代偿，这可能是由白细胞堵塞肺血管所致。我们观察到34例患者在血液透析期间出现白细胞减少（降至初始水平的20%），其中15例伴有肺功能受损。当我们将与透析器玻璃纸孵育过的自体血浆注入兔和羊体内时，突然出现白细胞减少和缺氧，肺动脉压加倍，肺淋巴流出量增至五倍。组织学检查显示严重的肺血管白细胞淤滞和间质水肿。该综合征可通过预先灭活补体来预防，但通过注入经酵母聚糖激活补体的血浆可再次引发。因此，补体介导的白细胞淤滞引起的急性肺功能障碍可能在玻璃纸膜血液透析的急性心肺并发症中起主要作用。
