Jackson R M, Veal C F
Birmingham VA Medical Center, Alabama.
Am J Med Sci. 1989 Jul;298(1):44-50. doi: 10.1097/00000441-198907000-00009.
In a 1902 American Journal of the Medical Sciences case report, Riesman described "albuminous expectoration" following thoracentesis, a phenomenon that is now recognized as re-expansion pulmonary edema (RPE). Both cellular and biochemical mechanisms that produce lung injury in RPE have been described recently. Pathophysiologically, this unilateral edematous lung injury resembles the adult respiratory distress syndrome (ARDS) because both are characterized by intra-alveolar-activated neutrophils and markedly increased lung capillary permeability. Biochemical mechanisms that operate in RPE are analogous to those in diverse re-oxygenation (reperfusion) injuries that have been described recently in the heart, kidney, brain, and intestine. Re-oxygenated lung tissue appears to produce excess superoxide and other cytotoxic oxygen metabolites, although lung xanthine oxidase, the commonly recognized source of these oxidants, is exceedingly low. Riesman's critical analyses of the re-expansion edema fluid in his case provided an impetus for others to hypothesize that increased permeability pulmonary edema in RPE represented re-oxygenation injury of the lung microvasculature.
在1902年《美国医学科学杂志》的一篇病例报告中，里斯曼描述了胸腔穿刺术后出现的“含蛋白痰液”，这一现象现在被认为是复张性肺水肿（RPE）。最近已经描述了在RPE中导致肺损伤的细胞和生化机制。从病理生理学角度来看，这种单侧肺水肿性肺损伤类似于成人呼吸窘迫综合征（ARDS），因为两者都以肺泡内活化的中性粒细胞和肺毛细血管通透性显著增加为特征。RPE中起作用的生化机制类似于最近在心脏、肾脏、大脑和肠道中描述的各种再氧合（再灌注）损伤中的机制。尽管通常认为这些氧化剂的来源——肺黄嘌呤氧化酶含量极低，但再氧合的肺组织似乎会产生过量的超氧化物和其他细胞毒性氧代谢产物。里斯曼对其病例中复张性水肿液的批判性分析促使其他人推测，RPE中通透性增加的肺水肿代表了肺微血管的再氧合损伤。
