Good J T, Antony V B, Reller L B, Maulitz R M, Sahn S A
Am Rev Respir Dis. 1983 Jun;127(6):702-4. doi: 10.1164/arrd.1983.127.6.702.
To determine the possible mechanisms responsible for the low pH pleural effusion associated with esophageal rupture we evaluated the following possibilities: (1) gastric acid reflux, (2) bacterial metabolism, and (3) leukocyte metabolism. Neither elimination of gastric hydrogen ion contribution by distal esophageal ligation nor elimination of bacteria with antibiotics prevented the progressive fall in pleural fluid pH after esophageal rupture. Only elimination of polymorphonuclear leukocytes from the pleural space by rendering animals leukopenic with nitrogen mustard, prevented a low pH effusion after esophageal rupture. It appears that pleural fluid leukocyte metabolism is primarily responsible for the low pH effusion associated with esophageal rupture.
为了确定与食管破裂相关的低pH值胸腔积液的可能机制，我们评估了以下几种可能性：（1）胃酸反流；（2）细菌代谢；（3）白细胞代谢。通过食管远端结扎消除胃氢离子的作用，或使用抗生素消除细菌，均不能阻止食管破裂后胸腔积液pH值的逐渐下降。只有通过用氮芥使动物白细胞减少，从而消除胸腔内的多形核白细胞，才能防止食管破裂后出现低pH值胸腔积液。看来，胸腔积液白细胞代谢是食管破裂相关的低pH值胸腔积液的主要原因。
