Pardy B J, Dudley H A
Surg Gynecol Obstet. 1977 Feb;144(2):259-69.
Pulmonary insufficiency is occasionally a life-threatening sequel to severe nonthoracic trauma. A similar disturbance of pulmonary function may be a feature of hepatic cirrhosis, fulminant hepatic failure, liver homotransplantation and major hepatic resection for blunt injury. In addition to the respiratory changes, other associations common to both post-traumatic pulmonary insufficiency and liver disease are disturbance of consciousness and susceptibility to infection by organisms normally found in the gastrointestinal tract. If failure of some aspect of liver function is responsible for the development of pulmonary insufficiency, it is likely that it is the hepatic reticulo-endothelial cells rather than the parenchymal cells which are concerned, because hepatic parenchymal cell failure is not a feature of post-traumatic pulmonary insufficiency. It is suggested that the hepatic reticuloendothelial system normally protects the lungs by acting as a prepulmonary filter removing and inactivating noxious macromolecular and particulate matter in the blood, such matter arising mainly from the intestine and the blood coagulation and fibrinolytic systems. Experimental evidence indicates that hypovolemia increases the load of circulating phagocytosable material and depresses activity of the hepatic reticuloendothelial system, while trapping of the pulmonary reticuloendothelial system is considerably enhanced. This noxious material, normally dealt with by the hepatic reticuloendothelial system, may accumulate during and after hypovolemia in active form in the lungs as a result of the action of three mechanisms: direct pulmonary reticuloendothelial phagocytosis from the blood, transfer in hepatic reticuloendothelial cells from liver to lungs and uptake from the blood by polymorphonuclear leukocytes which become sequestered in the lungs. The ensuing pulmonary injury caused by this material may then be manifested by progressive pulmonary insufficiency and the impairment of activity of the hepatic reticuloendothelial system by the presence of gram-negative infection. The reticuloendothelial system has been largely neglected in man, and it is considered that evaluation of reticuloendothelial activity in injured patients may lead to the definition of a syndrome of failure of the reticuloendothelial system of which pulmonary insufficiency may be an integral part.
肺功能不全偶尔是严重非胸部创伤危及生命的后遗症。类似的肺功能紊乱可能是肝硬化、暴发性肝衰竭、肝同种异体移植以及钝性损伤后肝大部切除的特征。除了呼吸变化外，创伤后肺功能不全和肝脏疾病共有的其他关联包括意识障碍和对胃肠道常见微生物感染的易感性。如果肝功能某些方面的衰竭是肺功能不全发生的原因，那么可能涉及的是肝网状内皮细胞而非实质细胞，因为创伤后肺功能不全并非以肝实质细胞衰竭为特征。有人提出，肝网状内皮系统通常通过充当肺前过滤器来保护肺，去除并使血液中的有害大分子和颗粒物失活，这些物质主要来自肠道以及凝血和纤维蛋白溶解系统。实验证据表明，血容量不足会增加循环中可吞噬物质的负荷，并抑制肝网状内皮系统的活性，而肺网状内皮系统的捕获能力则会显著增强。这种通常由肝网状内皮系统处理的有害物质，可能在血容量不足期间和之后，由于三种机制的作用，以活性形式在肺中蓄积：从血液中直接被肺网状内皮细胞吞噬、从肝脏经肝网状内皮细胞转移至肺以及被聚集在肺中的多形核白细胞从血液中摄取。这种物质随后导致的肺损伤可能表现为进行性肺功能不全，以及革兰氏阴性菌感染导致肝网状内皮系统活性受损。网状内皮系统在人类中在很大程度上被忽视了，有人认为评估受伤患者的网状内皮活性可能会明确一种网状内皮系统衰竭综合征，肺功能不全可能是其一个组成部分。
