Liver-lung interactions in critical illness.
Liver-lung interactions in critical illness.
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DOI：
10.1007/978-3-642-79715-6_7
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发表时间：
1994
期刊：
影响因子：
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通讯作者：
G. Matuschak
中科院分区：
文献类型：
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作者：
G. Matuschak
尽管肝脏在宿主防御稳态以及免疫、生化和代谢调节中起着核心作用，但由于多种原因，肝脏并未被认为是影响急性呼吸窘迫综合征(ARDS)预后的关键因素。肝病患者经常被排除在研究之外，肝功能障碍通常被“肝功能测试”非特异性地定义[1]。肝脏不像肺和其他器官那样便于研究，急性肝功能障碍也不像急性肺损伤那样直接明显[2，3]。我们提出了一个扩展的概念，即败血症和创伤相关的ARDS是全身免疫调节紊乱的中央肺部表现；肺损伤的发病机制和解决与全身宿主防御的更基本的紊乱有关[2-8]。这种重新定位意味着了解ARDS患者肝功能改变影响肺功能的途径可能具有治疗作用。在这里，我们研究了肝脏功能通过影响宿主防御的四个相互关联的元素来调节ARDS肺损伤的易感性和解决：(A)控制全身内毒素血症、菌血症和败血症和创伤的血管活性副产物，(B)调节单核吞噬细胞(Kupffer细胞)内源性炎症介质的产生和输出，(C)这些介质的代谢失活和解毒，以及(D)在中间代谢和控制炎症反应中必不可少的急性期蛋白质的合成。作为一个推论，我们评估了临床和实验证据表明，肝脏功能的改变增加了肺部炎症和死亡率，这是由于一种细胞因子：血管内和下呼吸道内炎症的二十烷基轴。
Though acknowledged to have a central role in host defense homeostasis as well as immunological, biochemical, and metabolic regulation, the liver has not been recognized as pivotal to outcome in the acute respiratory distress syndrome (ARDS) for several reasons. Patients with liver disease have often been excluded from study, and hepatic dysfunction has often been nonspecifically defined by “liver function tests” [1]. The liver is not as accessible for study as the lung and other organs, and acute liver dysfunction is not as immediately evident as is acute lung injury [2, 3]. We have proposed an expanded conception of sepsis- and trauma-related ARDS as the central pulmonary manifestation of a generalized disorder of immunoregulation; the pathogenesis and resolution of lung injury are linked to more fundamental derangements in systemic host defense [2–8]. This reorientation implies that understanding the pathways by which changes in hepatic performance affect pulmonary function in ARDS may have therapeutic utility. Here we examine the thesis that hepatic performance modulated predisposition and resolution of lung injury in ARDS by affecting four interrelated elements of host defense: (a) control of systemic endotoxemia, bacteremia, and vasoactive byproducts of sepsis and trauma, (b) regulation of the production and export of endogenous inflammatory mediators by mononuclear phagocytes (Kupffer cells), (c) metabolic inactivation and detoxification of these mediators, and (d) synthesis of acute-phase proteins essential in intermediary metabolism and control of the inflammatory response. As a corollary, we assess clinical and experimental evidence suggesting that alterations in hepatic performance augment lung inflammation and mortality owing to a cytokine:eicosanoid axis of inflammation within the intravascular compartment and lower respiratory tract.