Lee Marlon A, Yatani Atsuko, Sambol Justin T, Deitch Edwin A
Department of Surgery, New Jersey Medical School Newark, NJ, USA.
Int J Clin Exp Med. 2008;1(2):171-80. Epub 2008 Mar 31.
Acute injury-induced cardiac contractile dysfunction occurs even in young and otherwise healthy individuals after major injuries, and significantly contributes to morbidity and mortality in patients with pre-existent cardiac diseases as well as in patients who develop multiple organ dysfunction syndrome. Recent studies indicate that post-injury acute cardiac failure is the result of an exaggerated cardiac inflammatory response resulting in an inflammatory cardiomyopathy characterized by decreased cardiac contractility. Over the past decade, many of the effector molecules involved in this process have been identified as having some involvement in generating a myocardial inflammatory response. However, less is known about the agents and processes involved in triggering this inflammation-induced decrease in cardiac contractility. Consequently, in this review, the concept of the heart responding to major injury like an innate immune organ will be presented, the various effector molecules and mechanisms leading to myocyte contractile dysfunction will be reviewed and data indicating that the acute cardiac contractile dysfunction observed after trauma is due to gut-derived intestinal lymph factors will be reviewed.
急性损伤诱发的心脏收缩功能障碍即使在遭受重大创伤的年轻且原本健康的个体中也会发生,并且在患有既往心脏病的患者以及发生多器官功能障碍综合征的患者的发病和死亡中起重要作用。最近的研究表明,损伤后急性心力衰竭是心脏炎症反应过度的结果,导致以心脏收缩力下降为特征的炎症性心肌病。在过去十年中,许多参与这一过程的效应分子已被确定在引发心肌炎症反应中发挥了一定作用。然而,对于引发这种炎症导致心脏收缩力下降的因素和过程了解较少。因此,在本综述中,将阐述心脏像先天免疫器官一样对重大损伤作出反应的概念,回顾导致心肌细胞收缩功能障碍的各种效应分子和机制,并回顾表明创伤后观察到的急性心脏收缩功能障碍是由肠道来源的肠淋巴因子引起的数据。