Matsuda Naoyuki, Hattori Yuichi
Department of Molecular and Medical Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyoma, Japan.
J Smooth Muscle Res. 2007 Aug;43(4):117-37. doi: 10.1540/jsmr.43.117.
Sepsis is the leading cause of mortality in critically ill patients. In this pathological syndrome, septic shock and sequential multiple organ failure correlate with poor outcome. The pathophysiology of sepsis with acute organ dysfunction involves a highly complex, integrated response that includes activation of number of cell types, inflammatory mediators, and the hemostatic system. Central to this process may be alterations in vascular functions. This review article provides a growing body of evidence for the potential impact of vascular dysfunction on sepsis pathophysiology with a major emphasis on the endothelium. Furthermore, the role of apoptotic signaling molecules in the mechanisms underlying endothelial cell injury and death during sepsis and its potential value as a target for sepsis therapy will be discussed, which may help in the assessment of ongoing therapeutic strategies.
脓毒症是危重症患者死亡的主要原因。在这种病理综合征中,感染性休克和序贯性多器官功能衰竭与不良预后相关。伴有急性器官功能障碍的脓毒症病理生理学涉及高度复杂的综合反应,包括多种细胞类型、炎症介质和止血系统的激活。这一过程的核心可能是血管功能的改变。这篇综述文章提供了越来越多的证据,证明血管功能障碍对脓毒症病理生理学的潜在影响,主要侧重于内皮细胞。此外,还将讨论凋亡信号分子在脓毒症期间内皮细胞损伤和死亡机制中的作用及其作为脓毒症治疗靶点的潜在价值,这可能有助于评估当前的治疗策略。