Department of Intensive Care, Erasmus Medical Center, Erasmus University of Rotterdam, s Gravendijkwal 230, 3015 CE, Rotterdam, The Netherlands.
J Mol Med (Berl). 2010 Feb;88(2):127-33. doi: 10.1007/s00109-009-0585-6. Epub 2010 Jan 30.
Sepsis results from the interaction between a host and an invading pathogen. The microcirculatory dysfunction is now considered central in the development of the often deadly multiple organ dysfunction syndrome in septic shock patients. The microcirculatory flow shutdown and flow shunting leading to oxygen demand and supply mismatch at the cellular level and the local activation of inflammatory pathways resulting from the leukocyte-endothelium interactions are both features of the sepsis-induced microcirculatory dysfunction. Although the host response through the inflammatory and immunologic response appears to be critical, there are also evidences that Gram-positive and Gram-negative bacteria can exert different effects at the microcirculatory level. In this review we discuss available data on the potential bacterial-specific microcirculatory alterations observed during sepsis.
脓毒症是宿主与入侵病原体相互作用的结果。目前认为，在感染性休克患者中经常致命的多器官功能障碍综合征的发展中，微循环功能障碍起着核心作用。微循环血流停止和分流导致细胞水平的氧需求和供应不匹配，以及白细胞-内皮相互作用导致局部炎症途径的激活，这些都是脓毒症引起的微循环功能障碍的特征。尽管宿主反应通过炎症和免疫反应似乎至关重要，但也有证据表明革兰氏阳性和革兰氏阴性细菌在微循环水平上可以产生不同的影响。在这篇综述中，我们讨论了关于脓毒症期间观察到的潜在细菌特异性微循环改变的现有数据。
