The Human Microcirculation: Regulation of Flow and Beyond.
The Human Microcirculation: Regulation of Flow and Beyond.
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DOI：
10.1161/circresaha.115.305364
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发表时间：
2016-01-08
影响因子：
20.1
通讯作者：
Beyer AM
中科院分区：
文献类型：
--
作者：
Gutterman DD;Chabowski DS;Kadlec AO;Durand MJ;Freed JK;Ait-Aissa K;Beyer AM
微循环负责协调血管张力的调整，使局部组织的灌注量与氧气需求相匹配。除了这种代谢扩张，微血管系统还通过内皮释放一系列异常多样的化合物，包括一氧化氮、其他活性氧物种和花生四烯酸代谢产物，在调节血管张力方面发挥关键作用。动物模型为健康和疾病中的血管调节机制提供了极好的洞察力。然而，人类微循环的某些独特方面是本综述的重点。提出血管-实质沟通是多模式的，血管释放一氧化氮引起扩张，并通过抑制炎症和增殖来维持正常的实质功能。同样，在疾病或应激状态下，内皮细胞释放ROS既可介导扩张，又可导致实质炎症，从而导致细胞功能障碍、血栓形成和纤维化。文中还提出了导致这种应激诱导的血管扩张介质移位的一些途径。这一范式可能有助于解释为什么微血管功能障碍是心血管事件的如此强大的预测因子，并有助于确定新的治疗和预防方法。
The microcirculation is responsible for orchestrating adjustments in vascular tone to match local tissue perfusion with oxygen demand. Beyond this metabolic dilation, the microvasculature plays a critical role in modulating vascular tone by endothelial release of an unusually diverse family of compounds including nitric oxide, other reactive oxygen species, and arachidonic acid metabolites. Animal models have provided excellent insight into mechanisms of vasoregulation in health and disease. However there are unique aspects of the human microcirculation that serve as the focus of this review. The concept is put forth that vasculo-parenchymal communication is multimodal, with vascular release of nitric oxide eliciting dilation and preserving normal parenchymal function by inhibiting inflammation and proliferation. Likewise, in disease or stress, endothelial release of ROS both mediates dilation and parenchymal inflammation leading to cellular dysfunction, thrombosis, and fibrosis. Some pathways responsible for this stress-induced shift in mediator of vasodilation are proposed. This paradigm may help explain why microvascular dysfunction is such a powerful predictor of cardiovascular events, and help identify new approaches to treatment and prevention.