Bench-to-bedside review: microvascular dysfunction in sepsis--hemodynamics, oxygen transport, and nitric oxide.
Bench-to-bedside review: microvascular dysfunction in sepsis--hemodynamics, oxygen transport, and nitric oxide.
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DOI：
10.1186/cc2353
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发表时间：
2003-10
期刊：
影响因子：
--
通讯作者：
Ellis CG
中科院分区：
文献类型：
--
作者：
Bateman RM;Sharpe MD;Ellis CG
微循环是一个复杂的综合系统，它在整个组织中供应和分配氧气。红细胞（RBC）通过与血红蛋白的协同结合促进对流氧运输。在微循环中，氧从RBC扩散到邻近组织中，在那里被线粒体消耗。有证据表明，红细胞作为氧气的输送者和局部氧气梯度的“传感器”。在血管床内，RBC通过小动脉张力主动分布，并通过流变因素被动分布，包括血管几何形状和RBC变形性。微血管氧转运由微血管几何形状、血液动力学和RBC血红蛋白氧饱和度决定。脓毒症导致微血管氧转运异常，因为大量毛细血管停止流动，微循环无法补偿功能性毛细血管密度的降低。所产生的RBC流量的不均匀分布导致氧输送与氧需求不匹配，这影响临界氧输送和氧提取率。一氧化氮（NO）通过调节小动脉张力、红细胞变形性、白细胞和血小板与内皮细胞的粘附以及血容量来维持微血管稳态。NO还调节线粒体呼吸。在脓毒症期间，NO过度产生介导全身性低血压和微血管反应性，并且似乎对微血管血流具有保护作用。
The microcirculation is a complex and integrated system that supplies and distributes oxygen throughout the tissues. The red blood cell (RBC) facilitates convective oxygen transport via co-operative binding with hemoglobin. In the microcirculation oxygen diffuses from the RBC into neighboring tissues, where it is consumed by mitochondria. Evidence suggests that the RBC acts as deliverer of oxygen and 'sensor' of local oxygen gradients. Within vascular beds RBCs are distributed actively by arteriolar tone and passively by rheologic factors, including vessel geometry and RBC deformability. Microvascular oxygen transport is determined by microvascular geometry, hemodynamics, and RBC hemoglobin oxygen saturation. Sepsis causes abnormal microvascular oxygen transport as significant numbers of capillaries stop flowing and the microcirculation fails to compensate for decreased functional capillary density. The resulting maldistribution of RBC flow results in a mismatch of oxygen delivery with oxygen demand that affects both critical oxygen delivery and oxygen extraction ratio. Nitric oxide (NO) maintains microvascular homeostasis by regulating arteriolar tone, RBC deformability, leukocyte and platelet adhesion to endothelial cells, and blood volume. NO also regulates mitochondrial respiration. During sepsis, NO over-production mediates systemic hypotension and microvascular reactivity, and is seemingly protective of microvascular blood flow.
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