Impaired tissue oxygen delivery is a major cause of organ damage and failure in critically ill patients, which can occur even when systemic parameters, including cardiac output and arterial hemoglobin saturation, are close to normal. This review addresses oxygen transport mechanisms at the microcirculatory scale, and how hypoxia may occur in spite of adequate convective oxygen supply. The structure of the microcirculation is intrinsically heterogeneous, with wide variations in vessel diameters and flow pathway lengths, and consequently also in blood flow rates and oxygen levels. The dynamic processes of structural adaptation and flow regulation continually adjust microvessel diameters to compensate for heterogeneity, redistributing flow according to metabolic needs to ensure adequate tissue oxygenation. A key role in flow regulation is played by conducted responses, which are generated and propagated by endothelial cells and signal upstream arterioles to dilate in response to local hypoxia. Several pathophysiological conditions can impair local flow regulation, causing hypoxia and tissue damage leading to organ failure. Therapeutic measures targeted to systemic parameters may not address or may even worsen tissue oxygenation at the microvascular level. Restoration of tissue oxygenation in critically ill patients may depend on restoration of endothelial cell function, including conducted responses.

中文翻译：

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微血管流量调节受损对代谢-灌注匹配和器官功能的影响

组织供氧受损是危重患者器官损伤和衰竭的主要原因，即使在包括心输出量和动脉血红蛋白饱和度在内的全身参数接近正常时也会发生这种情况。这篇综述讨论了微循环尺度的氧气转运机制，以及尽管有足够的对流氧气供应，缺氧如何发生。微循环的结构本质上是异质的，血管直径和流动路径长度变化很大，因此血流速度和氧气水平也有很大变化。结构适应和流量调节的动态过程不断调整微血管直径以补偿异质性，根据代谢需要重新分配流量以确保足够的组织氧合。传导反应在流量调节中起关键作用，传导反应由内皮细胞产生和传播，并向上游小动脉发出信号以响应局部缺氧而扩张。几种病理生理状况会损害局部流量调节，导致缺氧和组织损伤，导致器官衰竭。针对全身参数的治疗措施可能无法解决甚至可能恶化微血管水平的组织氧合。危重患者组织氧合的恢复可能取决于内皮细胞功能的恢复，包括传导反应。造成缺氧和组织损伤，导致器官衰竭。针对全身参数的治疗措施可能无法解决甚至可能恶化微血管水平的组织氧合。危重患者组织氧合的恢复可能取决于内皮细胞功能的恢复，包括传导反应。造成缺氧和组织损伤，导致器官衰竭。针对全身参数的治疗措施可能无法解决甚至可能恶化微血管水平的组织氧合。危重患者组织氧合的恢复可能取决于内皮细胞功能的恢复，包括传导反应。