Cain S M
Clin Chest Med. 1983 May;4(2):139-48.
Peripheral O2 uptake is mandated to subserve the energy requirements of tissue and organ systems in an obligatory aerobe such as the human. In addition to this basic need, local O2 demand may also be increased by more general bodily conditions such as fever, increased catecholamine levels, or alkalosis. Blood flow, which brings O2 to the periphery, is closely regulated at the local level to meet O2 demand except where other functional requirements, such as filtering by the kidney, may intervene. In addition to regulation of total flow at the tissue level, the distribution of flow at the microcirculatory level is another important regulatory feature because it determines the capillary surface area available to extract O2. Dominant vasoconstrictor tone is modulated at the local level by a metabolically linked substance such as adenosine or possibly by a direct effect of PO2 on the microvasculature. The precapillary vessels that control distribution are more sensitive to local hypoxia than are the resistance vessels so that blood flow redistribution is a first-line defense. The total blood flow response is made more sensitive by activity of beta-adrenergic vasodilator receptors which are active in this counterpoised system of local blood flow control. Disruption of the microvasculature, such as by microembolization, makes O2 uptake more dependent upon O2 supply than is normally the case. This event is accompanied by a loss of autoregulatory ability. In view of the myriad potential effectors on microvascular smooth muscle, the true wonder is that blood flow and O2 delivery generally are so strongly meshed with O2 uptake at every level of functional organization in the body. It would hardly be surprising, then, if disruption in one part of the system, such as the pulmonary circulation, had a counterpart in the peripheral circulation. This was alluded to in the possible association of O2 supply dependency in the periphery and severe ventilation-perfusion abnormality in the lung during ARDS. It reminds us that deranged processes that are revealed by relatively routine measurements may not be restricted to a single target organ.
在像人类这样的 obligatory aerobe 中,外周氧摄取必须满足组织和器官系统的能量需求。除了这种基本需求外,诸如发热、儿茶酚胺水平升高或碱中毒等更普遍的身体状况也可能增加局部氧需求。将氧气输送到外周的血流在局部水平受到密切调节,以满足氧需求,除非其他功能需求(如肾脏过滤)可能会干预。除了在组织水平调节总血流量外,微循环水平的血流分布是另一个重要的调节特征,因为它决定了可用于提取氧气的毛细血管表面积。优势血管收缩张力在局部水平由诸如腺苷等代谢相关物质调节,或者可能由氧分压对微血管的直接作用调节。控制分布的毛细血管前血管比阻力血管对局部缺氧更敏感,因此血流再分布是一线防御。β-肾上腺素能血管舒张受体的活性使总血流反应更敏感,该受体在这种局部血流控制系统中起作用。微血管的破坏,如微栓塞,使氧摄取比正常情况更依赖于氧供应。这一事件伴随着自动调节能力的丧失。鉴于对微血管平滑肌有无数潜在的效应器,真正奇妙的是,在身体功能组织的每个层面,血流和氧输送通常都与氧摄取紧密匹配。那么,如果系统的一部分(如肺循环)出现紊乱,在外周循环中也有相应表现,这就不足为奇了。这在成人呼吸窘迫综合征期间外周氧供应依赖性与肺部严重通气-灌注异常的可能关联中有所提及。它提醒我们,通过相对常规测量揭示的紊乱过程可能不限于单个靶器官。