Department of Anaesthesia, Clinical Science Institute, National University of Ireland-Galway, Galway, Ireland.
Anesthesiology. 2010 Feb;112(2):462-72. doi: 10.1097/ALN.0b013e3181ca361f.
Acute respiratory distress syndrome is a devastating disease that causes substantial morbidity and mortality. Mechanical ventilation can worsen lung injury, whereas ventilatory strategies that reduce lung stretch, resulting in a "permissive" hypercapnic acidosis (HCA), improve outcome. HCA directly reduces nonsepsis-induced lung injury in preclinical models and, therefore, has therapeutic potential in these patients. These beneficial effects are mediated via inhibition of the host immune response, particularly cytokine signaling, phagocyte function, and the adaptive immune response. Of concern, these immunosuppressive effects of HCA may hinder the host response to microbial infection. Recent studies suggest that HCA is protective in the earlier phases of bacterial pneumonia-induced sepsis but may worsen injury in the setting of prolonged lung sepsis. In contrast, HCA is protective in preclinical models of early and prolonged systemic sepsis. Buffering of the HCA is not beneficial and may worsen pneumonia-induced injury.
急性呼吸窘迫综合征是一种严重的疾病，可导致较高的发病率和死亡率。机械通气可加重肺损伤，而减少肺牵张的通气策略可导致“允许性”高碳酸血症（HCA），从而改善预后。HCA 在临床前模型中直接减轻非脓毒症引起的肺损伤，因此在这些患者中具有治疗潜力。这些有益的影响是通过抑制宿主免疫反应介导的，特别是细胞因子信号、吞噬细胞功能和适应性免疫反应。值得关注的是，HCA 的这种免疫抑制作用可能会阻碍宿主对微生物感染的反应。最近的研究表明，HCA 在细菌性肺炎引起的脓毒症早期阶段具有保护作用，但在长时间肺部感染时可能会加重损伤。相比之下，HCA 在早期和长时间全身性脓毒症的临床前模型中具有保护作用。HCA 的缓冲没有益处，反而可能加重肺炎引起的损伤。
