CIBER de Enfermedades Respiratorias, Instituto de Salud Carlos III, Barranco de la Ballena s/n, Las Palmas de Gran Canaria, Spain.
Minerva Anestesiol. 2011 Jun;77(6):647-53.
Unequivocal evidence from both experimental and clinical research has shown that mechanical ventilation can damage the lungs and initiate an inflammatory response, possibly contributing to extrapulmonary organ dysfunction. This type of injury, referred to as ventilator-induced lung injury (VILI), resembles the syndromes of acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). VILI can trigger a complex array of inflammatory mediators, resulting in a local and systemic inflammatory response. Substances produced in the lungs can be translocated into the systemic circulation as a result of injury to the pulmonary epithelium and to the capillary endothelium. This type of injury forms the basis for the use of low tidal volumes (5-7 mL/kg of predicted body weight) during mechanical ventilation of patients with ALI/ARDS. The recognition of VILI has prompted a number of investigators to suggest that ALI/ARDS may be, in part, a product of our efforts to mechanically ventilate patients rather than the progression of the underlying disease. On the other hand, current scientific evidence supports a link between VILI and the development of extrapulmonary organ dysfunction, similar to how most severe cases of sepsis are clinically manifested. In addition, functional genomics approaches using a gene array methodology to measure lung gene expression have identified differential patterns of gene expression in animal models of VILI, similar to those gene pathways activated during experimental and clinical sepsis. In this line of thought, we hypothesize that injurious mechanical ventilation could be responsible for the perpetuation and worsening of sepsis in some patients and for the development of a sepsis-like syndrome in others.
明确的实验和临床研究证据表明，机械通气会损伤肺部并引发炎症反应，可能导致肺外器官功能障碍。这种损伤称为呼吸机相关性肺损伤（VILI），类似于急性肺损伤（ALI）和急性呼吸窘迫综合征（ARDS）的综合征。VILI 可以触发一系列复杂的炎症介质，导致局部和全身炎症反应。由于肺上皮和毛细血管内皮的损伤，肺部产生的物质可能转移到体循环中。这种损伤形式是在机械通气治疗 ALI/ARDS 患者时使用小潮气量（5-7ml/kg 预测体重）的基础。对 VILI 的认识促使许多研究人员提出，ALI/ARDS 可能部分是我们机械通气治疗患者的结果，而不是潜在疾病的进展。另一方面，目前的科学证据支持 VILI 与肺外器官功能障碍的发展之间存在联系，类似于大多数严重脓毒症的临床表现。此外，使用基因阵列方法测量肺基因表达的功能基因组学方法在 VILI 的动物模型中识别出了基因表达的差异模式，类似于在实验和临床脓毒症中激活的基因途径。基于这一思路，我们假设，损伤性机械通气可能是导致某些患者脓毒症持续和恶化以及其他患者发生类似脓毒症综合征的原因。
