Chest
Postgraduate Education Corner: Contemporary Reviews in Critical Care MedicinePathogenetic Significance of Biological Markers of Ventilator-Associated Lung Injury in Experimental and Clinical Studies
Section snippets
Biologic Markers of Inflammation in Clinical Studies
The role of the innate immune response and inflammation in the pathogenesis of VILI has been widely studied in recent years. Although some have suggested that inflammation may not be integral to the initiation of VILI, clearly a preponderance of data in this field support a major pathogenetic role for inflammation and lung neutrophil recruitment. The majority of biological markers identified in plasma, serum, pulmonary edema fluid, and BAL fluid in experimental studies are cytokines and
Experimental Studies of Ventilator-Attributable Injury
In an effort to understand and extend data from clinical trials, many investigators have attempted to model ventilator-attributable injury under more controlled experimental conditions. One of the most commonly used models is the VILI model in which normal lungs are injured with overtly harmful high or low lung volumes. Others have attempted to model the effects of more physiologic ventilator settings on previously injured lungs. This type of model, termed VALI, may more directly mimic the
Clinical Implications
Measurement of biological markers in experimental and clinical studies has provided insight into the pathogenesis of VALI. Both clinical and experimental data have characterized VALI as a condition of ongoing lung inflammation resulting from overdistention of the lung and potentially from excessively low lung volume. Although experimental studies have not been entirely concordant with clinical studies, there are several remarkable similarities. Temporal changes in plasma levels of IL-6, IL-8,
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Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).
The authors have no conflicts of interest to disclose.
This work was supported by National Institutes of Health grants HL69900 (Dr. Frank) and HL51856 (Dr. Matthay).