Regional lung strain and the metabolic signature of injury*.
Regional lung strain and the metabolic signature of injury*.
复制标题
局部肺应变和损伤的代谢特征*。
DOI：
10.1097/ccm.0000000000000383
复制
发表时间：
2014
影响因子：
8.8
通讯作者：
Hubmayr,RolfD
中科院分区：
文献类型：
--
作者：
Hubmayr,RolfD
Editorials1746 www. ccmjournal. org July 2014• Volume 42• Number 7 appear preferentially strained during breathing even though a nondependent region with a much larger alveolar FRC might have received the same volume of inspired gas. Furthermore, the two regions may not have experienced identical stresses, in part because the two regions differ with respect to prestress (the local transpulmonary pressure at FRC) and because the stress/strain relationship of lung parenchyma is nonlinear over the physiologic volume range. These observations and arguments are intended as cautionary note against the assumption that there is a single strain threshold, which forecasts the risk of biotrauma. This uncertainty exists, because in the intact chest local deformations cannot be referenced to the unstressed dimensions of the tissue network. Referencing ventilation to alveolar volume at total lung capacity (TLC) could in theory minimize the confounding influence of lung distortion, because the maximally stressed lung is uniformly expanded at TLC. The uncertainty about the existence of a unique straininjury threshold begs the question how macrostrain at the level of a single acinus relates to the known cell and molecular injury mechanisms thought to operate in affected lungs (13). Large alveolar volume excursions are certain to stress surfactant kinetics and may thereby mediate local flooding, tissue distortion, and generate interfacial stress of sufficient magnitude to wound adjacent airway and alveolar epithelial cells. Large parenchymal deformations are also certain to raise the tensile stress of alveolar walls, of the connective tissue matrix, and of cell-cell and cell-matrix contacts and can thereby trigger the release of bioactive molecules. in that context, it should be noted that inflation of the lungs to high pressures and volumes activated proinflammatory mechanotransduction responses only when accompanied by large tissue strains. This is consistent with numerous prior reports on the lung protective effects of PEEP dating back as far as 1974 to the classic experiments by Webb and Tierney (14).One of the hallmarks of ARDS in humans is the apparent flooding and collapse of dependent diaphragm apposed lung regions. The cyclic recruitment and derecruitment of neighboring unstable units is considered a major contributing factor in the evolution of the biotrauma syndrome. Of note, large tidal ventilation when limited to several hours in otherwise normal sheep was not associated with appreciable accumulation of interstitial or alveolar edema. it is therefore not entirely clear, if so-called opening and collapse contributed to the injury phenotype described by Wellman et al (11). For the same reason, we can only speculate if the mechanism by which
DOI：
10.1186/cc10034
发表时间：
2011
期刊：
Critical care (London, England)
影响因子：
--
作者：
Mattingley JS;Holets SR;Oeckler RA;Stroetz RW;Buck CF;Hubmayr RD
通讯作者：
Hubmayr RD
影响因子：
3.3
作者：
MEAD, J;TAKISHIMA, T;LEITH, D
通讯作者：
LEITH, D