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. 2018 May 24;22:136. doi: 10.1186/s13054-018-2051-8

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — A novel heterogeneous lung injury model in which the impact of any mechanical breath can be tested in both normal (“baby lung”) and the injured (acute respiratory distress syndrome (ARDS)) lung tissues. Heterogeneous injury was caused to very specific areas of lung tissue by instillation of Tween-20 via bronchoscopy into the dependent portion of the diaphragmatic lobe with the pig in the supine position. The remaining lung tissue not exposed to Tween-20 was normal. Following Tween-20 injury animals were split into two groups: either high dynamic strain (H_DS) caused by an extended expiratory duration or low dynamic strain (L_DS) with a very short expiratory duration. Both groups were exposed to over-distension (plateau airway pressure 40 cmH₂O). It is currently believed that high plateau airway pressures (≥ 30 cmH₂O) causes ventilator-induced lung injury (VILI) in a heterogeneous ARDS lung by over-distending (OD) the remaining normal tissue (i.e. the baby lung) [34]. The goal of the study was to identify if OD would cause VILI in the baby lung, if OD would exacerbate tissue damage in the Tween-20-injured lung tissue, and if dynamic strain played a role in lung tissue injury and/or protection. Gross Lung Photos: The top panel (a-d) shows the whole lung and the cut lung surface at necropsy. In the OD + L_DS group (a, c) the lung was prevented from collapsing at expiration by using a very short expiratory duration. In the OD + H_DS group (b, d) the lung was allowed to collapse during expiration by extending the expiratory duration. This study demonstrates that OD did not grossly injure the normal lung tissue, nor did it exacerbate injury in the tissue injured with Tween-20 (a, c), as long as the dynamic strain was minimal. The lung is uniformly inflated (top panel a) and the cut lung surface appears well-inflated without interlobular edema (top panel c). OD combined with H_DS (top panel b, d) exacerbated damage in the Tween-20-injured tissue and directly injured the baby lung. The lung showed marked atelectasis, extending into the normal lobes that were not exposed to Tween 20 (top panel b). The cut surface showed extensive atelectasis, interlobular edema (clear jelly-like substance between lobules), and significant airway water and edema foam in the airways (top panel d). This study demonstrates that OD + H_DS exacerbated injury to the Tween-20-damaged tissue and caused direct VILI injury to the normal tissue not exposed to Tween 20, whereas OD + L_DS caused no injury to the baby lung and did not exacerbate injury in the Tween-20-injured tissue. Lung Histology: The bottom panel shows representative histology staining in both the normal tissue (N_T) and the Tween-20-injured lung tissue (ALI_T) in both the OD + H_DS and OD + L_DS groups. OD + H_DS caused severe injury to the N_T and exacerbated injury in the ALI_T tissues. Arrows indicate infiltration of inflammatory white blood cells and the arrowhead identifies the presence of fibrin deposits in the airspace (i.e pulmonary edema). This pathology was not seen in the OD + L_DS group and the star shows the improved alveolar patency as compared with the OD + H_DS group. This study suggests that OD alone does not injury the baby lung unless combined with high dynamic strain [23]