{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T13:56:21Z","timestamp":1775483781949,"version":"3.50.1"},"reference-count":73,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2019,2,1]],"date-time":"2019-02-01T00:00:00Z","timestamp":1548979200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Low\u2013tidal volume (Vt) ventilation might protect healthy lungs from volutrauma but lead to inflammation resulting from other mechanisms, namely alveolar derecruitment and the ensuing alveolar collapse and tidal reexpansion. We hypothesized that the different mechanisms of low- and high-volume injury would be reflected in different mechanical properties being associated with development of pulmonary inflammation and mortality: an increase of hysteresis, reflecting progressive alveolar derecruitment, at low Vt; an increase of elastance, as a result of overdistension, at higher Vt. Mice were allocated to \u201cprotective\u201d (6 ml\/kg) or \u201cinjurious\u201d (15\u201320 ml\/kg) Vt groups and ventilated for 16 hours or until death. We measured elastance and hysteresis; pulmonary IL-6, IL-1\u03b2, and MIP-2 (macrophage inflammatory protein 2); wet-to-dry ratio; and blood gases. Survival was greater in the protective group (60%) than in the injurious group (25%). Nonsurvivors showed increased pulmonary cytokines, particularly in the injurious group, with the increase of elastance reflecting IL-6 concentration. Survivors instead showed only modest increases of cytokines, independent of Vt and unrelated to the increase of elastance. No single lung strain threshold could discriminate survivors from nonsurvivors. Hysteresis increased faster in the protective group, but, contrary to our hypothesis, its change was inversely related to the concentration of cytokines. In this model, significant mortality associated with pulmonary inflammation occurred even for strain values as low as about 0.8. Low Vt improved survival. The accompanying increase of hysteresis was not associated with greater inflammation.<\/jats:p>","DOI":"10.1165\/rcmb.2018-0100oc","type":"journal-article","created":{"date-parts":[[2018,9,10]],"date-time":"2018-09-10T18:16:46Z","timestamp":1536603406000},"page":"179-188","source":"Crossref","is-referenced-by-count":25,"title":["Relation between Respiratory Mechanics, Inflammation, and Survival in Experimental Mechanical Ventilation"],"prefix":"10.1093","volume":"60","author":[{"given":"Margit V.","family":"Szabari","sequence":"first","affiliation":[{"name":"Department of Anesthesia, Critical Care and Pain Medicine"},{"name":"Department of Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazue","family":"Takahashi","sequence":"additional","affiliation":[{"name":"Department of Radiology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Feng","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, Critical Care and Pain Medicine"},{"name":"Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph J.","family":"Locascio","sequence":"additional","affiliation":[{"name":"Department of Neurology, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Chao","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, Critical Care and Pain Medicine"},{"name":"Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edward A.","family":"Carter","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marcos F.","family":"Vidal Melo","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, Critical Care and Pain Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1170-8699","authenticated-orcid":false,"given":"Guido","family":"Musch","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, Critical Care and Pain Medicine"},{"name":"Department of Anesthesiology, Washington University in St. Louis, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2019,2,1]]},"reference":[{"key":"2026012222061002700_bib1","doi-asserted-by":"crossref","first-page":"1301","DOI":"10.1056\/NEJM200005043421801","article-title":"Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome","volume":"342","author":"Brower","year":"2000","journal-title":"N Engl J 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