Therapeutic hypothermia attenuates physiologic, histologic, and metabolomic markers of injury in a porcine model of acute respiratory distress syndrome. Issue 9 (4th May 2022)

• Record Type: Journal Article
• Authors: Angus, Sarah A.; Henderson, William R.; Banoei, Mohammad M.; Molgat‐Seon, Yannick; Peters, Carli M.; Parmar, Hanna R.; Griesdale, Donald E. G.; Sekhon, Mypinder; Sheel, Andrew William; Winston, Brent W.; Dominelli, Paolo B.
• Is Part Of: Physiological reports. Volume 10:Issue 9(2022)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-05-04
• Subjects: hemodynamics -- inflammation -- lung injury -- respiratory mechanics; Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.15286
• Languages: English
• ISSNs: 2051-817X

Abstract

Abstract: Acute respiratory distress syndrome (ARDS) is a lung injury characterized by noncardiogenic pulmonary edema and hypoxic respiratory failure. The purpose of this study was to investigate the effects of therapeutic hypothermia on short‐term experimental ARDS. Twenty adult female Yorkshire pigs were divided into four groups ( n = 5 each): normothermic control (C), normothermic injured (I), hypothermic control (HC), and hypothermic injured (HI). Acute respiratory distress syndrome was induced experimentally via intrapulmonary injection of oleic acid. Target core temperature was achieved in the HI group within 1 h of injury induction. Cardiorespiratory, histologic, cytokine, and metabolomic data were collected on all animals prior to and following injury/sham. All data were collected for approximately 12 h from the beginning of the study until euthanasia. Therapeutic hypothermia reduced injury in the HI compared to the I group (histological injury score = 0.51 ± 0.18 vs. 0.76 ± 0.06; p = 0.02) with no change in gas exchange. All groups expressed distinct phenotypes, with a reduction in pro‐inflammatory metabolites, an increase in anti‐inflammatory metabolites, and a reduction in inflammatory cytokines observed in the HI group compared to the I group. Changes to respiratory system mechanics in the injured groups were due to increases in lung elastance (E) and resistance (R) (ΔE from pre‐injury = 46 ± 14 cmH2 O L −1, p < 0.0001; ΔR from pre‐injury: 3 ± 2 cmH2 O L −1 s −, p = 0.30) rather than changes to the chest wall (ΔE from pre‐injury: 0.7 ± 1.6 cmH2 O L −1, p = 0.99; ΔR from pre‐injury: 0.6 ± 0.1 cmH2 O L −1 s −, p = 0.01). Both control groups had no change in respiratory mechanics. In conclusion, therapeutic hypothermia can reduce markers of injury and inflammation associated with experimentally induced short‐term ARDS. Abstract : We sought to determine if therapeutic hypothermia was effective at reducing injury and inflammation in a porcine model of acute respiratory distress syndrome. Injury score was determined by the presence of alveolar fibrin deposition, alveolar inflammatory cell infiltration, and interstitial and intra‐alveolar edema. Injury score was significantly lower in the hypothermic injured group relative to the normothermic injured group.