Cardiac Effects of Hyperoxia During Resuscitation From Hemorrhagic Shock in Swine.


Journal

Shock (Augusta, Ga.)
ISSN: 1540-0514
Titre abrégé: Shock
Pays: United States
ID NLM: 9421564

Informations de publication

Date de publication:
10 2019
Historique:
pubmed: 9 11 2018
medline: 24 7 2020
entrez: 9 11 2018
Statut: ppublish

Résumé

Hyperoxia (ventilation with FIO2 = 1.0) has vasoconstrictor properties, in particular in the coronary vascular bed, and, hence, may promote cardiac dysfunction. However, we previously showed that hyperoxia attenuated myocardial injury during resuscitation from hemorrhage in swine with coronary artery disease. Therefore, we tested the hypothesis whether hyperoxia would also mitigate myocardial injury and improve heart function in the absence of chronic cardiovascular comorbidity.After 3 h of hemorrhage (removal of 30% of the calculated blood volume and subsequent titration of mean arterial pressure to 40 mm Hg) 19 anesthetized, mechanically ventilated, and instrumented pigs received FIO2 = 0.3(control) or hyperoxia(FIO2 = 1.0) during the first 24 h. Before, at the end of and every 12 h after shock, hemodynamics, blood gases, metabolism, cytokines, and cardiac function (pulmonary artery thermodilution, left ventricular pressure-conductance catheterization) were recorded. At 48 h, cardiac tissue was harvested for western blotting, immunohistochemistry, and mitochondrial respiration.Except for higher left ventricular end-diastolic pressures at 24 h (hyperoxia 21 (17;24), control 17 (15;18) mm Hg; P = 0.046), hyperoxia affected neither left ventricular function cardiac injury (max. Troponin I at 12 h: hyperoxia:9 (6;23), control:17 (11;24) ng mL; P = 0.395), nor plasma cytokines (except for interleukin-1β: hyperoxia 10 (10;10) and 10 (10;10)/control 14 (10;22), 12 (10;15) pg mL, P = 0.023 and 0.021 at 12 and 24 h, respectively), oxidation and nitrosative stress, and mitochondrial respiration. However, hyperoxia decreased cardiac tissue three-nitrotyrosine formation (P < 0.001) and inducible nitric oxide synthase expression (P = 0.016). Ultimately, survival did not differ significantly either.In conclusion, in contrast to our previous study in swine with coronary artery disease, hyperoxia did not beneficially affect cardiac function or tissue injury in healthy swine, but was devoid of deleterious side effects.

Identifiants

pubmed: 30407373
doi: 10.1097/SHK.0000000000001283
doi:

Substances chimiques

3-nitrotyrosine 3604-79-3
Tyrosine 42HK56048U
Nitric Oxide Synthase Type II EC 1.14.13.39

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e52-e59

Auteurs

Thomas Datzmann (T)

Institute of Anesthesiological Pathophysiology and Process Engineering.
Department of Anesthesiology, University Hospital Ulm, Ulm, Germany.

Martin Wepler (M)

Institute of Anesthesiological Pathophysiology and Process Engineering.
Department of Anesthesiology, University Hospital Ulm, Ulm, Germany.

Ulrich Wachter (U)

Institute of Anesthesiological Pathophysiology and Process Engineering.

Josef A Vogt (JA)

Institute of Anesthesiological Pathophysiology and Process Engineering.

Oscar McCook (O)

Institute of Anesthesiological Pathophysiology and Process Engineering.

Tamara Merz (T)

Institute of Anesthesiological Pathophysiology and Process Engineering.

Enrico Calzia (E)

Institute of Anesthesiological Pathophysiology and Process Engineering.

Michael Gröger (M)

Institute of Anesthesiological Pathophysiology and Process Engineering.

Clair Hartmann (C)

Institute of Anesthesiological Pathophysiology and Process Engineering.
Department of Anesthesiology, University Hospital Ulm, Ulm, Germany.

Pierre Asfar (P)

CNRS UMR 6214, INSERM U1083, Université Angers.
Département de Réanimation Médicale et de Médecine Hyperbare, Centre Hospitalier Universitaire, Angers, France.

Peter Radermacher (P)

Institute of Anesthesiological Pathophysiology and Process Engineering.

Benedikt Lukas Nussbaum (BL)

Institute of Anesthesiological Pathophysiology and Process Engineering.
Department of Anesthesiology, University Hospital Ulm, Ulm, Germany.

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