The effect of targeted hyperoxemia in a randomized controlled trial employing a long-term resuscitated, model of combined acute subdural hematoma and hemorrhagic shock in swine with coronary artery disease: An exploratory, hypothesis-generating study
Creators: name: Datzmann, Thomas
name: Messerer, David Alexander Christian
name: Münz, Franziska
name: Hoffmann, Andrea
name: Gröger, Michael
name: Mathieu, René
name: Mayer, Simon
name: Gässler, Holger
name: Zink, Fabian
name: McCook, Oscar
name: Merz, Tamara
name: Scheuerle, Angelika
name: Wolfschmitt, Eva-Maria
name: Thebrath, Timo
name: Zuech, Stefan
name: Calzia, Enrico
name: Asfar, Pierre
name: Radermacher, Peter
name: Kapapa, Thomas
Publisher: name: Universität Ulm
Year: 2022
Subjects: subject: traumatic brain injury
subject: multimodal brain monitoring
subject: GFAP
subject: MAP-2
subject: protein S100β
subject: neuron-specific enolase
subject: mitochondrial respiration
subject: hyperoxemia
subject: DDC 610 / Medicine &amp; health
subject: Brain injuries, Traumatic
subject: Shock, Hemorrhagic
subject: Hematoma, Subdural
subject: Oxidative stress
subject: Mitochondria; Metabolism
subject: Schädel-Hirn-Trauma
subject: Hämorrhagischer Schock
subject: Subdurales Hämatom
subject: Oxidativer Stress
subject: Mitochondrium
subject: Hyperoxie

description: Controversial evidence is available regarding suitable targets for the arterial O2 tension (PaO2) after traumatic brain injury and/or hemorrhagic shock (HS). We previously demonstrated that hyperoxia during resuscitation from hemorrhagic shock attenuated cardiac injury and renal dysfunction in swine with coronary artery disease. Therefore, this study investigated the impact of targeted hyperoxemia in a long-term, resuscitated model of combined acute subdural hematoma (ASDH)-induced brain injury and HS. The prospective randomized, controlled, resuscitated animal investigation consisted of 15 adult pigs. Combined ASDH plus HS was induced by injection of 0.1 ml/kg autologous blood into the subdural space followed by controlled passive removal of blood. Two hours later, resuscitation was initiated comprising re-transfusion of shed blood, fluids, continuous i.v. noradrenaline, and either hyperoxemia (target PaO2 200 – 250 mmHg) or normoxemia (target PaO2 80 – 120 mmHg) during the first 24 h of the total of 54 h of intensive care. Systemic hemodynamics, intracranial and cerebral perfusion pressures, parameters of brain microdialysis and blood biomarkers of brain injury did not significantly differ between the two groups. According to the experimental protocol, PaO2 was significantly higher in the hyperoxemia group at the end of the intervention period, i.e., at 24 h of resuscitation, which coincided with a higher brain tissue PO2. The latter persisted until the end of observation period. While neurological function as assessed using the veterinary Modified Glasgow Coma Score progressively deteriorated in the control group, it remained unaffected in the hyperoxemia animals, however, without significant intergroup difference. Survival times did not significantly differ in the hyperoxemia and control groups either. Despite being associated with higher brain tissue PO2 levels, which were sustained beyond the intervention period, targeted hyperoxemia exerted neither significantly beneficial nor deleterious effects after combined ASDH and HS in swine with pre-existing coronary artery disease. The unavailability of a power calculation and, thus, the limited number of animals included, are the limitations of the study.