Normoxic ventilation after cardiac arrest reduces oxidation of brain lipids and improves neurological outcome

• Published in: Stroke (1970) 1998-08, Vol.29 (8), p.1679-1686
• Main Authors: Liu, Y, Rosenthal, R E, Haywood, Y, Miljkovic-Lolic, M, Vanderhoek, J Y, Fiskum, G
• Format: Article
• Language: English
• Subjects: Animals; Brain - blood supply; Brain - metabolism; Cardiac arrest; Cardiopulmonary Resuscitation; Cerebral Cortex - chemistry; Cerebral Cortex - metabolism; Chromatography, High Pressure Liquid; Corpus Striatum - chemistry; Corpus Striatum - metabolism; Dogs; Female; Heart Arrest - complications; Heart Arrest - metabolism; Heart Arrest - therapy; Hippocampus - chemistry; Hippocampus - metabolism; Ischemic Attack, Transient - etiology; Ischemic Attack, Transient - metabolism; Ischemic Attack, Transient - therapy; Lipid Metabolism; Mass Spectrometry; Oxidation-Reduction; Oxidative Stress - physiology; Oxygen Inhalation Therapy; Peroxides - analysis; Reperfusion Injury - etiology; Reperfusion Injury - metabolism; Reperfusion Injury - therapy; Treatment Outcome
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.str.29.8.1679

Increasing evidence that oxidative stress contributes to delayed neuronal death after global cerebral ischemia has led to reconsideration of the prolonged use of 100% ventilatory O2 following resuscitation from cardiac arrest. This study determined the temporal course of oxidation of brain fatty acyl groups in a clinically relevant canine model of cardiac arrest and resuscitation and tested the hypothesis that postischemic ventilation with 21% inspired O2, rather than 100% O2, results in reduced levels of oxidized brain lipids and decreased neurological impairment. Neurological deficit scoring and high performance liquid chromatography measurement of fatty acyl lipid oxidation were used in an established canine model using 10 minutes of cardiac arrest followed by resuscitation with different ventilatory oxygenation protocols and restoration of spontaneous circulation for 30 minutes to 24 hours. Significant increases in frontal cortex lipid oxidation occurred after 10 minutes of cardiac arrest alone with no reperfusion and after reperfusion for 30 minutes, 2 hours, and 24 hours (relative total 235-nm absorbing peak areas=7.1+/-0.7 SE, 17.3+/-2.7, 14.2+/-3.2, 16.1+/-1.0, and 14.0+/-0.8, respectively; n=4, P