Oxidant injury occurs rapidly after cardiac arrest, cardiopulmonary resuscitation, and reperfusion.

Abstract

Investigations conducted in cellular models show that reperfusion of ischemic tissue is associated with a burst of reactive oxidant species within minutes after reperfusion. Oxidant injury may play a role in the poor outcome typical of people resuscitated from cardiac arrest. The objective of the present study was to determine the presence and timing of oxidant injury in an in vivo model of cardiac arrest. Randomized controlled. University medical center laboratory. Domestic swine. We evaluated oxidant injury during and after 8 mins of cardiac arrest using a gas chromatography/mass spectrometry F2-isoprostane assay and compared these results with a matched control group. Baseline mean arterial, venous, and brain tissue F2-isoprostane levels were not significantly different when the cardiac arrest group was compared with the control group. However, in the group subjected to cardiac arrest and cardiopulmonary resuscitation we found significant (p < .0006) two- to three-fold increases in venous and arterial F2-isoprostane levels, which peaked between 15 and 30 mins after reperfusion and returned to baseline within 90 mins (p < .0006). Overall mean (+/- SE) brain tissue F2-isoprostane levels increased significantly to 370 +/- 60 vs. 140 +/- 60 ng/g tissue in the cardiac arrest group compared with the control group (p = .026). This study shows that F2-isoprostane measurement could be used to assess oxidant injury in an animal model of cardiac arrest and that oxidant injury occurs rapidly after cardiac arrest and reperfusion.