Cardiopulmonary-cerebral resuscitation with 100% oxygen exacerbates neurological dysfunction following nine minutes of normothermic cardiac arrest in dogs

Abstract

This study investigated the effects of normoxic (F IO 2 = 0.21), hyperoxic (F IO 2 = 1.0), and hyperoxic (F IO 2 = 1.0) plus antioxidant pretreatment (tirilizad mesylate) resuscitation on neurologic outcome following 9 min of normothermic (39 ± 1.0°C) cardiac arrest. Physiologic variables including arterial blood gases and neurologic outcome, which was assessed using a standardized scoring system, were followed over a 24-h period following resuscitation from cardiac arrest. Hyperoxically resuscitated dogs sustained significantly worse neurological deficit at 12 and 24 h (mean scores: 39 ± 3 and 49 ± 8, respectively) than did antioxidant pretreated hyperoxically resuscitated dogs (mean scores: 22 ± 1, P = 0.0007 and 22 ± 1, P = 0.004, respectively) and normoxically resuscitated dogs (mean scores: 28 ± 4, P = 0.025 and 33 ± 8, P = 0.041 respectively). These data suggest that oxidant injury has a major role in central nervous system dysfunction following successful resuscitation from 9 min of cardiac arrest. Also, resuscitation from cardiac arrest with hyperoxic F IO 2's may contribute to and further exacerbate neurologic dysfunction.