Oximetry-Guided normoxic resuscitation following canine cardiac arrest reduces cerebellar Purkinje neuronal damage

Background: Animal studies indicate that maintaining physiologic O-2 levels (normoxia) immediately after restoration of spontaneous circulation (ROSC) from cardiac arrest (CA) results in less hippocampal neuronal death compared to animals ventilated with 100% O-2. This study tested the hypothesis that beneficial effects of avoiding hyperoxia following CA are apparent in the cerebellum and therefore not limited to one brain region. Methods: Adult beagles were anesthetized and mechanically ventilated. Ventricular fibrillation CA was induced by electrical myocardial stimulation and cessation of ventilation. Ten min later, dogs were ventilated with 100% O-2 and resuscitated using 3 min of open chest CPR followed by defibrillation. Dogs were ventilated for 1 h with either 100% O-2 or with O-2 titrated rapidly to maintain hemoglobin O-2 saturation at 94-96%. FiO(2) was adjusted in both groups between one and 24 h post-arrest to maintain normoxic PaO2 of 80-120 mm Hg. Following 24 h critical care, dogs were euthanized and cerebellum analyzed for histochemical measures of neuronal damage and inflammation. Results and Conclusions: Hyperoxic resuscitation increased the number of injured Purkinje cells by 278% and the number of activated microglia/macrophages by 18% compared to normoxic resuscitation. These results indicate that normoxic resuscitation promotes favorable histopathologic outcomes in the cerebellum (in addition to hippocampus) following CA/ROSC. These findings emphasize the importance of avoiding unnecessary hyperoxia following CA/ROSC.