Abstract 88: Delayed Administration of Argon Reduces Ischemic Brain Damage and Preserves Functional Recovery After Cardiac Arrest in Rats

Abstract

Introduction: Argon is neuroprotective when given 1 hour after cardiac arrest (CA) in rats. Here, we investigated if a delayed administration of argon would also reduce neurologic dysfunction. Material and Methods: 18 male Sprague-Dawley rats were subjected to 7 mins of CA and 3 mins of cardiopulmonary resuscitation (CPR). Three hours after successful CPR, animals were randomized to ventilation with 70% argon for 1h in comparison to untreated controls receiving 70% nitrogen. A neurologic deficit score (NDS) was calculated on seven days following the experiment before the animals were killed and the brains harvested for histopathological analyses. Neuronal damage was semiquantitatively assessed by determining the proportion of neuronal cells showing shrunken and/or hypereosinophilic cytoplasm (HE staining) in combination with a loss of nuclear NeuN-immunoreactivity. Results: All animals survived. Untreated controls exhibited severe neurologic dysfunction while animals from the argon group showed significant improvements in the NDS at all points in time (Fig.1). This was paralleled by a significant reduction in the degree of ischemic brain damage in the neocortex, the basal ganglia and the hippocampal CA 3/4 region (Fig.2). Conclusions: Our study demonstrates that a one hour application of 70% argon, even when treatment was delayed for 3 hours after CA, provided a significant reduction in histopathological damage of the neocortex, basal ganglia and hippocampus which was associated with a marked improvement in functional neurologic recovery.