| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5998641 | Resuscitation | 2014 | 7 Pages |
PurposeArgon at a dosage of 70% is neuroprotective when given 1Â h after cardiac arrest (CA) in rats. In a rodent model, we investigated if the neuroprotective effects of argon are dose dependent and mediated by adenosine triphosphate dependent potassium (KATP) channels.MethodsForty-seven male Sprague-Dawley rats were subjected to 7Â min of CA and 3Â min of cardiopulmonary resuscitation (CPR). In protocol I animals were randomized to receive either 70% or 40% argon ventilation 1Â h after successful CPR or no argon-treatment. Animals of the second protocol also received 1Â h of 70% argon ventilation or no argon treatment but were randomized to a group receiving the KATP channel blocker 5-hydroxydecanoate (5-HD). For all animals a neurological deficit score (NDS) was calculated daily for seven days following the experiment before the animals were killed and the brains harvested for histopathological analyses.ResultsAll animals survived. Control animals exhibited severe neurologic dysfunction at all points in time as measured with the NDS. Argon treated animals showed significant improvements in the NDS through all postoperative days in a dose dependent fashion. This was paralleled by a significant reduction in the neuronal damage index in the neocortex and the hippocampal CA 3/4 region. Administration of 5-HD neither abolished the positive effects on functional recovery nor on histopathologic changes observed in the argon group.ConclusionOur study demonstrates a dose dependent neuroprotective effect of argon administration in this rodent model, which is not mediated via ATP dependent potassium channels.
