Abstract W P208: Treatment of Sodium Hydrogen Sulfide With Normothermia Reduces Neuronal Damage in the Striatum After Cardiac Arrest in Mice
Hydrogen sulfide donor, sodium hydrogen sulfide (NaHS), can induce hypothermia and attenuates ischemia reperfusion injury. The cerebroprotective mechanism of sulfide remains unclear. In order to exclude the hypothermic effect of sulfide, this study was designed to test whether NaHS treatment in mice after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR), followed by maintaining forced normothermia improved outcomes.
Methods: Adult male mice (20-26 g) were subjected to CA induced by intravenous KCL. After 8 min of CA, CPR was initiated with intravenous epinephrine, ventilation with 100% oxygen and chest compressions (rate 300/min). Mice were randomly assigned to 4 groups. In the normothermia group, mice were treated with either NaHS (3mg/kg) (n=20) or vehicle (n=19) intraperitoneally at 1 hr after CPR, then kept their head temperature above 35.0°C using a heating pad for 6 hr. In the hypothermia group, mice were treated with either NaHS (3mg/kg) (n=16) or vehicle (n=16) and kept at room temperature (26.0°C). Four days after CA/CPR, neurobehavioral assessments were performed and brains were removed for histological evaluation of neurons in the CA1 hippocampal region and the striatum.
Results: Head temperature decreased in the hypothermia groups after CPR. The mean head temperature at 6 hr after CPR in the hypothermia group was significantly lower in mice with NaHS compared to mice with vehicle (NaHS: 31.7 ± 2.4°C vs vehicle 34.0 ± 2.4°C). In the hypothermia group, neuronal injury in the striatum was small and similar between mice with NaHS and mice with vehicle (NaHS: 14 ± 10% vs vehicle: 20 ± 12%). In the normothermia group, injured neurons of the striatum was significantly less in mice with NaHS compared to mice with vehicle (NaHS: 22 ± 7% vs vehicle: 35 ± 22%, P<0.05). No difference was found in the CA1 region among all groups. Data are expressed as mean±SD.
Conclusions: In our mouse model of CA/CPR, CA induced spontaneous hypothermic response, which was enhanced by NaHS treatment. When the head temperature was kept constant, NaHS exerted neuroprotective effect in the striatum after CPR.
Author Disclosures: S. Nakayama: None. N. Taguchi: None. M. Tanaka: None.
- © 2014 by American Heart Association, Inc.