Effect of Tempol on Cerebral Resuscitation Caused by Asphyxia-Induced Cardiac Arrest.
BACKGROUND
This study was conducted to investigate the effect and mechanism of the nitrogen oxide 4-hydroxy- 2,2,6,6-tetramethylpiperidine (Tempol) on cerebral resuscitation caused by asphyxia-induced cardiac arrest.


METHODS
Airway occlusion-induced asphyxia at the end of expiration was used to establish the rat cerebral ischaemia-hypoxia injury model. A total of 90 adult male Sprague-Dawley rats were randomly divided into the three groups. The Tempol and conventional cardiopulmonary resuscitation (CPR) groups were further divided into four subgroups according to different time points.


RESULTS
After cerebral ischaemia, independent heart rate following asphyxia appeared earlier, and the success rate of primary recovery and the neurological function score of rats were higher in the Tempol group than in the conventional CPR group. The serum neuron-specific enolase (NSE) levels in the Tempol and conventional CPR groups were significantly higher within 6 to 48 h than that in the blank control group. The serum NSE level was significantly lower in the Tempol group than the conventional CPR group.


CONCLUSIONS
After global cerebral ischaemia-hypoxia, the antioxidant Tempol improved cerebral resuscitation by reducing oxidative stress injuries and post-CPR cerebral damage. The NSE level can be used as an early detection index in the diagnosis of global cerebral ischaemia-hypoxia injuries.


BACKGROUND
Cerebral ischemia; Neuron-specific enolase; Rats; Tempol.
Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province;
Dan
D
Bai
Departments of Respiratory Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, Hubei Province, China.
Xiaofeng
X
Wu
Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province;
Lingxin
L
Meng