Purpose: Cardiac arrest and resuscitation produce global cerebral ischemia and reperfusion injury to the brain, which lead to high mortality and delayed neuronal death. Adenosine has been suggested as an endogenous neuroprotective molecule, acting thr...
Purpose: Cardiac arrest and resuscitation produce global cerebral ischemia and reperfusion injury to the brain, which lead to high mortality and delayed neuronal death. Adenosine has been suggested as an endogenous neuroprotective molecule, acting through multiple potential mechanisms. We investigated the possible neuroprotective effects of adenosine on cerebral recovery following global ischemia induced by asphyxial cardiac arrest.
Methods: Twenty-four rats were randomized into three groups. Group Ⅰ,Ⅱ and Ⅲ had anesthesia, procedures, and asphyxia for 7 minutes and then survived to 72 hours. Group Ⅰ(n=8) was not administered N^6-L-phenylisopropyl adenosine(L-PIA). Group Ⅱ(n=8) was administered L-PIA(0.8 mg/kg), and group Ⅲ(n=8) was administered L-PIA (1.5 mg/kg), after spontaneous circulation. The dose-dependent neuroprotective effects of L-PIA were compared to the control by using a histopathological method.
Results: Histological observations of CA1 showed a more significant reduction of neuronal cell loss in groups Ⅱ and Ⅲ than in group I(p<0.05).
Histological observations of CA2 and CA3 didn't show a significant reduction of neuronal cell loss in groups Ⅱ and Ⅲ compared to group Ⅰ.
Conclusion: These results show that post-ischemic administration of adenosine protected against delayed neuronal damage in the hippocampal CA1 area following a 7-min asphyxial cardiac arrest in rats.