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• Meeting abstract
• Results
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Meeting abstract

Cardiac arrest (CA) is often followed by postischemic-anoxic encephalopathy. A ventricular fibrillation CA model in dogs was used in this study to understand the effect of oxygen free radical (OFR) and lactate (LA) in the postischemic-anoxic encephalopathy, and to explore the effect and mechanism of mild hypothermia (32-36°C) induced immediately with reperfusion after cardiac arrest (resuscitation).

Results

(i) The SOD levels in blood and CSF after resuscitation were lower than those before CA (P < 0.01), the LPO and LA levels in blood and CSF were significantly higher than those before CA (P < 0.01). (ii) The SOD level in CSF in mild hypothermia group was higher than that in normothermia group (P < 0.05), the LPO level in CSF was significantly lower than that in normothermia (P < 0.01). But the LA level in CSF and the SOD, LPO and LA levels in blood were not significantly different between these two groups, (iii) The total brain histopathologic damage scores in mild hypothermia group were lower than those in normothermia group (P < 0.01).

Conclusions

(i) The OFR and LA have some important effect in postischemic-anoxic encephalopathy. (ii) Mild hypothermia induced immediately with reperfusion after CA may improve cerebral outcome. (iii) The mechanism of this beneficial effect may be to reduce the generation of OFR and to mitigate the lipid peroxidation induced by OFR.

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