Abstract 14775: Regional TNFα Mapping in the Brain reveals the Striatum as a Neuroinflammatory Target after Ventricular Fibrillation Cardiac Arrest in Rats
Background: Neuroinflammation contributes to delayed neuronal death after cardiac arrest (CA). In a rat model of ventricular fibrillation (VF) CA, we tested the hypothesis that brain regions are differentially affected by inflammation, as reflected by brain tissue levels of tumor necrosis factor (TNF)α.
Methods: Using isoflurane anesthesia, adult male rats were intubated, cannulated and randomized to 6 or 8 min of VF or sham (anesthesia and surgery only) group. Body temperature was maintained at 37.0°C. Resuscitation was performed with drugs (epinephrine, sodium bicarbonate), mechanical ventilation and manual chest compressions (200/min). 3h after restoration of spontaneous circulation, tissue samples of cortex, striatum, hippocampus and cerebellum were obtained for ELISA.
Results: TNFα levels are presented in the figure above. 6 and 8 min VF caused a significant increase in TNFα vs. sham in the cortex (p=0.028), cerebellum (p=.009) and striatum (p<0.001), but not in hippocampus (p=.23). There was no difference in TNFα levels between 6 and 8 min VF groups in any brain region. In the 6 and 8 min VF groups, TNFα levels were highest in the striatum (p=0.004, p<0.001, striatum vs. other brain regions). No regional differences could be detected in the sham group.
Conclusions: While the role of neuroinflammation after CA is not yet fully elucidated, our results show a distinct regional pattern of early TNFα production, with highest levels in the striatum. Inflammation in the striatum could be a novel target for antiinflammatory therapies. The source of TNFα and its role remains to be defined in future experiments.
- © 2010 by American Heart Association, Inc.