Abstract 90: Histopathological Lesions in the Hippocampal CA1 Region After 6 and 8 Minutes of Cardiac Arrest in Rats
Introduction: Neuropathological damage in selectively vulnerable brain regions is an important outcome parameter in rodent models of ventricular fibrillation cardiac arrest (CA).
Hypothesis: Different durations of cardiac arrest influence the extent of neuronal loss and glial reaction in the cornu ammonis (CA1) region of the hippocampus.
Materials and Methods: CA was induced in male Sprague-Dawley rats, for 6 (n=7) or 8 min (n=6), 4 shams were included. Chest compressions, ventilation, drugs, and defibrillation were performed until return of spontaneous circulation (ROSC) was achieved. At day 14 animals were sacrificed. Brains were perfusion-fixed, embedded in paraffin and cut into 5 μm thick sections for histological evaluation. Viable neurons were counted in a 500 μm sector of CA1 in Nissl-stained sections. Immunohistochemistry was used to assess astrocyte and microglial activation semi-quantitatively with antibodies against GFAP and Iba1, respectively.
Results: In Nissl-staining the sham group had 79±4 viable neurons. The 8 min group showed significantly less viable neurons (37±10; p<0,001) and in the 6 min group there was a strong tendency (56±24; p=0,052) to less viable neurons. Furthermore, we detected a tendency to less viable neurons in the 8 min group compared to the 6 min group (p=0.085). Immunohistochemistry showed a statistically significant increase in staining intensity in astrocytes (6 min: 2±0.5; 8 min: 3±1; sham: 0±0) and microglia (6min: 3±0.5; 8 min: 4±1; sham: 0±0) in both CA groups. However, no significant differences were detectable between 6 min and 8 min group.
Conclusion: Both CA durations produced consistent histological damage with loss of viable neurons, but the 8 min group showed more homogeneous results. Unexpectedly, the duration of CA was of no consequence for the level of glial activation. That suggests a similar glial reaction after neuronal loss regardless of its extent.
Author Disclosures: U. Teubenbacher: None. W. Weihs: None. F. Ettl: None. I. Magnet: None. P. Kodajova: None. D. Grassmann: None. M. Wagner: None. A. Schober: None. A. Warenits: None. C. Testori: None. A. Janata: Research Grant; Modest; Austrian Science Foundation P24824. F. Sterz: None. S. Högler: None.
- © 2014 by American Heart Association, Inc.