Intracerebral hemorrhage (ICH) is the stroke subtype with the highest mortality and morbidity with 25% of patients dying within the first 48 h and a high incidence of poor outcomes. Because of high early mortality rates, an understanding of acute brain injury mechanisms is essential. In this study, we have investigated the putative role of acute inflammation in brain injury after experimental ICH. We depleted GR-1 + cells in mice by intraperitoneal administration of anti-GR-1 antibody or normal rat serum (control). We then induced ICH by infusion of autologous whole blood into the striatum and compared functional outcome and brain injury markers between the two groups. We found that administration of anti-GR-1 antibody led to a profound decrease in circulating GR-1 + cells (1.5 ± 0.34% vs. 50.3 ± 8.3% of CD45 + cells, p ≤ 0.01) and that brain neutrophils decreased by approximately 50% (p ≤ 0.05). We observed a reduction in astrocyte immunoreactivity in the GR-1 + cell-depleted group (p ≤ 0.05). Conversely, we did not find attenuation of brain edema or differences in behavioral deficits between the two groups. In summary, our results are promising and suggest that larger studies or different neutrophil manipulations may produce greater attenuation of injury after ICH.
- Intracerebral hemorrhage