Brain tissue at the edge of a surgical resection site is at risk for damage from direct trauma, retractor stretch, hemorrhage, edema, and electrocautery. In this study we used a new rodent model of surgically induced brain injury (SBI) to study this tissue at the edge of a resection site. The SBI model entails stereotaxic resection of part of the right frontal lobe. We tested pretreatment with erythropoietin, a known neuroprotectant, for protective effects in this model. Three groups of male Sprague-Dawley rats (280-330 g) were used: SBI without treatment (n = 63), SBI with EPO treatment (n = 76), and Sham surgery (n = 12). Rats were sacrificed 24 h, 72 h, and 7 days after SBI or Sham surgery. Postoperative assessment included mortality, histology, immunohistochemistry, Evans blue exudation, brain water content, and magnetic resonance imaging. No difference was found between untreated and EPO-treated groups in mortality, histology, TUNEL, magnetic resonance imaging, or blood-brain-barrier breakdown. The EPO-treated group had statistically more brain water content at 24 h than the untreated group. Immunohistochemistry demonstrated a qualitative increase in VEGF in the EPO-treatment group. We conclude that EPO does not ameliorate damage in SBI, and may increase brain edema early after surgery.
- Brain edema
- Surgically induced brain injury
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