Brain edema formation and complement activation in a rat model of subarachnoid hemorrhage.

Abstract

Previous studies have demonstrated that erythrocyte lysis and brain iron overload contribute to early brain injury after subarachnoid hemorrhage (SAH). Activation of the complement system and formation of the membrane attack complex can result in erythrocyte lysis and might, therefore, participate in such injury. This study, therefore, examined complement activation, blood-brain barrier (BBB) disruption, and brain edema in a rat SAH model.Subarachnoid hemorrhage was induced using a modified endovascular perforation technique. Brain complement activation was determined by Western blotting and immunohistochemistry. Brain edema was measured by dry/wet weight and BBB permeability assessed by measuring brain albumin levels.We found that there was expression of the membrane attack complex and clusterin in the frontal basal cortex and clot after SAH. The protein levels of the membrane attack complex were much higher in the frontal basal cortex at 72 h after SAH than those in sham (p < 0.01). We also found that brain water content was increased (81.9 ± 1.4 vs. 79.1 ± 0.2 % in sham, p < 0.05) and BBB was disrupted (albumin content: 10,695 ± 865 vs. 4,935 ± 3,121 pixels in sham, p < 0.01) 24 h after SAH.Our results suggest that complement activation after SAH might contribute to brain edema formation and BBB disruption after SAH.