The Role of Intracranial Pressure and Subarachnoid Blood Clots in Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats

Abstract Objective Early brain injury (EBI) after subarachnoid hemorrhage (SAH), which is considered a main factor leading to poor outcome, is thought to be caused by the elevation of intracranial pressure (ICP) and/or the presence of subarachnoid blood clots (SBC) itself. The purpose of this study was to examine whether ICP or SBC is more important to neurological deficit in the presence of apoptosis or edema. Methods A total of 42 rats were allocated to two groups: an endovascular perforation SAH model (the SAH group) and a cisterna magna saline injection model (the saline injection group). Statistical analysis of correlations among the ICP, the grade of clot volume, neuronal apoptosis, brain water content (brain edema), and neurological deficit was performed. Results In the SAH group, each of increased ICP and clot volume was correlated with neuronal apoptosis and brain edema. In the saline injection group, a raised ICP was associated with apoptosis, but it did not correlate with brain edema. Neuronal apoptosis (r = 0.75, p Conclusion The present study suggest that neuronal apoptosis is caused mainly by increased ICP, while brain edema is induced by SBC, and raised ICP could aggravate it in the presence of SBC. Brain edema could affect neurological deficit, but apoptosis alone may be less influential. Not only ICP but also SBC appear important for brain damage in the acute stage of SAH.