Inflammation in the brain after experimental subarachnoid hemorrhage.

OBJECTIVE: To study the occurrence of an inflammatory response in the brain after subarachnoid hemorrhage and its relation to the decrease in acute cerebral blood flow, subarachnoid blood proximity, and cell damage.
METHODS: Subarachnoid hemorrhage was induced in rats via endovascular perforation of the internal carotid artery or injection of blood into the prechiasmatic cistern. Cerebral blood flow was measured by laser Doppler flowmetry for 60 minutes. After 2 and 7 days, the brains were analyzed by immunohistochemistry using the following antibodies: OX6, ED1, intercellular adhesion molecule 1, tumor necrosis factor alpha, interleukin-1beta, interleukin-6, inducible nitric oxide synthase, and nestin. Deoxyribonucleic acid fragmentation was assessed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling.
RESULTS: In approximately half of the surviving animals (0-92%, depending on the marker and subgroup), signs of inflammation were detected. The most common findings were increased immunoreactivity to nestin, ED1, OX6, intercellular adhesion molecule 1, and tumor necrosis factor alpha. There was great variability in the intensity and the location of the inflammatory reaction among the animals, but tissues in proximity to the extravasated blood seemed to be especially affected. A significant correlation between the duration of cerebral blood flow under 30% of the baseline and the degree of the inflammation was observed. There was a strong correspondence between areas showing deoxyribonucleic acid fragmentation and inflammation.
CONCLUSION: Subarachnoid hemorrhage triggered an inflammatory reaction in the brain in a large fraction of the surviving animals, which may have contributed to cell death. Acute ischemic episodes and direct effect of blood seemed to be significant factors in its genesis.