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Platelet and Leukocyte Adhesion in the Microvasculature after SAH

Pathophysiology after subarachnoid hemorrhage (SAH) has not been well examined. We observed platelet-leukocyte-endothelial cell interactions as indexes of inflammatory and prothrombogenic responses in the acute phase of SAH, using an in vivo cranial window method. Subarachnoid hemorrhage was induced in C57Bl/6J mice by the endovascular perforation method. Regional cerebral blood flow (rCBF) was measured with laser-doppler flowmetry. The platelet-leukocyte-endothelial cell interactions were observed with an intravital microscopy 30 minutes, 2 hours, and 8 hours after SAH. The effect of P-selectin antibody and apocynin on these responses was examined, and compared with a different SAH model, in which autologous blood was injected into the foramen magnum. SAH was accompanied by a 60% decrease in rCBF, whereas no changes in rCBF were observed on the contralateral side. SAH elicited time- and size-dependent increases in rolling and adherent platelets and leukocytes in cerebral venules, attenuated by a P-selectin antibody, or apocynin. There was no significant blood cell recruitment in the blood-injected SAH model. SAH at the skull base induced P-selectin- and oxygen radical-mediated platelet-leukocyte-endothelial cell interactions in venules at the cerebral surface. These early inflammatory and prothrombogenic responses may cause a whole brain injury immediately after SAH.