Brain injury and cerebrovascular fibrin deposition correlate with reduced antithrombotic brain capillary functions in a hypertensive stroke model

Hemostasis factors may influence the pathophysiology of stroke. The role of brain hemostasis in ischemic hypertensive brain injury is not known. We st udied ischemic injury in spontaneously hypertensive rats in relation to cer ebrovascular fibrin deposition and activity of different hemostasis factors in brain microcirculation. In spontaneously hypertensive rats subjected to transient middle cerebral artery occlusion versus normotensive Wistar-Kyot o (W-K) rats, infarct and edema volumes were increased by 6.1-fold (P < 0.0 01) and 5.8-fold (P < 0.001), respectively, the cerebral blood flow (CBF) r educed during middle cerebral artery occlusion (MCAO) by 55% (P < 0.01), mo tor neurologic score increased by 6.9-fold (P < 0.01), and cerebrovascular fibrin deposition increased by 6.8-fold (P < 0.01). Under basal conditions, brain capillary protein C activation and tissue plasminogen activator acti vity were reduced in spontaneously hypertensive rats compared with Wistar-K yoto rats by 11.8-fold (r < 0.001) and 5.1-fold (r < 0.001), respectively, and the plasminogen activator inhibitor-1 antigen and tissue factor activit y were increased by 154-fold (P < 0.00001) and 74% (r < 0.01), respectively . We suggest that hypertension reduces antithrombotic mechanisms in brain m icrocirculation, which may enhance cerebrovascular fibrin deposition and mi crovascular obstructions during transient focal cerebral ischemia, which re sults in greater neuronal injury.