Hemorheological abnormalities in experimental cerebral ischemia and effects of protein kinase inhibitor on blood fluidity

The aim of this study was to investigate the mechanisms of the pathogenesis of hyperviscosity following cerebral ischemia, Focal ischemia was produced by embolic occlusion of the right middle cerebral artery (MCA) in rats for 1 hour, followed by recirculation. Twenty-four hours after MCA occlusion, fasudil, a protein kinase inhibitor, was administered intraperitoneally, Bl ood samples were taken from the abdominal aorta, and viscosity was measured using a cone-plate viscometer. The viscosity of whole blood in the ischemi c attack group was significantly increased compared with the sham operated group 24 hours after MCA occlusion, Fasudil dose-dependently and significan tly decreased the blood viscosity, and reduced to the normal range after ad ministration of 10 mg/kg of fasudil (sham-operated rats, 5.17 +/- 0.05 cP; pre dose/ischemic rats, 6.05 +/- 0.08 cP; post dose/ischemic rats, 5.23 +/- 0.14 cP; 37.5 sec(-1)). Our findings suggest that cerebral ischemia induce s a potent, systemic and longlasting hyperviscosity, and that the inhibitio n of protein kinases, especially rho kinase, is efficacious in preventing t his hyperviscosity. (C) 2000 Elsevier Science Inc. All rights reserved.