Abstract
Background and aim. The long-term effects and final outcome of cerebral ischemia is determined in large extent by functional status of cerebral hemodynamics. In the current study we investigated cerebral hemodynamics and blood rheology one week after transient global cerebral ischemia in rats. Materials and methods. Transient global cerebral ischemia was induced in anesthetized Wistar rats by clamping of both common carotid arteries for 12 min with simultaneous controlled hypotension to 45±3 mm Hg, followed by blood reinfusion. A week after ischemia rats were re-anesthetized, and subjected to blood flow experiments with blood flow velocity measurement or blood rheology study with measuring of hematocrit, RBC aggregation, RBC deformation and shear stress. Blood viscosity and yield shear stress were calculated. Peripheral vascular resistance was calculated from pulsation index. Results and discussion. Mean systolic and end diastolic blood flow velocity were increased in ischemic rats a week after global ischemia as compared to controls. Linear blood flow velocity was increased in parietal region and decreased in frontal and occipital regions in ischemic rats. We suppose this effect to be determined by long-term ischemic injury and no-reflow phenomenon. The pulsation index of cerebral circulation was also decreased a week after ischemia. This data, together with the fact of increased end diastolic blood flow velocity, suggests a decrease of cerebral vascular resistance and tone of brain vasculature. RBC aggregation and stability of aggregates were decreased in blood of ischemic rats, resulting in reduced blood viscosity. This can further ameliorate total peripheral resistance of brain micro-vessels. Conclusions. A week after global ischemia cerebral blood flow remains impaired, with decreased flow velocity in frontal and occipital regions and increased flow velocity in parietal region. Global ischemia also results in increase of diastolic blood flow velocity and decrease in pulsation index, which indicates a total decrease in cerebral peripheral vascular resistance. We suggest this phenomenon to be explained, at least in part, by altered rheological properties after cerebral ischemia.
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