Summary: As demonstrated in many studies ischemic brain injury causes microcirculatory disturbances which is reflected in changes in the rheological behavior of blood. This is caused by multifactorial interaction be tween blood cells and damaged endothelium in the capil lary network with release of tissue metabolites and by products of cellular injury with resulting increased cellu lar permeability producing a volume shift into the interstitium and, subsequently, a rise in the hematocrit density. Drop in perfusion pressure produces an increase in whole blood viscosity. By means of an oscillating cap illary rheometer and densimeter, the viscous and elastic parts of the complex viscosity of whole blood and plasma were measured from the ipsilateral internal jugular vein in
326during carotid clamping with increase in whole blood vis coelasticity and plasma density, although collateral circu lation was judged sufficient in the angiogram and cerebral perfusion pressure. These parameters not only returned to their initial value, but a significant amelioration was observed after installation of an intraluminal indwelling shunt as a response to improved orthograde flow and an enhanced shear velocity. We conclude that an increase in whole blood viscosity does correlate with decreased ce rebral blood flow. This response is immediate. Hemato crit density increases significantly as a result of fluid shift into the interstitium. These changes are reversible if blood flow is promptly restored. Key Words: Blood vis coelasticity-Plasma density-Blood density-Intralu minal shunt-Carotid endarterectomy-No-reflow phe nomenon.Ischemia can produce a perfusion defect in mi crovessels, which results in aggregation of erythro cytes and in stimulation of platelets and polymor phonuclear leucocytes (PMNL) followed by pro duction and release of substances that cause vasoconstriction, enhanced vessel patency, and fur ther chemotaxis (Bagge and Branemark, 1979;Litwin and Chapman, 1970). As blood flow and shear rate decrease to very low levels, complex vis cosity markedly increases (Sakuta, 1981). The phase interchange between both components, the phase angle <1>, separates the part of elastic en ergy stored in the circulating blood from the total energy required to keep it in motion (Fig. 1). Other factors that determine blood viscosity include he matocrit, erythrocyte aggregation, erythrocyte flex ibility, platelet aggregation, plasma viscosity, and shear rate (Kratky et aI., 1973). Flexibility or shear