Blood viscoelasticity response during carotid endarterectomy

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 between blood cells and damaged endothelium in the capillary network with release of tissue metabolites and by-products of cellular injury with resulting increased cellular 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 capillary 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 17 patients with unilateral occlusive carotid lesions during different stages of carotid endarterectomy. Our results show that fluid characteristics deteriorated significantly during carotid clamping with increase in whole blood viscoelasticity and plasma density, although collateral circulation 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 cerebral blood flow. This response is immediate. Hematocrit density increases significantly as a result of fluid shift into the interstitium. These changes are reversible if blood flow is promptly restored.