Changes in cell behaviour during ischaemic cerebrovascular disease

Abstract

The atherosclerotic process, along with the thrombotic events induce changes in blood and wall cells during the cerebro-vascular disease. Both the plaque, as a growing hindrance and a place for a chronic inflammation, and the underlying risk factors are acting upon the cells. A third actor is hypoxaemia occuring first as acute and transient episodes before a permanent setting behind the plaque. These changes disturb the flow and favour the wall cell adhesion. The platelets are shear induced activated. The red cells express a high aggregation related to elevated fibrinogen and specific disturbances linked to risk factors, acting also on deformability and adherence. Granulocytes are primed and exhibit a higher adhesion potency. Endothelial cells, in areas of microcirculation related to artery stenosis, are very susceptible to hypoxaemia which induces a fall in NO, a depletion of nucleotides, prothrombotic and adhesive properties and a decrease expression of thrombomodulin. This latter glycoproein appears as an interesting marker providing split fragments linked to O2-generation during the reperfusion injury. Finally the cells are also involved in cell-to-cell interactions. These changes greatly influence the vascular disease and should be specifically treated.