Tissue oxygen demand in regulation of the behavior of the cells in the vasculature.

The control of arteriolar diameters in microvasculature has been in the focus of studies on mechanisms matching oxygen demand and supply at the tissue level. Functionally, important vascular elements include endothelial cells (EC), vascular smooth muscle cells (VSMC) and red blood cells (RBC). Integration of these different cell types into functional units aimed at matching tissue oxygen supply with tissue oxygen demand is only achieved when all these cells can respond to the signals of tissue oxygen demand. Many vasoactive agents that serve as signals of tissue oxygen demand have their receptors on all these types of cells (VSMC, EC, and RBC) implying that there can be a coordinated regulation of their behavior by the tissue oxygen demand. Such functions of RBC as oxygen carrying by hemoglobin (Hb), rheology, and release of vasoactive agents are considered. Several common extra- and intracellular signaling pathways that link tissue oxygen demand with control of VSMC contractility, EC permeability, and RBC functioning are discussed

Oxidative injury in neonatal erythrocytes

Erythrocytes are continuously exposed to free radicals (FR) injury due to their high cellular oxygen concentration and heme iron. The autoxidation of oxyhaemoglobin to methaemoglobin, generating superoxide anion radical, represents the main source of FR in erythrocytes. The erythrocyte membrane is particularly sensitive to oxidative damage due to its high polyunsaturated fatty acid content, and hence, it represents an important system to evaluate the effect of oxidative stress (OS). Information on how red cells OS is triggered and mechanisms of erythrocytes oxidative pressure from plasma may provide a partial answer to questions about the causes of the anaemia of prematurity and about red cell involvement in hypoxia. The recent insights about the mechanism of oxidative injury of red cells and the evidence of relationships between erythrocyte, OS and hypoxia suggest that increased haemolysis is induced by severe hypoxia and acidosis in the perinatal perio