Abstract
As the main particulate component of the circulating blood, RBCs play major roles in physiological hemodynamics and impact all arterial wall pathologies. RBCs are the main determinant of blood viscosity, defining the frictional forces exerted by the blood on the arterial wall. This function is used in phylogeny and ontogeny of the cardiovascular (CV) system, allowing the acquisition of vasomotricity adapted to local metabolic demands, and systemic arterial pressure after birth. In pathology, RBCs collide with the arterial wall, inducing both local retention of their membranous lipids and local hemolysis, releasing heme-Fe++ with a high toxicity for arterial cells: endothelial and smooth muscle cells (SMCs) cardiomyocytes, neurons, etc. Specifically, overloading of cells by Fe++ promotes cell death. This local hemolysis is an event associated with early and advanced stages of human atherosclerosis. Similarly, the permanent renewal of mural RBC clotting is the major support of oxidation in abdominal aortic aneurysm. In parallel, calcifications promote intramural hemorrhages, and hemorrhages promote an osteoblastic phenotypic shift of arterial wall cells. Different plasma or tissue systems are able, at least in part, to limit this injury by acting at the different levels of this system.
Highlights
On the one hand, red blood cells (RBCs) or erythrocytes are the most abundant (4.5 106/mm3) circulating cells (90%)
These data demonstrate that senescent RBCs are frail and more sensitive to hemolysis and that their detrimental cytotoxicity on the arterial wall is mainly mediated by hemolysis and the powerful oxidative capacity of heme-ferrous iron
Erosion is relatively specific of the coronary circulation and predominates in epicardial conductance arteries, since shear stress is high in protodiastole, when the left ventricle relaxes, and flow abruptly invades the myocardium
Summary
On the one hand, red blood cells (RBCs) or erythrocytes are the most abundant (4.5 106/mm3) circulating cells (90%). Sickle cell anemia and malaria attacks share some similarities with this pathophysiology These data demonstrate that senescent RBCs are frail and more sensitive to hemolysis and that their detrimental cytotoxicity on the arterial wall is mainly mediated by hemolysis and the powerful oxidative capacity of heme-ferrous iron. Erosion is relatively specific of the coronary circulation (not observed in carotid arteries for instance) and predominates in epicardial conductance arteries, since shear stress is high in protodiastole, when the left ventricle relaxes, and flow abruptly invades the myocardium These cyclic transitory high frictional forces occur around 3.109 times during a lifespan of 80 years [1] and are responsible for endothelial abrasion. This specific pathology predominates in women [26], potentially linked to the hormonal environment [27] and/or a high coronary flow rate during pregnancy and preeclampsia [28]
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