Free radicals in arterial and venous blood. Its relation with the pathogenesis of atherosclerosis

pp 143-147

Abstract

Oxygen free-radicals are apparently involved in the pathogenesis of ageing and in the mechanisms that lead to atherosclerosis. Oxygen free-radicals are chemical species that have one unpaired electron in their external layer. Active oxygen is a concept that includes several oxygen-derived chemical species that are biologically active, such as superoxide anion, hidrogen peroxide, hydroxyl radical and singlet oxygen. They are reactive, unstable, and have a short mean life. Lipoperoxidation is produced as result of the action of oxygen, ozone and radiation or of numerous toxic substances on the poliinsaturated fatty acids of the biological membranes. The organisms that survive are the ones that have developed systems of antioxidant defense. The presence of lipoperoxides in tissues is shown by means of chemiluminiscence and by the method of the 2-thiobarbituric acid in blood, which allows to dose malondialdehyde a by-product of lipoperoxidation. Free-radicals damage the cell structures, membrane and mitochondria, denature lipoproteins and nucleic acids and alter the enzymatic systems and hemostatic factors. Iron and copper accelerated the process of lipoperoxidation. This paper reports on the levels of malondialdehyde in blood coming from the right ventricle (prelung) and from left ventricle (postlung) in patients undergoing hemodynamic tests. The role of lung in oxidation of lipoproteins and their implications in pathogenesis of atherosclerosis is evaluated. The results show that: a) The proportion of malondialdehyde is greater in blood coming from the left ventricle than from the right ventricle. b) As blood flows through the lung must suffer an oxidation process that denatures the native LDL lipoproteins, transforming them in oxidated lipoproteins which if they are hold by macro phages that penetrate through the endotelium may contribute to the formation of atheromatous lesions. c) The increase of postlung malondialdehyde oculd be a direct consequence of a greater pressure of O2 in arterial blood in relation to venous blood. It can be deduced that the arterial would be more exposed to oxidation stress than the venous bed. d) Therefore, blood flowing from the left ventricle would have more atherogenic capacity.