Abstract
Interest in the ground substance of vascular structures has been evoked by the advancement of histo-pathological studies on the atherosclerosis, emphasizing the possible role of mucopolysaccharide accumulation in the production of focal atheroma. Such histochemical observations on arterial mucopolysaccharide have stimulated the extension of the biochemical knowledge on their nature and metabolim. The questions were reviewed from the recent informations including some of our studies concerned. Our experiments at the first step were carried out on the gross aortic materials to overlook the changing pattern of total and fractionated AMPS with aging and atherosclerosis. At the next step, further microtechnique was introduced to permitting the analysis on the aortic material comprising as small as one intimal lesion, which was composed of the microscale extraction procedure including the selective precipitation with cation detergent and the densitometric determination of AMPS fractions after electrophoretic separation on cellulose acetate strip. The experiments have evidenced the facts that aging of aortic tissue appears to be characterized by a decline of total AMPS contents in aceton-dry tissue and a decrease in hyaluronic acid and chondroitinsulfate A or C content and an increase in chondroitinsulfate B, similarly to the aging skin or cartilage, and that the edematous lesions, perhaps an early phase of fibrous plaque, comprise both high AMPS value and hyaluronic acid content. The possible biological functions of AMPS on atherogenesis were also reviewed from the recent publications. AMPS was recognized to possess the properties of preventing thrombus formation and lipid deposition in the arterial wall through its antithrombin and lipid clearing activity and, on the other hand, those of inducing the fibrin and lipid deposit through physicochemical complex formation with fibrinogen and lipoprotein. The destruction or abnormal aggregation of AMPS in the ground substance might cause an increased permeability of the arterial wall to the circulating lipoprotein and also the destruction of connective tissue fibers, substantially inducing the atherosclerosis.
