HISTOCHEMICAL STUDIES OF HUMAN CORONARY ATHEROGENESIS: COMPARISON WITH AORTIC AND CEREBRAL ATHEROGENESIS.

Abstract

HomeCirculation ResearchVol. 13, No. 5Histochemical Studies of Human Coronary Atherogenesis: Comparison With Aortic And Cerebral Atherogenesis Free AccessResearch ArticlePDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessResearch ArticlePDF/EPUBHistochemical Studies of Human Coronary Atherogenesis: Comparison With Aortic And Cerebral Atherogenesis Frederick T. Zugibe, M.S., Ph.D. Frederick T. ZugibeFrederick T. Zugibe Basic Cardiovascular Research Section, General Medical Research, Veterans Administration Hospital, and the Department of Anatomy, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Search for more papers by this author Originally published1 Nov 1963https://doi.org/10.1161/01.RES.13.5.401Circulation Research. 1963;13:401–409AbstractA series of new histochemical techniques developed in our laboratory was employed in a study of human coronary arteries obtained from individuals ranging in age from fetal life to 70 years of age. Our conclusions are as follows:No apparent relationship exists between lipid and acid mucopolysaccharides with respect to staining intensity or distribution in any of the groups studied.The earliest morphological alteration in coronary arteries is a primary deposition of lipid. This lipid was observed within endo-thelial cells, as small subendothelial aggregates within macrophages and muscle fibers, or as extracellular deposits. The presence of lipid within the internal elastic membrane and fragmented elastic fibers was an infrequent finding.A comparison of this study with our previous histochemical studies of aorta and cerebral atherogenesis resulted in the following conclusions: At least two independent mechanisms may be responsible for the fatty changes occurring in these arteries; (a) infiltration of lipid via the endothelium and (b) degenerative changes within elastic elements. Lipid was never found in endothelial cells and muscle fibers in cerebral arteries, and was observed only occasionally in aortas. The most frequent site of lipid in cerebral arteries was within the internal elastic membrane while lipid was rarely found in the internal elastic membrane of coronary arteries and only occasionally in aortas.The ratio of chondroitin sulfate B to chon-droitin sulfate A or C increased with aging and severity of changes of elastic fibers in the area of the internal elastic membrane, with a concomitant increase in the ratio of coarse-to-fine collagen. It is suggested that this relationship indicates a reinforcement mechanism which strengthens the arterial wall at sites of fragmentation of the internal elastic membrane. Previous Back to top Next FiguresReferencesRelatedDetailsCited By Moore S (1989) Lipid Accumulation in the Vessel Wall Diseases of the Arterial Wall, 10.1007/978-1-4471-1464-2_13, (197-208), . Alavi M and Moore S (1985) Glycosaminoglycan composition and biosynthesis in the endothelium-covered neointima of de-endothelialized rabbit aorta, Experimental and Molecular Pathology, 10.1016/0014-4800(85)90088-7, 42:3, (389-400), Online publication date: 1-Jun-1985. Murata K (1985) Distribution of acidic glycosaminoglycans, lipids and water in normal human cerebral arteries at various ages., Stroke, 16:4, (687-694), Online publication date: 1-Jul-1985. Murata K and Yokoyama Y (1982) Acidic glycosaminoglycan, lipid and water contents in human coronary arterial branches, Atherosclerosis, 10.1016/0021-9150(82)90171-X, 45:1, (53-65), Online publication date: 1-Oct-1982. Adams C (1981) Arterial Histochemistry in Relation to Structure, Function and Disease Structure and Function of the Circulation, 10.1007/978-1-4615-7927-4_1, (1-155), . Murata K and Nakazawa K (1976) Composition of acidic glycosaminoglycans in human cerebral arteries, Atherosclerosis, 10.1016/0021-9150(76)90045-9, 25:1, (31-43), Online publication date: 1-Oct-1976. Lindner J (2016) Injury and Repair of Arterial Tissue, Angiology, 10.1177/000331977402501003, 25:10, (628-635), Online publication date: 1-Oct-1974. Berenson G, Radhakrishnamurthy B, Dalferes E and Srinivasan S (1971) Carbohydrate macromolecules and atherosclerosis, Human Pathology, 10.1016/S0046-8177(71)80021-7, 2:1, (57-79), Online publication date: 1-Mar-1971. Walton K, Williamson N and Johnson A (1970) The pathogenesis of atherosclerosis of the mitral and aortic valves, The Journal of Pathology, 10.1002/path.1711010302, 101:3, (205-220), Online publication date: 1-Jul-1970. Walton K and Williamson N (1968) Histological and immunofluorescent studies on the evolution of the human atheromatous plaque, Journal of Atherosclerosis Research, 10.1016/S0368-1319(68)80020-1, 8:4, (599-624), Online publication date: 1-Jan-1968. Martinazzi M, Capella C and Carnevali L (1968) Early sudanophilic lesions in femoral-popliteal and coronary arteries, Journal of Atherosclerosis Research, 10.1016/S0368-1319(68)80024-9, 8:4, (657-666), Online publication date: 1-Jan-1968. Smith E (1965) The influence of age and atherosclerosis on the chemistry of aortic intima, Journal of Atherosclerosis Research, 10.1016/S0368-1319(65)80065-5, 5:2, (241-248), Online publication date: 1-Mar-1965. November 1, 1963Vol 13, Issue 5Article InformationMetrics © 1963 American Heart Association, Inc.https://doi.org/10.1161/01.RES.13.5.401 Manuscript receivedMay 22, 1963Originally publishedNovember 1, 1963 PDF download Advertisement