The Journal of Japan Atherosclerosis Society
Online ISSN : 2185-8284
Print ISSN : 0386-2682
ISSN-L : 0386-2682
Volume 2, Issue 4
Displaying 1-7 of 7 articles from this issue
  • Ryozo OKADA, Nobutane HAZATO
    1975 Volume 2 Issue 4 Pages 217-223
    Published: January 01, 1975
    Released on J-STAGE: September 21, 2011
    JOURNAL FREE ACCESS
    A total of 390 aortas with widely scattered age range in Japanese autopsy cases was morphologically studied for intimal thrombosis. The internal surface of the aorta was divided into 6 segments; each two in the aortic arch, thoracic and abdominal aorta, and extent of lipid deposition, fibrous plaque and complicated lesions in the aortic intima was macroscopically estimated as well as that of thrombosis.
    The intimal thrombosis appeared first at the fourth decade of male and the sixth decade of female. The incidence of thrombosis was gradually increased with age up to 80% and 60% in the normotensive (lower than 150/90mmHg) oldest male and female respectively. Presence of hypertension accelerated apparently an increase of the incidence and extent of thrombosis. The extent of thrombosis was maximal at the abdominal aorta, the second at the aortic arch and minimal at the thoracic aorta.
    The incidence of thrombosis was varied by basic disease or disorders. Its difference was analysed by comparison of the age-corrected incidence of thrombosis. More than average incidence of thrombosis was observed in the ischemic and/or hypertensive heart disease with a special predominancy in male, idiopatic myocardiopathy and diabetes mellitus. Less than average incidence was seen in the rest of disease and significantly less incidence was in renal disease, blood disease and neoplasmas.
    If following organization of the intimal thrombosis made a progression or modification of aortic sclerosis, it should make an increase of fibrotic component, because accumulated thrombosis area with age was paralleled with intimal fibrosis area and not with lipidosis area. On the other hand, the thrombosis area per se was fairly paralleled with lipidosis area and not with fibrosis area. This evidence advocated the possibility that the intimal thrombosis could occur on the previously existed atheromatous lesion and its organization could make a fibrous cap or plaque on the atheroma. It suggested that the thrombosis was not primary element for atherogenicity but a modifying or accelerating factor for sclerosis.
    The significantly high incidence of thrombosis in male ischemic and/or hypertensive heart disease might postulate existence of thrombophilia or decrease of fibrinolytic activity in the aortic wall in this paticular disease.
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  • Minoru MORIMATSU, Teruyuki NAKASHIMA
    1975 Volume 2 Issue 4 Pages 225-237
    Published: January 01, 1975
    Released on J-STAGE: September 21, 2011
    JOURNAL FREE ACCESS
    The authors call attention to the existence of “cloudy thickening” as an initial change of human atheromatous plaque.
    Macroscopically, the lesions are gray, opaque and lack of distinct borderline against unaffected intimal surface. They may be circumscribed round or considerably elongated along the long axis of vessels.
    Microscopically, intimal edema is noticed and extracellular linear lipid is present along the internal elastic lamina.
    Electron microscopic examination reveals extracellular deposits of cellular debris (probably originated from imigrated mononuclear cells or other intimal cells) in the same position to that of lipid.
    Irreversible changing of cloudy thickening might depend on the amount of extracellular deposits and the increase of endothelial permeability.
    Fibrin deposition and its organization would be the most important factor when the lesion progresses to the severer atherosclerotic change.
    Estimation of Gore-Tejada's atherosclerotic index of human aortas performed by Mae supports the significancy of the cloudy thickening rather than that of the fatty streak or patch in the problem of atherogenesis.
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  • Akinobu SUMIYOSHI
    1975 Volume 2 Issue 4 Pages 239-244
    Published: January 01, 1975
    Released on J-STAGE: September 21, 2011
    JOURNAL FREE ACCESS
    There is a controversial problem what changes in the arterial intima are truly precursors of atheroma. Prior to the development of atheroma, varying degrees of fibrous thickening usually exist in the intima. Some investigators suggest that such intimal proliferative changes are the result of a physiological ageing process, but in my opinion, they are an integral part of the atherosclerotic process and “preatheromatous lesions”, because the degree of such changes displays wide variations from case to case in relation to age, thus it seems unlikely that age per se accounts for them.
    The purpose of this report is to discuss the significance of thrombus formation and infiltration of plasma proteins, particularly of fibrinogen (fibrin) and β-lipoprotein, into the arterial walls in the development of “preatheromatous lesions” and atherosclerosis.
    1. A preatheromatous lesion is derived from the organization of the mural thrombus.
    The mural white thrombus on the aorta of rabbits induced by insertion of polyethylene tubing was subsequently organized by modified smooth muscle cells and incorporated into the aortic wall, resulting in the fibrous thickening of the intima, “preatheromatous lesion”. Some of these lesions further became the atherosclerotic lesions resembling those found in man, without any cholesterol feeding.
    The endothelial damage and direct exposure of the subendothelial materials, mainly of microfibrils and collagen, were apparently necessary for the initiation of in vivo mural thrombus in the aorta.
    2. Plasma proteins, fibrinogen and β-lipoprotein, might pass through the aortic and large and medium-sized arterial walls of human. The endothelium and the elastic membrane of the arterial wall might act as a barrier to the passage of plasma proteins.
    The impairment of this filtration process and/or the increased permeability of fibrinogen and β-lipoprotein into the arterial wall would result in the deposition of fibrin and/or lipid which evoke the proliferation of smooth muscle cells and might play an important role in the development of atherosclerosis.
    The fibrin deposition tended to be detected earlier and more frequently than that of β-lipoprotein. This fact suggests that fibrin deposition might make a relatively major contribution in the development of preatheromatous lesion.
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  • Yoji YOSHIDA, Takashi JOSHITA, Hiroko SHINKAI, Yasuo TAKAYAMA, Noriyuk ...
    1975 Volume 2 Issue 4 Pages 245-255
    Published: January 01, 1975
    Released on J-STAGE: September 21, 2011
    JOURNAL FREE ACCESS
    Fatty streak, fat-free edema and thrombus as early lesions in genesis of atherosclerosis have been discussed. In this paper early lesions of atherosclerosis in human carotid and cerebral arteries are investigated.
    Both fatty streak (accumulation of foam cells in the intima) and fat-free edema in the intima can become early lesions.
    Groups of foam cells which accumulate in the intima disintegrate and undergo to atheroma (cell disintergration type atheroma, OONEDA). Collagenous and elastic fibers between foam cells disappear.
    Fat-free edema is followed by proliferation of intimal smooth muscle cells which produce collagenous and elastic fibers, and results in fibrosis in the intima. Collagenous fibers in the depths of the thickened intima can be seen to lighten in color and swell in varying degree. Electron microscopic examination reveals that many small lipid droplets, fine electron-dense materials similar to blood plasma protein and cell debris deposit between collagenous fibrils, as a result of which the fibrils split apart. Subsequently swollen fibers break down and undergo to atheroma (fiber disintegration type atheroma, OONEDA).
    Foam cells, fat-free edema and fatty swelling of collagenous fibers are often seen in the intima of which vascular permeability has been increased. Opening of intercellular junctions, degeneration, necrosis and desquamation of the endothelial cells are responsible for increase of endothelial permeability and can be frequently observed in areas where are marginal areas of the thickened intima and junctional areas between layers of the stratified thickened intima.
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  • Fujio NUMANO, Masahiko KOBAYASHI, Kinya MORIYA, Tomoe KUROIWA, Takeo T ...
    1975 Volume 2 Issue 4 Pages 257-266
    Published: January 01, 1975
    Released on J-STAGE: September 21, 2011
    JOURNAL FREE ACCESS
    It is well known that risk factors of atherosclerosis, such as hypertention, stress or hyperlipidemia, provoke the increase of vascular permeability to accumulate lipid in arterial wall. In fact, one shot treatment of angiotensin II, adrenaline, cholestrol or cigarett smoking induced experimentally edematous change in the aortic wall of experimental animals. In this studies, induction of atherosclerotic change in aortic wall of rabbits by repeated challenge with these risk factors were pursued histochemically and microbiochemically.
    4 groups of rabbits were respectively challenged every day with 1γ/kg of angiotensin II (IV), 1g/kg of cholestrol (PO), 1% cholestrol containing diet feeding (150g/day) or 1cc of saline (IV) or 10cc of saline through gastric tube as a placebo control for 2 weeks or 4 weeks.
    In 2 weeks' treated rabbits, histological study revealed commonly the intimal change in the aortic wall of rabbits challenged with cholestrol or angiotensin characterized with cell proliferation and a scanty of lipid accumulation.
    A decrease of PR, ATPase, a slight increase of acid pase, esterase and lipase activities were observed in the aortic wall of rabbits in all three groups, compared with those in placebo control rabbits.
    Microbiochemical assay of phosphofructokinase by Lowry's method modefied by us exhibited an increased activity in intima of all three groups. Especially statistically significant increase was certified in intima of cholestrol challenged groups.
    In 4 weeks treatment, foam cells began to appear in intima of both cholestrol challenged groups and lipase, esterase and G-6PDH activities became striking in media of these group.
    On the contrary, the decreased glycolytic enzyme activities such as PR, LDH, PFK, or MDH were remarkable in the middle part of media of the rabbits treated with angiotensin.
    A statistically significant decrease in the activity of PFK in this lesion was a found microbiochemically (P<0.05).
    These studies suggest that repeated challenges with one shot treatment of risk factors, such as epinephrine, angiotensin or cholestrol give commonly rise to intimal thickening characterized with cell proliferation and that further continuous challenges forces them to atherosclerotic change characterized with the quality of risk factors.
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  • 1975 Volume 2 Issue 4 Pages 267-272
    Published: January 01, 1975
    Released on J-STAGE: September 21, 2011
    JOURNAL FREE ACCESS
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  • With Special Reference to Prognosis and Infarct size
    K. Ueda, M. Sugiura, K. Kuramoto, T. Matsushita, K. Hiraoka, S. Ohkawa ...
    1975 Volume 2 Issue 4 Pages 273-277
    Published: January 01, 1975
    Released on J-STAGE: September 21, 2011
    JOURNAL FREE ACCESS
    In elderly patients with acute myocardial infarction, prognosis and complications were closely related to the serum levels of enzymes (GOT and CPK). In 14 autopsied cases with transmural infarction, there was a linear relation between serum GOT levels and infarct size. It was concluded that estimation of infarct size and prognosis of a case with acute myocardial infarction could be possible from the serum enzyme levels.
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