JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
Volume 40, Issue 1
Displaying 1-5 of 5 articles from this issue
  • REIZO KUSUKAWA, TSUNEO HOSHINO, GO TOMONAGA, IWAO MASHIRO, YUKIO SHIMO ...
    1976 Volume 40 Issue 1 Pages 1-11
    Published: February 20, 1976
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Utilizing the pressure-volume relationship, the indices of left ventricular diastolic compliance, SV/EDP-DP, and dV/VdP, ventricular stiffness index, I/P(dV/dP), and myocardial stiffness index, I/S(dD/dS) were evaluated of seven patients with normal left ventricle, eleven patients with hypertrophic and seven with congestive type of primary myocardial disease. Myocardial stiffness index was obtained from the equation of S=aekD, where S is a wall stress, a ; a constant, D; a length of short axis, K; a stiffness constant. The mean values and standard errors of the means of SV/EDP-DP, dV/dP, dV/VdP, I/P(dV/dP), and I/S(dD/dS) for normal group are 16.7±8.7 (ml/mmHg), 16.03±6.98 (ml/mmHg-1), 0.1259±0.0447 (mmHg-1) 0.0059±0.0032 (ml-1) and 0.603±0.153 (cm-1), for hypertrophic type are 10.5±5.5 (ml/mmHg), 3.91±2.13 (ml/mmHg-1), 0.0250±0.0239 (mmHg-1), 0.0308±0.0126 (ml-1), and 3.287±1.272 (cm-1). There were highly significant differences between normal and primary myocardial disease in each indices except SV/EDP-DP. I/P(dV/DO), and I/S(dD/dS) had highly significant differences between hypertrophic and congestive type, the latter is stiffer than the former. The compliance index was not sensitive enough to separate two types of primary myocardial disease.
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  • SAJIO SUMIDA
    1976 Volume 40 Issue 1 Pages 13-19
    Published: February 20, 1976
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
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  • JIN YAMAMOTO, JUN KIRA, MASATO MATSUNAGA, KOICHI OGINO, CHUICHI KAWAI
    1976 Volume 40 Issue 1 Pages 21-28
    Published: February 20, 1976
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The relationship between hypertension-inducing potency and renin content of kidney extract was analyzed in rats using Sephadex G-100, CM-Sephadex C-50, DEAE-Cellulose or Concanavalin A-Sepharose column chromatography. Hypertension-inducing potency of each fraction obtained was evaluated on the basis of the final blood pressure level attained by repeated injections into the test animals for 10 days. Hypertension-inducing potency was found mainly in the renin-containing fractions. And it seems reasonable to conclude that renin is implicated in the pathogenesis of hypertension produced by kidney extract. However, there were significant discrepancies between hypertension-inducing potency and renin content of subdivided fractions of these renin-containing eluates. Possible explanations for the discrepancies disclosed-including the possibility of the involvement of an unknown substance(s)-have been discussed. In addition, it was suggested from the result of Concanavalin A-Sepharose chromatography that rat renal renin has a glycoprotein nature.
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  • OSAMU TAKEICHI, TAKASHI NAGAO, YOSHIYUKI MIZUNUMA, KOUICHI MIKAWA, TSU ...
    1976 Volume 40 Issue 1 Pages 29-34
    Published: February 20, 1976
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Sequential histochemical studies were conducted to determine the level of monoamine oxidase (MAO) activity in the infarcted tissue of the experimental myocardial infarction in dog. MAO activity was not found in the normal heart muscle, but the activities were present in the wall of the coronary artery histochemically. Fibroblasts and collagen fibers began to take the place of the destroyed heart muscles in the infarcted area from 10 days after the coronary occlusion in dogs, and MAO activities were noted sporadically in the Fibroblasts and the interstices of the collagen fibers in the infarcted area. MAO activities increased histochemically in the Fibroblasts and the fiber interstices in the infarcted area 10 days or more after the coronary occlusion. These findings suggested the presence of the active collagen metabolism outside the myocardial cells in the infarcted area in the recovery stage of the experimental myocardial infarction. It was also suggested that the interstices of the collagen fibers in the myocardial wall constituted the lymphatic ducts outside the blood vessels and that the MAO activity in serum determined by the method in which tryptamine hydrochloride was used as substrate might indicate the grade of fibrosis of the myocardial tissue in the infarcted areas.
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  • SENRI HIRAKAWA, MASAHIKO KINOSHITA, SHOJI HAYASE
    1976 Volume 40 Issue 1 Pages 35-51
    Published: February 20, 1976
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    A simplified, non-invasive method for assessment of the performance of the right heart during supine leg exercise was described, which necessitated no more than a bicycle"ergometer"for leg exercise, a radiocardiograph for recording cardiac index (CI) and a"water"manometer for measuring cubital venous pressure (VP). Because the use of a cardiac catheter was omitted, right atrial pressure (RA), right ventricular diastolic pressure (RVd) or pulmonary arterial pressure (PA) were not measured. In 11 healthy subjects and 25 patients with primarily left-sided valvular disease and hypertension, the observed shift of CI-VP plot with exercise was similar to the published records of exercise-induced shift of CI-RA plot or CI-RVd plot in normal subjects and the same types of heart disease. With levels of load used in this study, a dividing line separating normal from abnormal elevation of VP during supine leg exercise (ΔVP) could be drawn at ΔVP=35 mm H2O and (2) in these types of heart disease, ΔVP in excess of 35 mm H2O was always associated with a"subnormal"increase in CI (ΔCI < 0.8 lit. min-1. M-2) with exercise, except in a few cases who appeared, clinically, to be in what may be termed"latent heart failure". Factors probably responsible for an impaired pumping ability of the right heart during exercise in left-sided heart disease were discussed, in relation to ΔVP.
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