JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
Volume 42, Issue 8
Displaying 1-8 of 8 articles from this issue
  • TOSHIHIRO MATSUMURA, TAKETOSHI KISHIMOTO, TSUTOMU MAEDA, MASANOBU MAEK ...
    1978 Volume 42 Issue 8 Pages 927-938
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Effects of prostaglandin A2 (PGA2) and E2 (PGE2) on renin release and intrarenal blood flow distribution were studied in dogs anesthetised with pentobarbital. Plasma renin activity (PRA) was measured by radioimmunoassay. Intrarenal distribution of blood flow was determined by means of a radioactive microsphere method. Intrarenal arterial administration (IRA) of PGA2 at a rate of 0.1 μg/min caused an increase in renal blood flow (RBF) and a slight increase in urine flow (UF) without any change of renal arterial pressure (RAP). Renal venous PRA was slightly but significantly increased following PGA2 infusion into the renal artery (0.1 μg/min). Doses of PGA2 (0.5 μg/min, IRA) and PGE2 (0.1 μg/min, IRA) had maximum effect on RBF without changing RAP. Both PGA2 (0.5 μg/min, IRA) and PGE2 (0.1 μg/min, IRA) increased RBF, UF and urinary sodium and potassium excretion, but did not influence on Glomerular filtration rate (GFR). PGA2 (0.5 μg/min, IRA) increased significantly arterial and renal venous PRA while, PGE2 (0.1 μg/min, IRA) had no effect on arterial or renal venous PRA. Concerning the intrarenal distribution of blood flow, both PGA2 (0.5 μg/min, IRA) and PGE2 (0.1 μg/min, IRA) resulted in an increased flow rate in each cortical zone, but the zonal response pattern was not uniform and was characterzed by a progressively proportional increase in flow from the superfical to the deep cortex. Thus, the percentage distribution was significantly changed, showing a redistribution of blood flow from the superficial cortex to the deep cortex. Intravenous administration (IV) of 0.5 μg/min PGA2 reduced blood pressure by 15-20 mmHg but did not change RBF. UF showed a slight decrease following PGA2 infusion intravenously (0.5 μg/min, IV) and increased significantly arterial and renal venous PRA. PGE2 (0.5 μg/min, IV) caused a reduction in RAP by 10-15 mmHg. RBF and UF showed a small increase following PGE2 infusion intravenously (0.5 μg/min). Both arterial and renal venous PRA were increased by intravenous administration of 0.5 μg/min PGE2, but the difference was not significant. The data suggested that both PGA2 and PGE2 have similar effects on renal hemodynamics and urine formation. It is likely that PGA2 stimulates renin release but PGE2 does not.
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  • KAZUHIRO ARIKAWA, AKIRA TAIRA, KAZUTAKE MURATA, YOSHIOMI HAMADA, HACHI ...
    1978 Volume 42 Issue 8 Pages 939-943
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
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  • YOZO MATSUDA, SHIGENOBU YAMADA, HIROYUKI KUROGANE, HIKARU SATO, KAZUMI ...
    1978 Volume 42 Issue 8 Pages 945-954
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The present study was designed to evaluate the left ventricular performance in man with the impedance cardiography which was deviced by Kubicek and associates. The Q-Z interval was compared with hemodynamic and angiographic indices of left ventricular performance in 36 patients in whom cardiac catheterization was carried out. Correlation coefficients between the Q-Z interval and other indices, that is Q-dp/dt, V max, Max dp/dt and Ejection Fraction were 0.91, -0.87, -0.71 and -0.54, respectively and all of them were statistically significant. A shortening of the Q-Z interval always corresponded to an increase of myocardial contractility and a prolongation of it corresponded to a decrease of myocardial contractility. In atrial pacing of 10 patients with sinus bradicardia, the Q-Z interval was not influenced by the heart rate. The usefulness of impedance cardiography is based on the good correlation between the interval from the onset of ventricular depolarization to the peak of the first derivative of the impedance cardiogram (Q-Z interval) and the interval from the onset of ventricular depolarization to the peak of the first derivative of left ventricular pressure (Q-dp/dt). From these results, it is postulated that the Q-Z interval is one of the valuable indices for the assessment of left ventricular performance.
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  • KIZUKU KURAMOTO, SATORU MATSUSHITA, JUNICHIRO MIFUNE, MAKOTO SAKAI, MO ...
    1978 Volume 42 Issue 8 Pages 955-960
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The validity of isoproterenol test in the diagnosis of ischemic heart disease in the aged was evaluated in 67 autopsied cases. The additional ST segment depression of 0.5 mm or greater of the ischemic type after the intravenous infusion of isoproterenol (ISP) at a rate of 0.02 μg/kg/min for five minutes was considered to be the positive test. The sensitivity in 25 severe coronary stenoses of 75% or more was 72.0%, and specificity in 42 mild coronary stenoses was 71.4%. The false negative results were observed in 6 cases of ten myocardial infarctions, and the false positive results were observed in 5 cases of seven stenotic valvular diseases. The sensitivity and specificity after excluding the myocardial infarction and stenotic valvular disease were 100% and 81.8%, respectively. ST depression at rest was a poor indication of the coronary stenosis, and the specificity of the ISP test in the abnormal resting ST depression was 64.7%. The increases in heart rate and cardiac index after ISP infusion were greater in severe coronary stenosis without myocardial infarction than in mild coronary stenosis, indicating the hypersensitivity to the beta-adrenergic stimulation. The hemodynamic responses in myocardial infarction to the ISP infusion were similar to the reponses in mild coronary stenosis. The isoproterenol test was a safe and useful method not only in the assessment of the coronary heart disease, but also in clarifying the pathophysiological mechanism.
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  • MINORU OHMAE
    1978 Volume 42 Issue 8 Pages 961-970
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Five cases of chronic acquired atrioventricular block were presented. Two cases (Cases 3 and 4) were thought to be primary block. Two other cases (Cases 1 and 2) were thought to be due to coronary sclerosis. One case (Case 5) was due to invasion of reticulosarcoma cells. Cases 1 and 2 showed bilateral bundle branch fibrosis, and cases 3 and 4, interruption of the penetrating portion of His bundle. In case 4, an abnormal conal muscle pressed against the His bundle. In case 5 reticulosarcoma cells invaded the S-A node, A-V node and bundle branches. Correlations between ECG and histology were discussed. The electrocardiographic finding were found to correlate well with the changes in the conduction system.
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  • AKIRA OOSHIMA
    1978 Volume 42 Issue 8 Pages 971-978
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    An immunohistochemical method and light microscopy were utilized to determine localization of prolyl hydroxylase in the cardiovascular tissues of hypertensive rats. The blood vessels and renal glomerulus from these animals demonstrated an enhanced immunoreaction for prolyl hydroxylase. As the most prominent staining was observed in medial smooth muscle cells of blood vessels, these are probably the major collagen-producing cells in arteriosclerotic lesions induced by hypertension. In the glomerulus, endothelial cells and probably mesangial cells are mainly responsible for the collagen formation. An intense immunoreaction was also found in the fibroblasts which proliferated in the area of myocardial fibrosis in hypertensive rats, while there was no specific staining in myocardial cells in either hypertensive or normotensive rats.
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  • KIKUKO IMAMURA
    1978 Volume 42 Issue 8 Pages 979-1002
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The morphology of the left ventricular myocardium of spontaneously hypertensive rats (SHR) (Okamoto and Aoki) was studied with light and electron microscopes, with special reference to a quantitative analysis of subcellular organelles and a description of the characteristics of the capillaries in myocardium. Paired groups of SHR and control Wistar-Kyoto rats were sacrificed at 3, 5, 9, 11, 15 and 21 weeks and one year of age. In the left ventricular lateral wall of SHR, starting at the age of 11 weeks, the cardiocytes became progressively thicker as the blood pressure rose and exhibited various ultrastructural alterations. In these cardiocytes, the proliferation of Z-band materials was occasionally present in the myofibrils, and was closely associated with the subsarcolemmal area and intercalated discs. Convolutions and extensive foldings of the intercalated discs were prominent. Mitochondrial abnormalities consisted of fragmentation and stacks of cristae, aggregates of small mitochondria and intramitochondorial α-glycogen rosettes. In one-year-old SHR, malaligned cardiocytes as well as myofibrils were seen in certain areas of the myocardium. In some cardiocytes, streaming and clumping of Z-band material, myofibrillolysis and proliferation of sarcoplasmic reticulum appeared. In addition, there were clusters of spherical microparticles, tubular aggregates and intramitochondrial inclusions, suggestive of degenerative changes. Stereological analysis of subcellular organelles in the hypertrophied cardiocytes of SHR revealed an increase of myofibrillar volume fractions and a decrease of mitochondrial volume fractions, resulting in an increase in the ratio of myofibrils to mitochondria. These findings differed from those in the posterior papillary muscle of the left ventricle in the same animal hearts. Thus, it is apparent that myocardial hypertrophy varies in each area of the myocardium due to different stresses during the course of its development. In the hypertrophied myocardium of SHR, the capillaries were seen to proliferate with the appearance of a "tunnel capillary", while interstitial fibrosis and hypertensive vascular lesions progressed with aging. The capillary proliferation maintained a constant diffusion distance from the capillary to the cardiocyte, probably as one of adaptation in cardiac hypertrophy in SHR.
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  • [in Japanese]
    1978 Volume 42 Issue 8 Pages 1003-1009
    Published: September 20, 1978
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    On the occasion of the Fourth Meeting of the International Society of Hypertension (ISH) in Sydney, 24-26 February 1976, a nomenclature committee was founded with the specific task to review the present nomenclature of the renin-angiotensin system (PAS) and to adopt it to the rules laid down by the Commission on Biochemical Nomenclature of the International Union of Pure and Applied Chemistry (IUPAC), and the International Union of Biochemistry (IUB). Apart from the members of the ISH-Committee1, the Council for High Blood Pressure Research of the American Heart Association also appointed a nomenclature committee2 which jointed the efforts of the ISH-Committee. Valuable suggestions came from scientists throughout the world in response to different memoranda which were drafted and circulated by the committee. It was agreed upon that there may be two kinds of nomenclature, one trivial working nomenclature with usually brief and historically grown names, and a second systematic nomenclature to be introduced if the substance is well enough characterized to allow such classification.
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