JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
Volume 51, Issue 1
Displaying 1-15 of 15 articles from this issue
  • BURTON E SOBEL
    1987 Volume 51 Issue 1 Pages 1-4
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Although coronary thrombolysis with fibrinolytic agents leads to restoration of patency of coronary arteries demonstratable angiographically, elucidation of the efficacy of the approach requires evaluation of its effect on the heart. Clot-selective fibrinolytic agents such as tissue-type plasminogen activator (t-PA) offer particular promise as therapeutic agents because they induce clot lysis without marked activation of the fibrinolytic system in the circulating blood and hence without marked fibrinogenolysis and predisposition to bleeding. Results of several large scale clinical trials demonstrate recanalization in approximately 75% of patients. Detection of recanalization may be achievable by analysis of plasma creatine kinase isoforms as a function of time, and in the research environment, with the use of positron emission tomography. This modality demonstrates restoration of regional perfusion and intermediary myocardial metabolism and provides an approach for calibration of conventional and more widely applicable diagnostic procedures such as scintigraphy.
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  • CHUICHI KAWAI
    1987 Volume 51 Issue 1 Pages 5-14
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
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  • SHIGEKI ITOH, KATSUYA KOBAYASHI, HISASHI. FUKUZAKI
    1987 Volume 51 Issue 1 Pages 15-24
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Late potentials (LPs) recorded using the signal averaging technique were studied sequentially in 12 cases with acute myocardial infarction (AMI) in order to clarify how LPs develop in relation to ventricular arrhythmias (VA) in this disorder. Within 7 days after the onset of AMI there were no significant differences between LP durations with and without VA, and the overall mean value was relatively short (15.9±5.0 msec). On the 14th day, these cases were clearly divided into two groups according to LP duration. The group with LP duration over 20 msec (n=56, average: 24.3±1.5 msec) exhibited a higher VA score and the other group with a shorter LP duration (n=7, average: 15.0±2.1 msec) had a lower VA score (4.3±0.9 vs 0.6±0.5, p<0.001). This tendency was observed even in the late phase, and data such as peak CPK, cardiac index and mean pulmonary capillary pressure obtained in the acute phase could not predict this separation. In conclusion, LPs appear slightly later following the onset of AMI and correspond with the appearance of VA in the late phase; thus, LPs are useful for the prediction of VA in the course of AMI.
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  • KAZUSHI TSUDA, MASATO KIKUUCHI, ICHIRO NISHIO, YOSHIAKI. MASUYAMA
    1987 Volume 51 Issue 1 Pages 25-32
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The present study was designed to evaluate the role of the presynaptic α2-adrenoceptor in the pathogenesis of hypertension. Norepinephrine overflow during sympathetic nerve stimulation and its changes by presynaptic α2-adrenoceptor inhibition were examined in the perfused mesenteric vasculatures of young and adult spontaneously hypertensive rats (SHR) compared with age-matched Wistar Kyoto rats (WKY). Electrical sympathetic nerve stimulation caused significantly greater overflow of endogenous norepinephrine from the adrenergic nerve terminals in young SHR than in age- matched WKY. Yohimbine, an α2-adrenoceptor blocking agent, facilitated norepinephrine overflow from the adrenergic nerve terminals. The effects of yohimbine on norepinephrine overflow and pressor responses to electrical nerve stimulation were less in young SHR than in age-matched WKY. Norepinephrine overflow in adult SHR was similar to that in adult WKY, and differences in the effect of yohimbine on norepinephrine overflow between SHR and WKY were not marked at this chronic stage. These results suggest that enhanced norepinephrine overflow in the mesenteric vasculatures can be observed only in young SHR; this may be due in part to an impaired negative feed-back mechanism on the nerve terminals by presynaptic 2-adrenoceptors.
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  • SENRI HIRAKAWA, MICHIO ARAKAWA, KENJIRO KAMBARA, JUMPEI IINUMA, KIDETA ...
    1987 Volume 51 Issue 1 Pages 33-40
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    In this study, we examined the pressure-volume (P-V) relationships of the pulmonary "venous" (P'V') system in anesthetized living dogs, and assessed compliance by fitting the derived data of the P-V relationships to the exponential function. By definition, the P'V' system consists of the pulmonary veins and the left atrium. The pulmonary "venous" volume (P'V'V) was determined with our modified double indicator dilution method using a single injection and double sampling technique. The mean left atrial pressure (P^-LA) was measured directly. To observe sequential changes over a wide range of the P-V relationships, dogs were studied from the control state through the volume-loaded state with dextran. The P'V'V ranged from 3.4 to 12.2 ml·kg-1 and the P^-LA from 3.2 to 40.6 mmHg. We fitted the data of the P-V relationships (n=24) to the exponential function, yielding an equation; P'V'V(ml·kg-1)=19(1-0.833(e-0.017P^-LA(mmHg))). We then differentiated an above equation to estimate the slope of this curve (static compliance), giving the equation: dV/dP(mlmmHg-1kg-1)=0.269(e0.017P^-LA(mmHg)). Therefore, at P^-LA of 10 mmHg (normal level), the compliance is 0.226 mlmmHg-1kg-1. The compliance, obtained with an application of the present results in dogs to man, (disregarding expected species differences), coincides well with that in man determined with our indirect method.
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  • TOSHIKUNI YANAGISHITA, NOBORU KONNO, EIICHI GESHI, TAKASHI KATAGIRI
    1987 Volume 51 Issue 1 Pages 41-50
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Alterations in the phospholipid component of membranes were studied in acute myocardial ischemia with respect to sarcoplasmic reticulum (SR) and mitochondria (Mt) in the carine heart and compared with changes in the phospholipid composition of intact membrane treated with exogenous phospholipases (PLases)A2 and C, in order to examine the mechanism of ischemic degradation. As early as 30 min after coronary ligation, the total phospholipid content of SR and Mt decreased significantly, 16.0% and 5.6% respectively. The patterns of SR and Mt phospholipids from the ischemic myocardia did not differ on the chromatograms from those of the non-ischemic myocardia, and no significant increases in lysophospholipids were found for up to 3 hrs. Among the components of phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE) decreased mainly during ischemia, and depletion of PC exceeded that of PE in SR. PLase C hydrolysed phospholipids yielded no lysophospholipids, compared to the production of a large amount of lysophospholipids by PLase A2. It was concluded that degradation of membrane phospholipids occurs in the early stage of myocardial ischemia mainly in PC and PE, which are the major components of membrane phospholipids. This may be an expression of irreversible changes, and the activation of PLase C was considered to play an important role in their degradation.
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  • YUJI MATSUOKA, EIICHI SENNARI, KUNIO HAYAKAWA
    1987 Volume 51 Issue 1 Pages 51-58
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    We encountered two children with chronic idiopathic myocarditis accompanied by marked right ventricular dilatation, who died of progressive right hear failure. A definitive diagnosis was made by histological examination of the myocardium at autopsy. The patients were both boys, aged 7 years and 1 year and 4 months, and a number of identical features were evident upon physical and laboratory examinations. No heart murmur was heard, and gallop rhythm was noted in distant heart sounds. Electrocardiogram revealed intraventricular block, low voltage QRS complex, and ST-T abnormality. Two-dimensional Doppler echocradiogram and right ventriculogram showed marked dilatation and decreased contractility of the right ventricle as well as tricuspid regurgitation. Thinning of the wall and marked dilatation of the right ventricle were confirmed at autopsy. Our observations showed that chronic myocarditis associated with tricuspid regurgitation may readily lead to marked right ventricular dilatation even exceeding the degree of left ventricular dilatation. Idiopathic myocarditis associated with such unusual features is relatively rare, and may present problems in differentiation from other congenital heart diseases causing dilatation and dysfunction of the right ventricle.
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  • HITONOBU TOMOIKE, SHUNICHI KASEDA, YOSHITOSHI URABE, MOTOOMI NAKAMURA
    1987 Volume 51 Issue 1 Pages 64-73
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Regional wall motion was analyzed to deduce the muscle property unique to regional contractile states. End-systolic pressure length relations were evaluated 1) under global changes in a contractile state, 2) under selective intracoronary administration of inotropic agents to produce regional hypo- or hyper-kinesis, and 3) before and after extension of size of the ischemia. Linearity of thee end-systolic pressure-length relation was confirmed in each perturbation; however, the behavior of this relation with regard to changes in the slope and X-axis intercept differed among the three situations. When the contractile state was altered globally by intravenous administration of inotropic agents such as dobutamine and propranolol, the slope of the end-systolic pressure-length relation changed in a manner similar to that seen with the pressure-volume relation or stress-strain relation, with no significant changes in the X-axis intercept. Namely, the level of global cardiac function determined the slope of the end-systolic pressure length relation. When regional hypokinesis was produced pharmacologically by selective intracoronary infusion of lidocaine, the X-axis intercept moved rightward, depending on the degree of regional hypokinesis. Expansion in the size of the ischemic area also shifted the X-axis intercept rightward. The latter two phenomena suggested that the hypokinetic segments were stretched by the surrounding intact myocardium. Accordingly, end-systolic pressure-length relations provide useful information concerning the functional state of regional myocardium. The systolic properties of the regional myocardium rendered hypokinetic have to be quantified so as to include the total geometry of the heart.
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  • MAKOTO AKAISHIM, WILLIAM S WEINTRAUB, RICHARD H HELFANT
    1987 Volume 51 Issue 1 Pages 74-82
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Several aspects of regional ischemic myocardial function determined by segment motion are discussed, based on our studies. Although global left ventricular function decreased progressively as the global severity of myocardial ischemia increased, there are several possible factors which may modify this relationship. As for the site of the ischemic area, occlusion of the left anterior descending artery resulted in a greater decrease in the left ventricular ejection fraction than occlusion of the left circumflex artery. Interaction between the ischemic myocardium and the non-ischemic myocardium may be a multi-factorial phenomenon rather than simple tandem stretching. The segment length motion during acute ischemia appears to be complicated. The segment motion of the severe ischemic myocardium during systole and diastole was explained for the most part by a uniform tension-length curve which was independent of changes in the loading condition. This non-linear elastic property was fundamental to the production of segment motion asynchrony. The wall motion of the hypokinetic segment might be explained by a combination of the active change in myocardial stiffness and the non-linear elastic property of the myocardium.
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  • HIROSHI NONOGIH, SHIGETAKE SASAYAMA, SHUNICHI MIYAZAKI, CHUICHI KAWAI
    1987 Volume 51 Issue 1 Pages 83-89
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Mechanisms related to increased left ventricular filling pressure associated with myocardial ischemia were studied in 13 patients with coronary artery disease. Single-plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter in the control and post-pacing periods. All patients developed typical anginal pain during pacing tachycardia. Seven patients (group I) demonstrated no significant changes in ejection fraction (EF) and peak systolic pressure-end-systolic volume ratio (P/Ves) after rapid pacing. End-diastolic pressure (EDP), however, increased significantly from 14.9±4.9 to 24.4±8.5 mmHg (p<0.01). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. In the normal segment, the end-diastolic length (EDL) was augmented by 13.6%, associated with a 22.4% increase in stroke excursion with pacing stress. In the ischemic segment, EDL remained unchanged, but stroke excursion was significantly reduced. The diastolic pressure-volume curve shifted directly upward or more to the right, while the diastolic pressure-length curve moved up on the single curve in the normal segment and shifted directly upward or more to the right, while the diastolic pressure-length curve moved up on the single curve in the normal segment and shifted directly upward in the ischemic segment, so that pressure was higher at any given segment length in the ischemic segment, indicating regional alteration of the diastolic properties. Thus, an ischemic response to pacing tachycardia Changes in the regional myocardial performance are consistent and the global function is determined by the interaction of changes in regional function of both normal and ischemic myocardium.
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  • TAKASHI SERIZAWA, SHIN-ICHI MOMOMURA, OSAMI KOHMOTO, TETSUO OHYA, HIRO ...
    1987 Volume 51 Issue 1 Pages 90-97
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    To investigate the mechanisms of altered myocardial diastolic stiffness and relaxation induced by myocardial oxygen deficit, we compared the hemodynamic effects of low flow ischemia (myocardial infarction model) and hypoxia in which the coronary flow was not reduced (angina pectoris model) in isolated retrograde perfused rabbit hearts. A 15-min hypoxia induced a significant increase in the left ventricular end diastolic pressure (LVEDP 10±3 to 21±7 mmHg, p<0.05), Po(-1±6 to 12±5 mmHg, p<0.01) and TB(41±8 to 54±10 ms, p<0.05), where Po and TB are the asymptote and the time constant of the isovolumetric left ventricular pressure decline (P=Po+A·e-t/TB), respectively. There was a close linear correlation between the delta Po and delta LVEDP (t=0.98, p<0.01), and between delta TB and delta LVEDP (r=0.73, p<0.05). Low flow ischemia increased Po (0±4 to 2±3 mmHg, p<0.05) and TB (43±4 to 50±11 mmHg, NS). When DPI 201-106, a cardiotonic agent, was given to the hypoxia moded by increasing the Ca++ sensitivity of contractile proteins, further increases were observed in LVEDP (to 258 mmHg, p<0.05) and Po (to 157 mmHg, p<0.05). DPI also increased LVEDP (72 to 94 mmHg, NS) and Po(to 44 mmHg, p<0.05) in the ischemia model, However, TB was not altered by DPI. Conclusions: 1) Po reflects the LVEDP, 2) The discrepancies between the changes of T and Po induced by DPI indicate different mechanisms underlying changes in LV diastolic stiffness and relaxation. 3) Both hypoxia and ischemia induced abnormalities in myocardial diastolic stiffness and relaxation.
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  • MASAHARU OZAKI, TAKASHI YAMAGISHI, TOHRU IKEZONO, TATSURO SHIMIZU, YUH ...
    1987 Volume 51 Issue 1 Pages 98-106
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    To assess left ventricular (LV) systolic and diastolic function globally and regionally and to study the relationship between regional asynchrony and global LV function in patients with stable effort angina pectoris (AP) without previous myocardial infarction, we conducted a resting gated radionuclide ventriculographic study in 15 control subjects (N group) and 22 AP patients with isolated disease of the left anterior descending coronary artery (LAD). In nine of these 22 AP patients, LV systolic and diastolic function before surgical revascularization (Aorto-Coronary Bypass) were compared with those after surgical revascularization. A computer program subdivided the image of the LV into four regions (septal, basal, lateral and apical) by our previously reported method.1, 2 The time-activity and first-derivative curves of the global LV and three regions (septal, lateral, apical; the basal region was not computed) LV were computed. In the global LV, the peak filling rate (PFR) normalized to LV end-diastolic volume (EDV) and the ratio of increment of filling volume at 100 msec from global end-systole (ES) to the EDV (%EFV), which was correlated with the time constant of LV pressure decay during isovolumic relaxation, 3 decreased (p<0.01, p<0.001, respectively) and time to PFR ('time interval from global ES to PFR) was greater (p<0.001) in the AP group than that in the N group. However, in the AP group, the ejection fraction (EF), normalized peak ejection rate (PFR) and %1/3SV, which was defined as the percent stroke volume ejected during the first third of the global LV ejection phase, were not different from these in the N group. With regard to REGIONAL LV FUNCTION, the regional %1/3SV decreased only in the septal region perfused by the stenosed vessel. There were no significant differences in regional EF or PER between the two groups. ASYNCHRONOUS differences in regional EF or PER between the two groups. ASYNCHRONOUS INDEXES were defined as the sum of the absolute value of the time differences between global and regional timing of PER, ES or PFR, and were expressed as TPER, TES, and TPFR, respectively. TES and TPF were significantly greater in the AP group (p<0.01, p<0.001, respectively). A negative correlation existed between TPF and global PFR (r=-0.65, p<0.001). After surgical revascularization, %EFV, PFR and asynchrony at the PFR (TPFR) improved (p<0.05, p<0.01, p<0.01, respectively). There was a good negative correlation between the changes in PFR after A-C Bypass operation and those in TPFR after A-C Bypass (r=0.828, p<0.01). Thus, in AP with one-vessel disease, regional asynchronous wall motion occurs between the side perfused by the stenosed vessel and the normally perfused side in late systole and early diastole, which may cause impairment of global LV filling, and these diastolic impairments are reversible.
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  • MASATSUGU HORIM, MASAFUMI KITAKAZE, YOSHIO ISHIDA, MICHITOSHI INOUE
    1987 Volume 51 Issue 1 Pages 107-113
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The goal of this study was to investigate the mechanisms of impaired relaxation in ischemic and reperfused hearts without asynergic wall motion. to test the hypothesis that muscle elongation during ischemia does not improve the slowed relaxation, the time constant (T) of the isovolumic left ventricular pressure decay was obtained during volume loading in 14 isolated perfused canine hearts. In the nonischemic condition (coronary perfusion pressure: 107±3 mmHg), T progressively decreased as the peak left ventricular pressure was increased by volume loading. In contrast, in the ischemic condition (coronary perfusion pressure: 51±3 mmHg), T did not decrease despite an increase in peak left ventricular pressure by volume loading. These results indicate that during ischemia the impaired relaxation is not improved by an increase in preload. Moreover, reperfusion after a brief ischemia also increased T despite an increase in the contractile force, i.e., left ventricular pressure. The maximal change in the relaxation rate occurred much earlier than the maximal change in the relaxation rate occurred much earlier than the maximal overshoot of the contractile force and coincided with an increase in coronary blood flow. These results indicate that prolongation of relaxation immediately after reperfusion is partly attributable to an increase in the electile force induced by the refilling of the coronary arteries. These mechanisms of impaired relaxation during ischemia and reperfusion may deteriorate ventricular filling and hence, cardiac output.
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  • YOICHI GOTO, MATSUHIKO HIRAMORI, HIROYUKI SUGA
    1987 Volume 51 Issue 1 Pages 114-119
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    We evaluated left ventricular (LV) regional work from a wall tension-regional area (T=A) loop using sonomicrometers in the excised cross-circulated canine left ventricle connected to a volume servo pump. Regional work assessed from a T-A loop closely agreed with the predicted value calculated from LV stroke work and percent regional area under conditions of the control state, dobutanime infusion, and global ischemia. In addition, globally integrated regional work over the entire ischemic and non-ischemic zones agreed closely with LV stroke work either before or after coronary occlusion. These results indicate that LV regional work can be assessed reliably from the T-A loop in both normal and regionally ischemic hearts. Regional work correlated linearly with end-diastolic regional area, indicating a regional Frank-Starling relation, and the slope of this relationship increased with dobutanime infusion and decreased with global ischemia. The correlation between regional work and LV stroke work was also linear and the regression line was the same during the control state and global ischemia, indicating a constant relationship between the work of a specific wall region and LV stroke work regardless of global changes in contractile state. However, after regional ischemia, this regression line apparently shifted downward because T-A loops in the ischemic region were extremely deformed and regional work markedly decreased. From these results, we concluded that T-A loops are a reliable and useful means of assessing regional contractile performance of the LV.
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  • MOTOAKI SUGAWARA, KIYOHARU NAKANO
    1987 Volume 51 Issue 1 Pages 120-124
    Published: January 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    We introduce a new method of defining regional work of the ventricle and evaluating regional myocardial function using the relationship between mean wall stress (σ) and the natural logarithm of the reciprocal of wall thickness (1n(1/H)). The σ-1 n (1/H) relationship was studied during pressure loading, contractility change, volume loading and the development of ischemia in ten anesthetized dogs. The validity of our method is discussed. At the time of cardiac catheterization, our method was applied to three human subjects: one with a normal heart, one with anterior acute myocardial infarction, and one with inferior acute myocardial infarction. The functioning state of a region of the ventricular wall was evaluated quantitatively by the amount of regional work per stroke.
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