JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
55 巻, 11 号
選択された号の論文の17件中1~17を表示しています
  • MAKOTO KONDO, YOUSUKE YUZUKI, HIROMASA SHIMIZU, ATSUO TANAKA, MIKIMARO ...
    1991 年 55 巻 11 号 p. 1045-1049
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    The usefulness of a scoring system with early technetium-99m pyrophosphate scintigraphy as a method for evaluating the efficacy of myocardial preservation after thrombolysis was studied. The mean time from the onset of acute myocardial infarction to injection of the tracer was 5.6±1.5h (range 2.8 to 11.9h). All 36 patients underwent successful recanalization. Patients with strongly positive technetium-99m pyrophosphate uptake in anterior acute myocardial infarction had a significantly lower regional ejection fraction and a significantly larger thallium-201 defect score than those with 2+ positive results in chronic stage. Similarly, in inferior acute myocardial infarction, the thallium-201 defect score was significantly larger in patients with strongly positive uptake than in those with 2+ and negative uptake scores. In conclusion. strongly positive results in early technetium-99m pyrophosphate scintigraphy within 12h after the onset of acute myocardial infarction may indicate failure in limiting the infarct size by coronary thrombolysis.
  • KENSUKE EGASHIRA, TETSUZI INOU, TSUTOMU IMAIZUMI, HITONOBU TOMOIKE, AK ...
    1991 年 55 巻 11 号 p. 1050-1056
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    Atrial natriuretic peptide (ANP) is recognized as an"endogenous vasodilator". The purpose of this study was to determine the effects of a clinical therapeutic dose of synthetic alpha-human ANP on the coronary circulation in 15 subjects with normal coronary arteries and normal ventricular function. The epicardial coronary arterial diameter was measured by selective coronary arteriography. Coronary blood flow was estimated from the arterial cross-sectional area and the flow velocity determined using an subselective intracoronary Doppler catheter. ANP, 0.03 micrograms/min/kg given intravenously over 15 minutes, caused a dilation of the large epicardial coronary artery (n=8): the diameter of the proximal left anterior descending artery dilated from 2.6±0.4 to 3.1±0.5mm (p<0.01). Mean anterial pressure decreased from 89±5 to 83±5mmHg (p<0.01): heart rate did not change during ANP infusion. Estimated coronary blood flow significantly increased (n=6, p<0.01). and thus the coronary vascular resistance decreased after ANP infusion. suggesting an ANP-induced dilation of resistance vessels. The present study demonstrates that in human subjects a clinical dose of ANP by intravenous infusion dilates both the large epicardial and small resistance coronary vessels. These results suggest a potenitally beneficial role for ANP in reducing the severity of myocardial ischemia in patients with ischemic heart disease.
  • JUNICH HASEGAWA, TORU TAKAMI, TAKAFUMI KANEDA, WATARU YAMANE, AKIRA HO ...
    1991 年 55 巻 11 号 p. 1057-1060
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    A middle aged woman with idiopathic long QT syndrome was found to have repetitive ventricular tachycardia of the "torsade de pointes" type. The arrhythmia was resistant to mexiletine and lidocaine, but was controlled by intravenous magnesium sulfate (MgSO4). The recurrent attacks were abolished by a bolus of 2.0g MgSO4, and extremely prolonged QTU interval was reduced by intravenous infusion of 5 mg/min MgSO4 for 36h. This case shows the effectiveness of intravenous magnesium in controlling the attack of torsade de pointes in patients with idiopathic long QT syndrome.
  • KANJI IGA, KENJIRO HORI, KATUJI KITAGUCHI, TADASHI MATSUMURA, HIROMITU ...
    1991 年 55 巻 11 号 p. 1061-1067
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    Eight cases of transient reversible segmental asynergy of the left ventricle thought not to be related to coronary artery lesions are reported. Three cases were associated with inflammatory reactions of unknown origin, and one each with lactic acidosis, abdominal surgery, hypoglycemia, tetanus and pneumonia. None of the patients had symptoms suggestive of ischemic heart disease before or after these episodes. Electrocardiograms before these episodes were all normal. Two-dimensional echocardiography was performed to evaluate abnormal electrocardiograms. Coronary angiography was performed in 4 of 8 cases and was normal in all 4 cases; 2 done as emergencies and 2 non-emergencies. Two ergonovine tests were negative. Left ventricular wall motion abnormalities. present mainly at the apex of the left ventricle, returned to normal in I to 4 weeks. Giant negative T waves in the chest leads during this recovery period were characteristic electrocardiographic features and normalized in 6 weeks on average . We believe that these episodes were not related to ischemia due to coronary artery disease, but to some metabolic humoral factors. An excellent prognosis can be expected if these abnormal metabolic circumstances can be resolved.
  • HITOSHI TANIO, TOSHIAKI KUMADA, MASATAKA HAYASHI, YOSHIHIRO HIMURA, YA ...
    1991 年 55 巻 11 号 p. 1068-1076
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    To evaluate the effects of a new phosphodiesterase inhibitor. E-1020 (1, 2-dihydro-6-methyl-2-oxo-5-(imidazo [1, 2-a] pyridin-6-yl)-3-pyridine carbonitrile hydrochloride monohydrate), on cardiovascular hemodynamics in acute heart failure, we compared its effects with those of dopamine on experimentally produced acute mitral regurgitation in dogs. After the production of mitral regurgitation by transmyocardial chordal sectioning and obtaining a stable state, dopamine (5μg/kg/min) was infused until the peak positive dP/dt (peak (+) dp/dt) increased to about 50% of the pre-dopamine value. After complete recovery. E-1020 (30μg/kg) was infused over 5 min and the data were obtained 10 min later. Both drugs equally increased peak ( + ) dp/dt, decreased systemic vascular resistance. and increased cardiac output. Left ventricular (LV) end-diastolic pressure. LV end-diastolic segment length (EDL). and mean left atrial (LA) pressure decreased with both drugs. The changes in EDL and mean LA pressure were larger with E-1020 than with dopamine (p<.01 and p<.05). Although mean inferior vena caval blood flow volume (mIVCF) increased and mean inferior vena caval pressure decreased with both drugs, the increment of mIVCF was smaller with E-1020 (p<.001). Thus. E-1020 had not only a positive inotropic effect but also a vasodilatory action both on resistance vessels and on capacitance vessels.
  • SHIGENORI ISHIKAWA, MASAAKI HONDA, SACHIKO YAMADA, SHIGEFUMI MORIOKA, ...
    1991 年 55 巻 11 号 p. 1077-1085
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    To investigate the changes in beta-adrenergic receptors in the right and left ventricles during the development of cardiac hypertrophy, right ventricular hypertrophy (RVH) was induced in rats by a single injection of monocrotaline (M) (60mg/kg). The rats demonstrated RVH at 2 weeks and severe RVH with congestive heart failure at 4 weeks after the injection. Changes in the beta-adrenergic receptors in the membrane fractions of both ventricles were examined in the M-treated vs. control rats using 125I-iodocyanopindolol (ICYP). Plasma and tissue catecholamines were measured. Plasma levels of nor-epinephrine (NE) and epinephrine (EP) showed no change at 2 weeks after the injection. However. at 4 weeks there was a significant increase in NE (p<0.01), but not in EP. There was no significant change in NE or EP in either ventricle at 2 weeks vs. the controls. However, at 4 weeks there was a significant increase in both NE and EP in the right ventricle (RV) (p<0.05). NE in the left ventricle (LV) tended to increase. but not a significant extent (p<0.1). With the development of RVH at 2 weeks, the maximum number of binding sites (Bmax) in both the RV and LV showed a significant decrease (p<0.01). There was a 21% decrease of Bmax in the RV and 15% in the LV at 2 weeks vs. the controls. At 4 weeks, the changes in Bmax were more prominent, with a 57% decrease in the RV and 22% in the LV. At 2 weeks the dissociation constant (Kd) of the RV decreased significantly (p<0.01), but the Kd of the LV showed no significant difference vs the control. At 4 weeks. Kd of the ventricles in the M-treated rats showed no significant difference vs. the control. These observations suggest that during the development of RVH, beta-adrenergic receptors were down-regulated not only in the hypertrophic RV but also in non-hypertrophic LV.
  • KENJI IIZUKA, HIDEAKI KAWAGUCHI, HISAKAZU YASUDA
    1991 年 55 巻 11 号 p. 1086-1093
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    This study was undertaken to investigate the correlation between hypoxic cell injury and protease activity, as well as the effects of α1-, and β-adrenergic blocking agents and calcium antagonists during hypoxia. Cell death during hypoxia rose to 80% after 6h. Calpain activity increased to 4 units during hypoxia, much higher than the 0.7 units seen in aerobic condition at 6h. This activity was markedly inhibited by calpain-specific inhibitor I (n-acetyl-leucyle-leucyle-norleucinal). α1-adrenergic blocking agents did not affect calpain activity and cell death under hypoxia. On the other hand, β-adrenergic blocking agents and calcium antagonists suppressed the calpain activity and decreased cell death during hypoxia. These β-adrenergic blocking agents and calcium antagonists also inhibited intracellular calcium-influx during hypoxia. These results suggest the β-adrenergic receptor stimulation activates adenylate cyclase activity and enhances calcium-influx during hypoxia. The elevated intracellular calcium concentration then stimulates calpain activity under hypoxia. These results prove that β-adrenergic blocking agents and calcium antagonists prevent protein degradation during hypoxic cell injury.
  • KOH ARAKAWA, THEDORE PAPAZOGLOU, THANASSIS PAPAIOANNOU, WEI QIANG SHI, ...
    1991 年 55 巻 11 号 p. 1094-1105
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    In order to develop a reliable laser-induced fluorescence (LIF) guided laser angioplasty system, real time, pulse-by-pulse fluorescence spectra were recorded and the same fiberoptic was used for both detection of the fluorescence and for atheromatous tissue ablation. A 308nm XeCl excimer laser served as the laser source for both the induction of fluorescence and the ablation. The fluorescence signal was induced at high laser energies during ablation without any serious change in the fluorescence pattern. A new characteristic fluorescence peak at 540nm for atheromatous tissue was observed after treatment with chlortetracycline hydrochloride (CTC). This allowed the development of an algorithm and a subsequent index to discriminate the atheromatous tissue from the normal tissue. During atheromatous tissue ablation, this index changed as normal tissue was approached, thereby avoiding vessel perforation. Our results suggest that monitoring of this index through the catheter delivering the laser energy enhances selective ablation while simultaneously reducing the risk of vessel perforation.
  • MASAO ENDOH
    1991 年 55 巻 11 号 p. 1108-1117
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    The relationship between changes in intracellular Ca+2 transients and isometric contractions has been assessed in intact cardiac muscle preparations, superficial cells of which have been microinjected with the Ca+2-sensitive bioluminescent protein aequorin. Regulation of myocardial contractility by physiological and pathophysiological intervention is achieved by either (1) modulation of intracellular Ca+2 mobilization. or (2) modulation of Ca+2 sensitivity of myofibrils, or both. Regulation of contractility by changes in heart rate a well established frequency-force relationship that plays an important role in the cardiac pumping function in situ is mainly achieved by mechanism (1), other mechanisms becoming involved depending on the range of frequency of stimulation. The length-dependent regulation of contractility (length-tension relationship in vitro or Frank-Starling's law, or ventricular function curve in situ) is achieved essentially by mechanism (2). Catecholamines promote mechanism (1) through activation of β- and/or α -adrenoceptors, α-adrenoceptor stimulation being much less effective than β-stimulation in this respect. β-Adrenoceptor stimulation decreases, while a -stimulation may increase the Ca+2-sensitivity of contractile proteins. Subsequent to exposure of muscle preparations to Ca+2 free solution, a prominent and reversible dissociation of force of contraction from Ca+2 transients was produced when the [Ca+2]0 was gradually returned to the level of the normal Krebs-Henseleit solution ([Ca+2]0=2.5mM). The aequorin-injected multicellular intact myocardial cell preparation provides an excellent experimental paradigm through which to address the physiological. pharmacological and pathophysiological modulation of E-C coupling in mammalian cardiac muscle. The subcellular mechanism involved, especially in the pathophysiological modulation of Ca+2 signaling process in myocardial cells, awaits further study.
  • NOBORU KANEKO, KUNIHIKO TERAOKA, YOSHIFUMI HORIKAWA, TATSURO UCHIDA, R ...
    1991 年 55 巻 11 号 p. 1118-1123
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    Using a modified Langendorff system. we established an experimental model of kinetic cell death in the rat heart. After calcium (5.5mM) was loaded for 20 min and 10-7 mol isoproterenol was then delivered to the perfusion medium. the hearts developed tonic contracture. Histological examination of the myocardium revealed widespread kinetic cell death. Stimulation of α -adrenoceptors with phenylephrine did not induce kinetic cell death. even after calcium loading. In our kinetic cell death model in the rat, the outflow of creatine phosphokinase into the perfusion medium was increased after isoproterenol application. with a peak occurring at 45 min. The peak transient increase in the intracellular calcium ion concentration (the Ca-transient) was measured using Fura2/AM, and was found to be augmented by increasing the calcium concentration of the perfusion medium. These results suggest that in the presence of an increased intracellular calcium concentration. even slight stimulation of β-adrenoceptors can easily induce myocardial injury.
  • TERUHIKO TOYO-OKA, MINORU MORITA, WOO SEE SHIN, YOKO OKAI-MATSUO, TSUN ...
    1991 年 55 巻 11 号 p. 1124-1126
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
  • TSUNEHIKO KUZUYA, HISAKAZU FUJI, SHIRO HOSHIDA, AKIRA KITABATAKE, MICH ...
    1991 年 55 巻 11 号 p. 1127-1131
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    Free radicals derived from polymorphonuclear leukocytes (PMN) have been suggested to play an important role in myocardial ischemia-reperfusion injury. To define the mechanism by which activated PMN exacerbate ischemic myocardial damage. we investigated the extent of cell injury. free radical generation and lipid peroxidation in embryo mouse myocardial cells co-incubated with activated PMN. The generation of free radicals derived from PMN correlated with the extent of myocardial cell injury. Among the cell sheets preconditioned with hypoxic and glucose free medium. PMN-adhered myocardial cells were initially injured after adding PMN activator. extending to adjacent cells. Chemiluminescence emission and thiobarbituric acid reactive substance in the co-incubated cells were markedly increased and sustained compared with those in each cell monoincubation. The augmented lipid peroxidation was related to the progression of myocardial cell injury. These results indicate that PMN-derived free radicals cause membrane disruption, contributing to the progression of myocardial injury.
  • AKIRA MATSUMORI, IKUTARO OKADA, TAKEHIKO YAMADA, SHINGO MARUYAMA, CHUI ...
    1991 年 55 巻 11 号 p. 1132-1137
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    The pathogenesis of myocardial cell injury in myocarditis and cardiomyopathy was investigated. The presence of viral genomes in the murine heart in experimental coxsackievirus B3 myocarditis was studied by Northern blotting analysis using a 32P-labeled cDNA probe from the 5' end sequence. The strongest signal of positive autoradiograms was always at about 7.4 kilobases, corresponding to the size of the complete genome of the virus. Successive infections with coxsackievirus and encephalomyocarditis (EMC) virus infection showed simultaneous acute myocarditis and healed myocarditis, and the results suggest that successive virus infections cause additional myocardial damage, and develop lesions similar to chronic myocarditis or dilated cardiomyopathy. Antiheart auto-antibody, induced during EMC virus infection, reacted predominantly with myosin. Indium-111 antimyosin scintigraphy showed positive in some of the patients with cardiomyopathy, and the uptake was inversely correlated with left ventricular function. When mice were injected with antimyosin antibody, mouse immunoglobulin G was detected in hearts in the chronic stage of EMC virus myocarditis, in myocytes surrounding fibrosis and calcification, suggesting deposition of antimyosin antibody. Although further study is necessary to clarify the mechansim of uptake of antimyosin in cardiomyopathy, antimyosin anti-body may accumulate in viable myocytes with ongoing degeneration as well as in necrosis.
  • TOHRU IZUMI, MAKOTO KODAMA, MICHIO FUJIWARA
    1991 年 55 巻 11 号 p. 1138-1143
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    In this paper, the ability of human cardiac myosin to provoke autoimmune myocarditis was investigated. Myosin fractions were immunized into A.SW. mice. Lewis rats or Hartley guinea pigs. All of the immunized rats displayed overt symptoms of myocarditis and, in a few cases, died from it. The hearts of these rats were enlarged and discolored. Histologically, the muscles of the heart were characterized by remarkable cell infiltration, extensive myofiber necrosis and the appearance of polynuclear giant cells. Neither mice nor guinea pigs showed such disease profile. In this novel experimental model, the disease state was transferable by T lymphocytes. Thus, cardiac myosin was shown to provoke muscle cell damage through a T cell mediated autoimmune process.
  • CHIHARU KISHIMOTO, HIROSHI OCHIAI, SHIGATAKE SASAYAMA
    1991 年 55 巻 11 号 p. 1144-1148
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    To address unresolved questions, experimental models of viral myocarditis may be of great value. In this study, immunological mechanisms of myocardial dam-age in coxsackievirus B3 myocarditis in mice were investigated. The results showed that susceptibility to viral infection is primarily determined by the gene-tic background of the host, that the severity of myocarditis depends not upon B cells but upon T cells, and that antigen-specific T cells play a pivotal role in the pathogenesis of acute coxsackievirus B3 myocarditis.
  • ISSEI KOMURO, YOUICHI KATOH, EITETSU HOH, FUMIMARO TAKAKU, YOSHIO YAZA ...
    1991 年 55 巻 11 号 p. 1149-1157
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    To examine the molecular mechanisms by which mechanical stimuli induced cardiac hypertrophy and injury, we cultured rat neonatal cardiocytes in deform-able dishes and imposed an in vitro mechanical load by stretching the adherent cells. Myocyte stretching increased total cell RNA content and mRNA levels of c-fos. Marked accumulation of c-fos mRNA followed increases in intracellular Na+ and protein kinase C activation. The accumulation of c-fos mRNA by cardiocyte stretching was suppressed by protein kinase C inhibitors but not by stretch channel blockers. Moreover, myocyte stretching increased inositol phosphate levels. and activation of protein kinase C by phorbolesters stumulated the expression of c-fos. We also examined TGFβ expression in the heart. TGFβ is known to he stimulated by protein kinase C activation. and the mRNA level of TGFβ was increased in in vivo heart by pressure overload. Furthermore, collagen synthesis was stimulated by TGFβ in cultured fibroblasts from hearts. These findings suggest that hemodynamic overload may stimulate cardiac hypertrophy and induce cardiac injury (fibrosis) through protein kinase C activation.
  • TAKAYUKI OZAWA, SATORU SUGIYAMA, MASASHI TANAKA, KAZUKI HATTORI
    1991 年 55 巻 11 号 p. 1158-1164
    発行日: 1991/11/20
    公開日: 2008/04/14
    ジャーナル フリー
    Since mitochondria occupy a pivotal position in energy metabolism, mitochondrial dysfunction is directly linked with disturbances in cellular function. Mitochondria possess their own DNA, which codes 13 subunits of the mitochondrial energy transducing system; the other subunits are coded by nuclear DNA. Recent advances in gene technology, especially the polymerase chain reaction (PCR), permit us to analyze mitochondrial DNA mutations in a small quantity of tissue. We devised rapid and accurate methods to detect mitochondrial DNA mutations, i.e., the primer shift PCR method and the PCR-Southern method. We also developed a method to determine DNA sequences directly without cloning. Using these methods, we revealed that multiple mitochondrial DNA mutations exist in the myocardium of patients with cardiomyopathy. One mutation was based on the following directly repeated sequence: 5'-CATCAACAACCG-3'. This sequence exists in both the ATPase6 gene and the D-loop region, and pseudo-recombination occurs at that directly repeated sequence resulting in a 7.4 kbp deletion. Accordingly, some subunits of the mitochondrial energy transducing system can not be biosynthesized by these deleted mitochondrial DNA, and energy transduction is substantially depleted. Even without reduction of blood supply, mitochondrial DNA mutations can induce a chronic ischemia-like state in the myocardium, which might be a factor in the genesis of cardiomyopathy.
feedback
Top