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Hiroshi Iwao - One of the best experts on this subject based on the ideXlab platform.
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Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates
Hypertension Research, 2009Co-Authors: Yasukatsu Izumi, Hideaki Okatani, Masayuki Shiota, Takafumi Nakao, Go Kito, Katsuyuki Miura, Hiroshi IwaoAbstract:Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a β-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating Myocytolysis, showed that increased Myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardioMyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca^2+-ATPase 2A2 and adenylate cyclase 7; renin–angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferator-activated receptor-γ co-activator-1α, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of β-blockers.
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Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates
Hypertension Research, 2009Co-Authors: Yasukatsu Izumi, Hideaki Okatani, Masayuki Shiota, Takafumi Nakao, Go Kito, Katsuyuki Miura, Ryota Ise, Hiroshi IwaoAbstract:Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a beta-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating Myocytolysis, showed that increased Myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardioMyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca(2+)-ATPase 2A2 and adenylate cyclase 7; renin-angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferator-activated receptor-gamma co-activator-1alpha, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of beta-blockers.
Yasukatsu Izumi - One of the best experts on this subject based on the ideXlab platform.
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Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates
Hypertension Research, 2009Co-Authors: Yasukatsu Izumi, Hideaki Okatani, Masayuki Shiota, Takafumi Nakao, Go Kito, Katsuyuki Miura, Hiroshi IwaoAbstract:Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a β-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating Myocytolysis, showed that increased Myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardioMyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca^2+-ATPase 2A2 and adenylate cyclase 7; renin–angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferator-activated receptor-γ co-activator-1α, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of β-blockers.
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Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates
Hypertension Research, 2009Co-Authors: Yasukatsu Izumi, Hideaki Okatani, Masayuki Shiota, Takafumi Nakao, Go Kito, Katsuyuki Miura, Ryota Ise, Hiroshi IwaoAbstract:Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a beta-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating Myocytolysis, showed that increased Myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardioMyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca(2+)-ATPase 2A2 and adenylate cyclase 7; renin-angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferator-activated receptor-gamma co-activator-1alpha, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of beta-blockers.
John G. Clement - One of the best experts on this subject based on the ideXlab platform.
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Early Histopathologic and Ultrastructural Changes in the Heart of Sprague-Dawley Rats Following Administration of Soman:
Toxicologic Pathology, 1996Co-Authors: Leander Tryphonas, John P. Veinot, John G. ClementAbstract:Male Sprague-Dawley rats were given atropine methylnitrate (20 mg/kg) and HI-6 (125 mg/kg) ip 10 min before a single injection of 130 μg soman/kg sc, and the heart was examined by light and electron microscopy 10, 25, 45, 90, and 180 min after the onset of seizures. Seizures appeared within 6-11 min after treatment. Control rats were given saline sc in place of soman. Early myocardial lesions consisting of hypercontraction and hyperextension of sarcomeres, focal Myocytolysis, and contraction bands were detected in individual or groups of myocardial fibers. Hypercontraction was characterized by shortening of the sarcomere length, disappearance of the I and H bands, and thickening of the Z line. In contrast, hyperextended sarcomeres had thickened I and H bands. Myocytolysis was characterized by a progressively severe focal dissolution of myofilaments and edema of the affected sarcoplasmic area. Contraction bands appeared to result from the breakdown of markedly hypercontracted myofibril bundles. Due to the ...
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Histomorphogenesis of soman-induced encephalocardiomyopathy in Sprague-Dawley rats.
Toxicologic Pathology, 1995Co-Authors: Leander Tryphonas, John G. ClementAbstract:Although myocardial damage caused by soman has been previously reported, its relation to brain damage is unclear. In order to clarify this relationship, we examined the histomorphogenesis of central nervous system (CNS) and myocardial lesions in Sprague-Dawley rats, given atropine methylnitrate (20 mg/kg) and HI-6 (125 mg/kg) ip 10 min before a single injection of 0 or 130 micrograms soman/kg (sc) and sacrificed 45 min and 1.5 hr, 3 hr, 24 hr, and 72 hr later. Bilaterally symmetrical CNS damage began with vacuolation of the neuropil and was followed by astrocytic degeneration and neuronal necrosis culminating in liquefaction necrosis and focal hemorrhage. The cerebral cortex, limbic system, thalamus, and substantia nigra were common target sites. Repair in affected sites was characterized by capillary endothelial cell proliferation, microgliosis, and reversal of microvacuolation. Myocardial damage began with Myocytolysis and contraction bands and evolved into coagulative Myocytolysis and replacement fibrosis with a transient recruitment of acute inflammatory cells. The left ventricle, especially its free wall and papillary muscles, was consistently affected. There was good correlation among seizures, CNS damage, and myocardial lesions at all times following treatment. The results support the view that CNS lesions are associated with protracted seizure activity and provide evidence that myocardial damage is neurogenic.
L. M. Nepomnyashchikh - One of the best experts on this subject based on the ideXlab platform.
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Lytic and contracture-lytic prenecrotic damage to cardiomyocytes: photochemical fluorochrome staining and fluorescent microscopy of the myocardium.
Bulletin of Experimental Biology and Medicine, 2002Co-Authors: V. G. Zimmermann, L. M. NepomnyashchikhAbstract:Acute prenecrotic damage to cardiomyocytes of lytic (Myocytolysis, cytolysis) and contracture-lytic (primary lumpy degradation of myofibrils) types during ischemic and metabolic alteration of the myocardium are detected at the photooptic level by means of photochemical fluorochrome staining and examination under fluorescent light. Comparison of the fluorescent and polarization microscopic pictures showed that changes in cardiomyocytes are determined by local mass redistribution in the sarcomere compartments and transformations of birefraction of myofibrillar system components during necrobiosis. These changes are determined by lysis and coagulation processes in protein structures of sarcomeres.
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Alterative and plastic insufficiency of cardiomyocytes: isoproterenol-induced damage to myocardium during anthracycline cardiomyopathy.
Bulletin of Experimental Biology and Medicine, 2001Co-Authors: E. L. Lushnikova, L. M. Nepomnyashchikh, D. E. SemenovAbstract:The development of regenerative and plastic myocardial insufficiency induced by anthracycline antibiotic rubomycin is accompanied by a decrease in cardiomyocyte sensitivity to damage produced by synthetic catecholamine isoproterenol. The incidence and the size of coagulation necrosis foci of cardiomyocytes developed 6 h after isoproterenol injection significantly decreased with increasing in the interval between rubomycin injection and subsequent administration of isoproterenol. In Wistar rats receiving rubomycin 3-5 days prior to isoproterenol and exhibiting signs of regenerative and plastic insufficiency, no cardiomyocyte contracture, intracellular Myocytolysis, or lump degradation characteristic of cardiac insufficiency induced by endo- and exogenous catecholamines were found.
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Structural features of acute focal metabolic injuries to somatic muscle fibers caused by dimethylparaphenylenediamine
Bulletin of Experimental Biology and Medicine, 1999Co-Authors: M. A. Bakarev, L. M. Nepomnyashchikh, V. G. TsimmermanAbstract:The pathological picture of an acute disorder of cell metabolism caused by dimethylparaphenylenediamine consists of typical focal reactions of striated muscles to injury: myofibril contractures and intracellular Myocytolysis. Analysis of the pathological process demonstrates the time course of contracture injuries as a succession of overcontracture (first-third degree contractures) and necrobiotic phases (fourth degree contracture), followed by lump degradation and macrophagal resorption. Two polar types of contractures are clearly differentiated by the size, shape and structural and metabolic characteristics of target fibers: “ribbons“ and ”medallions”. Disappearance of Z strips, disaggregation, disorientation, and fragmentation of myofibrils are typical of intracellular Myocytolysis. The observed changes form the morphological basis for acute disease of striated muscles.
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General pathological processes in somatic muscles in W/SSM rats with genetically determined metabolic myopathy
Bulletin of Experimental Biology and Medicine, 1998Co-Authors: L. M. Nepomnyashchikh, M. A. Bakarev, V. G. TsimmermanAbstract:Hypertrophy, atrophy, and dystrophy, which reflect the balance between alterative and compensatory-adaptive processes at all levels of structural organization, predominate among structural changes in W/SSM rats with metabolic myopathy under conditions of progressive chronic disorders of cellular homeostasis. Primary universal reactions of striated muscles to damage (myofibril contractures and intracellular Myocytolysis) are observed at the ultrastructural level. Increased incidence of focal changes and the time course of morphological and stereological parameters in a constantly functioning organ (diaphragm) indicate that working muscle fibers are most susceptible to injury.
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Electron microscopic characteristic of major types of acute damage to cardiomyocytes
Bulletin of Experimental Biology and Medicine, 1997Co-Authors: L. M. NepomnyashchikhAbstract:The major (independent) types of acute damage to cardiomyocytes: myofibrillar contractures, intracellular Myocytolysis, primary crumpy degradation, and cytolysis are characterized ultrastructurally. It is shown that dystrophic and necrobiotic changes in the myocardium are mosaic, implying that prior to electron microscopic examination cardiomyocytes should be studied in polarized light.
Go Kito - One of the best experts on this subject based on the ideXlab platform.
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Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates
Hypertension Research, 2009Co-Authors: Yasukatsu Izumi, Hideaki Okatani, Masayuki Shiota, Takafumi Nakao, Go Kito, Katsuyuki Miura, Hiroshi IwaoAbstract:Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a β-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating Myocytolysis, showed that increased Myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardioMyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca^2+-ATPase 2A2 and adenylate cyclase 7; renin–angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferator-activated receptor-γ co-activator-1α, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of β-blockers.
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Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates
Hypertension Research, 2009Co-Authors: Yasukatsu Izumi, Hideaki Okatani, Masayuki Shiota, Takafumi Nakao, Go Kito, Katsuyuki Miura, Ryota Ise, Hiroshi IwaoAbstract:Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a beta-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating Myocytolysis, showed that increased Myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardioMyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca(2+)-ATPase 2A2 and adenylate cyclase 7; renin-angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferator-activated receptor-gamma co-activator-1alpha, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of beta-blockers.
