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  • 1
    Electronic Resource
    Electronic Resource
    Preconditioning and Antioxidant Defense against Reperfusion Injury (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 723 (1994), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1994.tb36721.x
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  • 2
    Electronic Resource
    Electronic Resource
    A biphasic change in contractile proteins during the development of cardiac hypertrophy in pigs (1987)
    Springer
    Basic research in cardiology 82 (1987), S. 1-8 
    Details
    ISSN: 1435-1803
    Keywords: cardiac hypertrophy ; myosin ATPase ; actin-activated myosin ATPase ; myofibrillar ATPase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A non-failing hypertrophy of the left ventricle was produced in the pig heart by supravalvular banding of aorta for 4, 8 and 12 weeks and the myosin and myofibrillar adenosine triphosphatase activities were measured. A significant increase in myosin Ca2+-ATPase activity was seen at 4 weeks of hypertrophy, but at 8 and 12 weeks this activity was significantly decreased compared to sham control. Similar changes were also seen in actin-activated myosin ATPase activities at 4, 8 and 12 weeks of hypertrophy. There were no changes in the K+- and NH4 +-EDTA-stimulated ATPase activities of myosin. Basal ATPase activities of myofibrils were decreased at 4 and 8 weeks of hypertrophy and there was no change in this activity at 12 weeks of hypertrophy. Ca2+ stimulated ATPase activity of myofibrils was significantly increased at 4 weeks, normal at 8 weeks and significantly reduced at 12 weeks of hypertrophy. The changes in ATPase activities were not due to any alterations of proteins by high concentrations of salts during the purification of myosin. The non-hypertrophied right ventricle from the banded animals did not show any change in the basal or Ca2+ stimulated myofibrillar ATPase activities. It is suggested that hypertrophy of the myocardium is accompanied by specific changes in the enzyme activities of the contractile proteins and the biphasic responses may correlate with the functional state of the myocardium subjected to a chronic increase in pressure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907047
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  • 3
    Electronic Resource
    Electronic Resource
    Time-course of cardiac myocyte injury due to oxidative stress (1992)
    Springer
    Molecular and cellular biochemistry 111 (1992), S. 25-31 
    Details
    ISSN: 1573-4919
    Keywords: myocardial cations ; lipid peroxide ; high energy phosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Time course of changes in cell morphology, cation content, lipid peroxidation and high energy phosphates was examined in isolated rat cardiac myocytes exposed to oxygen radicals for 0 to 20 min. Xanthine (2 mM) and xanthine oxidase (10 U/L) mixture was used as a source of oxygen radicals. A significant decrease in the number of rod-shape cells with a concomitant increase in the number of hypercontracted cells was observed within 5 min of exposure to xanthine-xanthine oxidase (x-xo). At 10,15 and 20 min of exposure to x-xo, there was a time-dependant increase in the number of round cells. Lipid peroxide content, as indicated by the thiobarbituric acid reactive material, was significantly and progressively increased between 10 to 20 min of perfusion with x-xo. In myocytes exposed to x-xo, Ca2+ and Na+ were increased by 15% and 45% at 15 min and by 55% and 100% at 20 min respectively. Levels of adenosine tri- and di- phosphates were significantly depressed and that of adenosine mono- phosphate were higher at 20 min. These data support the hypothesis that reactive oxygen intermediates can directly influence myocyte structure and function, but these changes seem to occur more slowly in isolated myocytes than in whole hearts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229570
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  • 4
    Electronic Resource
    Electronic Resource
    Free radicals in health and disease (1988)
    Springer
    Molecular and cellular biochemistry 84 (1988), S. 121-122 
    Details
    ISSN: 1573-4919
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00421045
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  • 5
    Electronic Resource
    Electronic Resource
    Adriamycin-induced leakage of lysosomal enzymes in vitro (1988)
    Springer
    Molecular and cellular biochemistry 81 (1988), S. 89-94 
    Details
    ISSN: 1573-4919
    Keywords: heart lysosomes ; lysosomal permeability ; enzyme leakage ; superoxide radical ; adriamycin effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Chronic treatment of rats with adriamycin has been shown to affect myocardial lysosomes as well as enzyme activities in the serum fraction. In this study, we examined in vitro effects of adriamycin (10−6 to 10−3 M) on the lysosomal fraction isolated from rat ventricular tissue. Morphological examination revealed that the isolated fraction was mainly vesicular in nature. Higher concentrations of adriamycin (10−3 M) caused a significant loss of acid phosphatase and N-acetyl-B-d-glucosaminidase activity from the lyosomal vesicles. The enzyme leakage was not accompanied by any intravesicular localization of lanthanum, an extravesicular electron dense tracer. Preincubation of lysosomal vesicles with 10 μg/ml superoxide dismutase did not protect against adriamycin-induced loss of lysosomal enzymes. The study shows that adriamycin induces loss of lysosomal enzymes in vitro and the superoxide radical may not be involved in this change.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00225656
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  • 6
    Electronic Resource
    Electronic Resource
    Probucol treatment reverses antioxidant and functional deficit in diabetic cardiomyopathy (1996)
    Springer
    Molecular and cellular biochemistry 160-161 (1996), S. 283-288 
    Details
    ISSN: 1573-4919
    Keywords: oxidative stress ; superoxide dismutase ; glutathione peroxidase ; catalase ; lipid peroxidation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Earlier we reported that probucol treatment subsequent to the induction of diabetes can prevent diabetes-associated changes in myocardial antioxidants as well as function at 8 weeks. In this study, we examined the efficacy of probucol in the reversal of diabetes induced myocardial changes. Rats were made diabetic with a single injection of streptozotocin (65 mg/kg, i.v.). After 4 weeks of induction of diabetes, a group of animals was treated on alternate days with probucol (10 mg/kg i.p.), a known lipid lowering agent with antioxidant properties. At 8 weeks, there was a significant drop in the left ventricle (LVSP) and aortic systolic pressures (ASP) in the diabetic group. Hearts from these animals showed an increase in the thiobarbituric acid reacting substances (TBARS), indicating increased lipid peroxidation. This was accompanied by a decrease in the myocardial antioxidant enzymes activities, superoxide dismutase (SOD) and glutathione peroxidase (GSHPx). Myocardial catalase activity in the diabetic group was higher. In the diabetic + probucol group both LVSP and ASP showed significant recovery. This was also accompanied by an improvement in SOD and GSHPx activities and there was further increase in the catalase activity. Levels of the TBARS were decreased in this group. These data provide evidence that diabetic cardiomyopathy is associated with an antioxidant deficit which can be reversed with probucol treatment. Improved cardiac function with probucol may be due to the recovery of antioxidants in the heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00240060
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  • 7
    Electronic Resource
    Electronic Resource
    Subcellular changes during cardiac hypertrophy and heart failure due to bacterial endocarditis (1980)
    Springer
    Basic research in cardiology 75 (1980), S. 81-91 
    Details
    ISSN: 1435-1803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei katheterisierten Kaninchen wurde Streptococcus viridans bzw. Kochsalzlösung (bei Kontrolltieren) injiziert und der Zeitverlauf der Veränderungen in der Herzaktion der myokardialen Ultrastruktur (Membransysteme, Myofibrillen) sowie dem Gehalt an Kationen, zyklischem AMP, Noradrenalin und energiereichem Phosphat verfolgt. Sowohl bei in infizierten als auch bei den nichtinfizierten Tieren ergab sich, daß die Myokardhypertrophie einer verstärkten Aktivität des sympathischen Nervensystems folgt, wie aus der Steigerung der Herzfrequenz sowie des Gehaltes an Noradrenalin- und zyklischem AMP hervorging. Der Rückgang in der Aktivität der sarkolemmalen Na+−Ka+-ATPase-Aktivität war von kontraktilem Versagen begleitet und ging einem Abfall des myokardialen K+-Gehalts und einem Anstieg des Na+-Gehalts voraus. Die Minderung der sarkolemmalen Ca2+-Bindungsaktivität könnte zu einem Rückgang der Ca2+-Aufnahme beitragen und die Minderung des myokardialen Ca2+-Gehaltes und der kontraktilen Aktivität erklären. Diese Veränderungen waren auch von einer reduzierten mikrosomalen Ca2+-Bindung und von einer verminderten mitochondrialen RCI begleitet. Eine reduzierte Aktivität der oxidativen Phosphorylierung in den Mitochondrien bewirkte einen Rückgang der Vorräte an energiereichem Phosphat. Ein Abfall der sarkolemmalen, mitochondrialen und myofibrillären ATPase-Aktivität und der sarkolemmalen Adenylatcyclase wurde in späteren Stadien der bakteriellen Endokarditis beobachtet, in denen auch ausgedehnte Zellschädigungen vorlagen. Diese Beobachtungen lassen vermuten, daß die myokardiale Hypertrophie bei bakterieller Endokarditis Folge eines erhöhten Spiegels an zyklischem AMP ist, während das nachfolgende Herzversagen und die Zellschädigung bei dieser Erkrankung auf Defekte verschiedener Membransysteme-begleitet von myokardialem Ca2+-Defizit-bezogen werden kann.
    Notes: Summary Rabbits were catheterized and injected with saline (uninfected) orStreptococcus viridans (infected) to study the time course of changes in heart function, ultrastructure, membrane systems, myofibrils, and myocardial cations, cyclic AMP, norepinephrine and high energy phosphate contents. Myocardial hypertrophy in both infected and uninfected animals was found to follow increased activity of sympathetic nervous system as indicated by increased heart rate as well as norepinephrine and cyclic AMP contents. The decrease in sarcolemmal Na+−K+ ATPase activity was associated with contractile failure and preceded the observed decrease in myocardial K+ and increase in Na+ contents. The decrease in sarcolemmal Ca2+ binding activity may contribute in decreasing calcium entry and explain decreased myocardial Ca2+ contents and contractile activity; these changes were also accompanied by decreased microsomal calcium binding as well as depressed mitochondrial RCI. Depression in mitochondrial oxidative phosphorylation activity was found to result in declining high energy phosphate stores. Decreases in sarcolemmal, mitochondrial and myofibrillar ATPase activities as well as sarcolemmal adenylate cyclase activity were observed in late stages of bacterial endocarditis, at which time extensive myocardial cell damage was also apparent. These observations suggest that myocardial hypertrophy due to bacterial endocarditis may be a consequence of elevated levels of cyclic AMP whereas subsequent heart failure and cell damage in this disease may be due to defects in different membrane systems accompanied by a myocardial calcium deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02001398
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  • 8
    Electronic Resource
    Electronic Resource
    Negatively charged sites and calcium binding in the isolated rat heart sarcolemma* (1981)
    Springer
    Basic research in cardiology 76 (1981), S. 16-28 
    Details
    ISSN: 1435-1803
    Keywords: heart sarcolemma ; sarcolemmal calcium binding ; surface charge ; colloidal iron staining, membrane-bound enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Beim isolierten Sarkolemm vom Rattenherzen wurde die Färbung mit kolloidalem Eisen, Ca-Bindung und Enzym-Aktivitäten untersucht. Die Färbung mit kolloidalem Eisen zeigte eine hohe Dichte negativ geladener Stellen an der Zelloberfläche. Es wurde festgestellt, daß diese Membranfraktion über Ca-Bindungsaktivität sowohl bei niedriger (0,1 mM) als auch bei hoher (1,25 mM) Ca-Konzentration verfügt. Vorbehandlung des Sarkolemms mit Trypsin, Phospholipase C oder Neuraminidase führte sowohl zu einer Abnahme der Färbung mit kolloidalem Eisen als auch zu einer verminderten Bindungsaktivität für Calcium bei hohen Ca-Konzentrationen. Die Ca-Bindung bei niedrigen Konzentrationen wurde sowohl durch Trypsin als auch durch Neuraminidase vermindert. Die Aktivität der Mg2+-ATPase, Ca2+-ATPase und Na+−K+-ATPase wurde durch Neuraminidase und Trypsin-Behandlung verändert, während Behandlung mit Phospholipase C nur die Na+−K+-ATPase beeinflußte. Es ergibt sich die Schlußfolgerung, daß sowohl den negativen Oberflächenladungen als auch den Ca-Bindungsstellen des isolierten Sarkolemms vom Rattenherzen ein Mosaik von Biomolekülen zugrunde liegt, welches Proteine, Phospholipide und Glycoproteine enthält, und daß Änderungen der Oberflächenladung die Aktivität membrangebundener Enzyme beeinflussen können.
    Notes: Summary Colloidal iron staining, calcium binding and enzyme activities were studied in the isolated rat heart sarcolemma. Colloidal iron staining of the sarcolemma revealed a high density of negatively charged sites associated with the cell surface. This membrane fraction was found to have calcium binding activity at both low (0.1 mM) and high (1.25 mM) concentrations of calcium. Pretreatment of the sarcolemma with either trypsin, phospholipase C or neuraminidase, was associated with a reduction in colloidal iron staining as well as decreased calcium-binding activity at high concentrations of calcium. Calcium binding at low concentrations was decreased by both trypsin and neuraminidase. Mg2+ ATPase, Ca2+ ATPase, and Na+−K+ ATPase activities were altered by neuraminidase and trypsin treatments, whereas phospholipase C treatment altered Na+−K+ ATPase only. It is concluded that both surface negative charge and calcium-binding sites associated with the isolated rat heart sarcolemma are contributed by a mosaic of biomolecules including proteins, phospholipids and glycoproteins, and alterations in the surface charge may influence the activities of membrane-bound enzymes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01908160
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  • 9
    Electronic Resource
    Electronic Resource
    Cardiac alpha- and beta-adrenergic receptor alterations in diabetic cardiomyopathy (1982)
    Springer
    Basic research in cardiology 77 (1982), S. 610-618 
    Details
    ISSN: 1435-1803
    Keywords: diabetic cardiomyopathy ; adrenergic receptors in rat heart ; alpha and beta receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wurde der Einfluß eines chronischen, experimentellen Diabetes auf die adrenergen Rezeptoren des Rattenherzens untersucht. Diabetes wurde durch Streptozotocin (65 mg/kg i.v.) erzeugt. Die Untersuchungen wurden 8 Wochen nach Verabreichung durchgeführt. Es wurden positive und negative dF/dt-Werte (Geschwindigkeit der Kraftentwicklung) von isolierten Papillarmuskeln bestimmt. Die durch Isoproterenol und Methoxamin gesteigerte Kraftentwicklung war bei Ratten mit Diabetes vermindert. Die Bindungseigenschaften von Beta-und Alpha-rezeptoren in den Membranen des Herzens wurden mit Hilfe von3H-dihydroalprenolol und3H-dihydroergocryptin bestimmt. Im diabetischen Myokard war die Zahl der Beta- und Alpharezeptor-Bindungsstellen vermindert, nicht jedoch die Affinitätskonstanten. Die verringerte Beta- und Alpharezeptoren-Dichte im Herz könnte für die verminderte Ansprechbarkeit der Mechanik auf adrenerge Reize bei der diabetischen Kardiomyopathie verantwortlich sein.
    Notes: Summary The effect of chronic experimental diabetes on the adrenergic receptors in the rat heart was investigated. Diabetes was induced by streptozotocin (65 mg/kg; i.v.) administration, animals were sacrificed 8 weeks later, and positive as well as negative dF/dt values were determined in isolated papillary muscle preparations. Stimulation of the contractile force generation by isoproterenol and methoxamine was attenuated in diabetic preparations. Beta-and alpha-adrenergic receptor bindings were determined in cardiac membranes by employing3H-dihydroalprenolol and3H-dihydroergocryptine respectively. Reduced number of beta- and alpha-receptor binding sites without changes in the affinity constants were observed in diabetic myocardium. Such a decrease in alpha- and beta-receptor density in the heart may account for the depressed contractile responsiveness to adrenergic stimuli in diabetic cardiomyopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01908314
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  • 10
    Electronic Resource
    Electronic Resource
    Calcium movements in relation to heart function (1982)
    Springer
    Basic research in cardiology 77 (1982), S. 117-139 
    Details
    ISSN: 1435-1803
    Keywords: calcium movement ; cardiac physiology ; cardiac pathophysiology ; calcium regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es ist allgemein anerkannt, daß Calcium von besonderer Bedeutung für die Funktion der Myokardzelle ist. Trotzdem ist über die genaue Natur der Calcium-Wirkung sowie auch über die mögliche Bedeutung von Calcium für das Absterben einer Myokardzelle wenig bekannt. Fortschritte in der Erforschung der Calcium-Bewegungen im Herzen ermöglichen neue Vorstellungen über die Rolle des Calciums unter physiologischen und pathophysiologischen Bedingungen. Offensichtlich bestehen enge Beziehungen zwischen Calcium-Bewegungen und elektrophysiologischen Abläufen, kontraktiler Funktion, Membranintegrität und Energiemetabolismus. Insbesondere wurde eine neue Theorie entwickelt, die den giemetabolismus. Insbesondere wurde eine neue Theorie entwickelt, die den Inositphosphatid-Umsatz und die Aktivierung der Ca-abhängigen ATPase berücksichtigt im Hinblick auf die Mechanismen und die Kontrolle des Calcium-Eintritts in die Zelle bei Erregung. Änderungen in der Regulierung des Calcium-Stoffwechsels können die Ca-Verteilung in der Zelle beeinflussen und dadruch Herzfunktion und Stoffwechsel verändern. Die Rolle, die Calcium bei der Entwicklung pathologischer Zustände im Myokard spielt, wird im Lichte der Forschungsergebnisse bei Verwendung unterschiedlicher experimenteller Ansätze diskutiert. Es wird postuliert, daß Überladung der Zelle mit Calcium und Calcium-Mangel der Zelle zum kontraktilen Versagen des Herzens und zum Zelltod beitragen durch eine Anzahl definierter Mechanismen. Im Hinblick auf eine sachgerechte Behandlung kardialer Störungen stellt sich daher die Aufgabe, die genaue Natur der Prozesse zu klären, die mit Calcium-Überbeladung oder Calcium-Mangel einhergehen.
    Notes: Summary It is widely recognized that calcium is of singular importance in the viability of the myocardial cell, nonetheless little is known concerning the precise nature of the action of calcium in myocardium as to how it maintains the life of the cell and how it may dictate the death of the cell. However, recent advances in research involved with the study of calcium movement in the heart have been highly valuable for the formulation of new concepts with respect to the physiological and pathological aspects of calcium metabolism in the myocardium. It is becoming clear that calcium movements are closely related to cardiac electrophysiological events, contractile function, membrane integrity and energy metabolism. In particular, a novel theory involving phosphatidylinositol turnover and Ca2+-dependent ATPase activation has been advanced regarding the mechanism and control of calcium entry into the cardiac cell upon excitation. Alterations in the regulation of calcium metabolism through the interaction of a number of separate, elements may affect calcium distribution in the cell and thereby may change cardiac function and metabolism. The part calcium plays in the genesis of pathological states in the myocardium is discussed in the light of research employing various experimental protocols. Intracellular calcium overload and deficiency are postulated to contribute to cardiac contractile failure and cell death through a number of distinct mechanisms. It is now a real challenge to understand the precise nature of processes associated with the occurrence of intracellular calcium overload or intracellular calcium deficiency in order to achieve proper management of cardiac disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01908167
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