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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
    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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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Differences in sarcolemmal preparations: Cell surface material and membrane sidedness (1983)
    Springer
    Basic research in cardiology 78 (1983), S. 451-461 
    Details
    ISSN: 1435-1803
    Keywords: isolated sarcolemma ; cell surface material ; sialic acid ; membrane sidedness ; sarcolemmal enzymes ; calcium binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two different procedures were employed for the isolation of sarcolemma from the rat heart and the membranes were studied with respect to the presence of cell surface material as well as their functional characteristics. Both hypotonic shock-LiBr treatment method (fraction HL) and sucrose density gradient method (fraction S) yielded membranes enriched 8 to 13 fold with respect to Na+−K+ ATPase and adenylate cyclase activites in comparison to heart homogenate. Cell surface material was demonstrated on the outer surface of the vesicles only in fraction HL with cationic dyes, lanthanum and ferritin, applied either to the isolated fractions or perfused in the heart through coronaries. Fraction HL also had high sialic acid content. ATP independent Ca2+ binding in fraction HL was about 6 times more than that in fraction S which had little sialic acid and showed no cell surface staining with cationic dyes. On the other hand, ATP-dependent Ca2+ binding and Ca2+-stimulated Mg2+ dependent ATPase activities in fraction S were 4 to 6 times higher than those in fraction HL. Epinephrine stimulated adenylate cyclase in fractions HL and S by 24 and 3% whereas ouabain was found to inhibit Na+−K+ ATPase in these fractions by 80 and 10% respectively. A mild treatment of the membranes with deoxycholate to eliminate the semipermeable characteristics or effects of sidedness of the vesicles resulted in an almost complete ouabain inhibition of Na+−K+ ATPase in both fractions. These data suggest that presence of cell surface material as well as membrane sidedness has an important role inin vitro expression of functional characteristics of sarcolemma. It is emphasized that sarcolemmal preparations containing cell surface material will provide information more realistic to the native conditionsin situ.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02070168
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  • 5
    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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  • 6
    Electronic Resource
    Electronic Resource
    Reduced myocardial injury due to exogenous oxidants in pressure induced heart hypertrophy (1991)
    Springer
    Basic research in cardiology 86 (1991), S. 273-282 
    Details
    ISSN: 1435-1803
    Keywords: Oxygenradical injury ; antioxidants ; hyperfunctionalhypertrophy ; lipid peroxidation ; heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in myocardial function, structure, high energy phosphates and lipid peroxide content were examined in hypertrophied hearts exposed to partially reduced forms of oxygen (PRFO) in an ex vivo system. Heart hypertrophy in rats was produced by narrowing of the abdominal aorta for 6, 12, 24, and 48 weeks. During this period, a stable hypertrophy and hyperfunction with no clinical signs of heart failure is reported to be accompanied by an increase in myocardial superoxide dismutase and glutathione peroxidase activities and a decrease in lipid peroxide content (Gupta and Singal, Circ. Res. 64:398–406, 1989). A 10-min perfusion of sham control hearts with PRFO caused a significant decline in the developed force, ± dF/dt and a rise in resting tension. These changes due to PRFO were significantly less in all groups of hypertrophied hearts. PRFO produced 80.8 ± 4.2 % increase in malondialdehyde (MDA) content in sham controls, while different groups of hypertrophied hearts showed significantly lesser increase (range 45–50 %) in MDA. PRFO resulted in loss of myocardial ATP and CP in control and hypertrophied groups, but this loss was significantly less in all groups of hypertrophied hearts. Both quantitative and qualitative ultrastructural changes due to PRFO were also found to be less in hypertrophied hearts. There were no significant differences among 6- to 48-week hypertrophy groups in their response to PRFO. The study suggests that endogenous antioxidants may serve as putative stabilizers of myocardial subcellular as well as contractile functions against oxidative stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02190607
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  • 7
    Electronic Resource
    Electronic Resource
    Alterations in heart sarcolemmal Ca2+-ATPase and Ca2+-binding activities due to oxygen free radicals (1990)
    Springer
    Basic research in cardiology 85 (1990), S. 45-54 
    Details
    ISSN: 1435-1803
    Keywords: freeradicals ; hydrogen peroxide ; Ca2+-ATPase ; Ca2+-binding ; heart sarcolemma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of oxygen free radicals on Ca2+/Mg2+ ATPase and ATP-independent Ca2+-binding activities were examined in rat heart sarcolemma. Membranes were incubated with different oxygen radical generating media such as xanthine + xanthine oxidase, hydrogen peroxide, and hydrogen peroxide + Fe2+. In the presence of xanthine + xanthine oxidase, Ca2+ ATPase activity was stimulated and this effect was prevented by the addition of superoxide dismutase. Hydrogen peroxide also showed a significant increase in Ca2+-ATPase activity in a dose-dependent manner and this effect was blocked by catalase. On the other hand, a combination of hydrogen peroxide + Fe2+ decreased Ca2+-ATPase activity; this depression was prevented by the addition of D-mannitol. The observed change in Ca2+-ATPase activity due to oxygen free radicals was associated with changes in Vmax, whereas Ka remained unaffected. Both xanthine + xanthine oxidase and hydrogen peroxide increased whereas, hydrogen peroxide + Fe2+ inhibited the ATP-independent Ca2+-binding activities. It is suggested that oxygen free radicals may influence Ca2+ movements in the cell by altering the Ca2+/Mg2+ ATPase and Ca2+-binding activities of the membrane and these effects may be oxygen-radical species specific.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907013
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  • 8
    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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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Significance of adaptation mechanisms in adriamycin induced congestive heart failure (1992)
    Springer
    Basic research in cardiology 87 (1992), S. 512-518 
    Details
    ISSN: 1435-1803
    Keywords: Adrenergic changes cardiomyopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Natural history of myocardial dysfunction due to chronic contractile deficit consists of physiological and pathophysiological adaptations culminating in congestive heart failure. Among the mechanisms considered is the combination of compensatory as well as the harmful overcompensatory role of the adrenergic system during the genesis of a congestive heart failure “spiral” due to the chronic treatment with adriamycin. Refractoriness of this spiral to various inotropic agents may involve reduced sympathetic support of the myocardium, structural loss of contractile elements and abnormalities of the Ca2+ metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788661
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