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  • 1
    Electronic Resource
    Electronic Resource
    Oxygen free radicals and calcium homeostasis in the heart (1994)
    Springer
    Molecular and cellular biochemistry 139 (1994), S. 91-100 
    Details
    ISSN: 1573-4919
    Keywords: sarcolemma ; myofibrils, Na+/Ca2+ exchange ; sarcoplasmic reticulum ; cardiac contraction ; Ca2+ pump
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Many experiments have been done to clarify the effects of oxygen free radicals on Ca2+ homeostasis in the hearts. A burst of oxygen free radicals occurs immediately after reperfusion, but we have to be reminded that the exact levels of oxygen free radicals in the hearts are yet unknown in both physiological and pathophysiological conditions. Therefore, we should give careful consideration to this point when we perform the experiments and analyze the results. It is, however, evident that Ca2+ overload occurs when the hearts are exposed to an excess amount of oxygen free radicals. Though ATP-independent Ca2+ binding is increased, Ca2+ influx through Ca2+ channel does not increase in the presence of oxygen free radicals. Another possible pathway through which Ca2+ can enter the myocytes is Na+−Ca2+ exchanger. Although, the activities of Na+−K+ ATPase and Na+−H+ exchange are inhibited by oxygen free radicals, it is not known whether intracellular Na+ level increases under oxidative stress or not. The question has to be solved for the understanding of the importance of Na+−Ca2+ exchange in Ca2+ influx process from extracellular space. Another question is ‘which way does Na+−Ca2+ exchange work under oxidative stress? Net influx or efflux of Ca2+?’ Membrane permeability for Ca2+ may be maintained in a relatively early phase of free radical injury. Since sarcolemmal Ca2+-pump ATPase activity is depressed by oxygen free radicals, Ca2+ extrusion from cytosol to extracellular space is considered to be reduced. It has also been shown that oxygen free radicals promote Ca2+ release from sarcoplasmic reticulum and inhibit Ca2+ sequestration to sarcoplasmic reticulum. Thus, these changes in Ca2+ handling systems could cause the Ca2+ overload due to oxygen free radicals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944207
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Oxygen free radicals and calcium homeostasis in the heart (1994)
    Springer
    Molecular and cellular biochemistry 135 (1994), S. 99-108 
    Details
    ISSN: 1573-4919
    Keywords: sarcolemma ; myofibrils ; Na+/Ca2+ exchange ; sarcoplasmic reticulum ; cardiac contraction ; Ca2+ pump
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Many experiments have been done to clarify the effects of oxygen free radicals on Ca2+ homeostasis in the hearts. A burst of oxygen free radicals occurs immediately after reperfusion, but we have to be reminded that the exact levels of oxygen free radicals in the hearts are yet unknown in both physiological and pathophysiological conditions. Therefore, we should give careful consideration to this point when we perform the experiments and analayze the results. It is, however, evident that Ca2+ overload occurs when the hearts are exposed to an excess amount of oxygen free radicals. Though ATP-independent Ca2+ binding is increased, Ca2+ influx through Ca2+ channel does not increase in the presence of oxygen free radicals. Another possible pathway through which Ca2+ can enter the myocytes is Na+−Ca2+ exchanger. Although, the activities of Na+−K+ ATPase and Na+−Ca2+ exchanger. Although, the activities of Na+−H+ exchange are inhibited by oxygen free radicals, it is not known whether intracellular Na+ level increases under oxidative stress or not. The question has to be solved for the understanding of the importance of Na+−Ca2+ exchange in Ca2+ influx process from extracellular space. Another question is ‘which way does Na+−Ca2+ exchange work under oxidative stress? Net influx or efflux of Ca2+?’ Membrane permeability for Ca2+ may be maintained in a relatively early phase of free radical injury. Since sarcolemmal Ca2+-pump ATPase activity is depressed by oxygen free radicals, Ca2+ extrusion from cytosol to extracellular space is considered to be reduced. It has also been shown that oxygen free radicals promote Ca2+ release from sarcoplasmic reticulum and inhibit Ca2+ sequestration to sarcoplasmic reticulum. Thus, these changes in Ca2+ handling systems could cause the Ca2+ overload due to oxygen free radicals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00925965
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    31P-NMR magnetization transfer study of reperfused rat heart (1993)
    Springer
    Molecular and cellular biochemistry 119 (1993), S. 121-127 
    Details
    ISSN: 1573-4919
    Keywords: saturation transfer ; nuclear magnetic resonance ; reperfused heart ; high-energy phosphate ; ATP ; creatine phosphate ; inorganic phosphate ; cardiac performance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The relationships between pressure rate product (PRP) and flux(PCr → ATP) or flux(Pi → ATP) were studied in isolated perfused rat hearts by the method of saturation transfer using31P-NMR during the preischemic and reperfusion periods. The hearts were made ischemic for 15 min, followed by 60 min of reperfusion. PRP was almost completely depressed, and recovered to 60^ of the control level (preischemic period) after reperfusion. The ATP level during reperfusion was significantly decreased, whereas there was no significant change in PCr level. Pi level of reperfused hearts was significantly higher than that in the control. Both flux(PCr → ATP) and flux(Pi → ATP) were significantly decreased during the reperfusion period (both p〈0.05). However, the flux(PCr → ATP)/PRP ratio during reperfusion did not differ from that of the control. This result indicates that the decrease in flux(PCr → ATP) was matched by a similar decrease in cardiac performance. In contrast, the flux(Pi → ATP)/PRP ratio during reperfusion was significantly decreased compared to that of control. These results suggest that the stunned heart needs less ATP turnover in proportion to its depressed contractile activity, and flux(Pi → ATP) may limit the recovery of postischemic performance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926862
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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