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  • 1
    Electronic Resource
    Electronic Resource
    Lipid peroxidation during myocardial reperfusion (1992)
    Springer
    Molecular and cellular biochemistry 111 (1992), S. 49-54 
    Details
    ISSN: 1573-4919
    Keywords: thiobarbituric acid test ; liquid chromatography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Reperfusion of heart muscle after prolonged ischaemia is associated with metabolic and functional abnormalities and eventual cell death. Free radical induced lipid peroxidation of cell membranes is thought to be a major mechanism in the evolution of reperfusion damage. The evidences in support for this kind of damage are based on tissue malondialdehyde quantitation by the thiobarbituric acid test (TBA-test). In an attempt to verify this topic we have subjected isolated and Langendorff perfused rabbit hearts to a period of 60 minutes of severe ischaemia plus 30 minutes of reperfusion. At appropriate time points malondialdehyde was determined in the tissue by means of TBA-test and directly by reversed phase, high pressure, liquid chromatography (HPLC). We have found no correlation between the two compared assays. During reperfusion, there was the formation of non-lipid related, malondialdehyde-like, TBA-reactive substance which leads to overstimations of the extent of lipid peroxidation. On the contrary, by direct HPLC quantitation, there was a decrease of tissue malondialdehyde during ischaemia and during the early phases of reperfusion. Our results demonstrate that TBA-test is not a reliable index of malondialdehyde accumulation in organ system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229573
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Occurrence of oxidative stress during myocardial reperfusion (1992)
    Springer
    Molecular and cellular biochemistry 111 (1992), S. 61-69 
    Details
    ISSN: 1573-4919
    Keywords: oxygen free radicals ; myocardial ischaemia ; myocardial reperfusion ; heart damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Reperfusion, without doubt, is the most effective way to treat the ischaemic myocardium. Late reperfusion may however cause further damage. Myocardial production of oxygen free radicals above the neutralizing capacity of the myocytes is an important cause of this reperfusion damage. There is evidence that prolonged ischaemia reduces the naturally occurring defence mechanisms of the heart against oxygen free radicals, particularly mitochondrial manganese superoxide dismutase, and intracellular pool of reduced glutathione. Consequently, reperfusion results in a severe oxidative damage, as evidenced by tissue accumulation and release of oxidized glutathione. An oxygen free radical-mediated impairment of mechanical function also occurs during reperfusion of human heart. In fact we observed during surgical reperfusion of coronary artery disease (CAD) patients, a prolonged and sustained release of oxidized glutathione;the degree of oxidative stress was inversely correlated with recovery of mechanical and haemodynamic function. These findings represent the rationale for therapeutic interventions which increase the cellular antioxidant capacities and improve the efficacy of myocardial reperfusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229575
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    The effect of propionyl-L-carnitine on the ischemic and reperfused intact myocardium and on their derived mitochondria (1991)
    Springer
    Cardiovascular drugs and therapy 5 (1991), S. 57-65 
    Details
    ISSN: 1573-7241
    Keywords: Propionyl-L-carnitine ; ischemia ; reperfusion ; mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess whether propionyl-L-carnitine protects rabbit heart against the deterioration caused by ischemia and reperfusion, isolated hearts were infused with a medium containing it in different concentrations. During control, normoxic perfusion, and 60 minutes of low-flow ischemia (37°C) followed by 30 minutes of reperfusion, diastolic, and developed pressures were monitored; coronary effluent was collected and assayed for lactate and creatine phosphokinase (CPK); mitochondria were harvested and assayed for oxidative phosphorylation and calcium content; and tissues for concentration of adenosine triphosphate (ATP) and creatine phosphate. Propionyl-L-carnitine reduced the ischemic deterioration of mitochondrial function and the depletion of tissue stores of ATP. On reperfusion, hearts treated with it recovered better than the untreated hearts with respect to left ventricular performance, replenishment of ATP and CP stores, and mitochondrial function. The reperfusion-induced mitochondrial calcium overload and release of CPK were also reduced. The effect of propionyl-L-carnitine was dose dependent. At 10-8 M it failed to modify ischemic and reperfusion damage but protected well at 10-7 M. No further protection was obtained at 10-6 M. Propionyl-L-carnitine thus protects the myocardium against some of the deleterious effects of ischemia and reperfusion. In particular it protects mitochondrial function, perhaps partly by preventing mitochondrial calcium overload. Because this protection occurs in the absence of a negative inotropic effect during normoxia or of a coronary dilatatory effect during ischemia, it cannot be attributed to an energy-sparing effect or to the improvement of oxygen delivery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00128244
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    Paper (German National Licenses)
    Fulltext
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