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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Molecular Basis of Disease 1227 (1994), S. 53-59 
    ISSN: 0925-4439
    Keywords: Mitochondrial function ; Oxidative metabolism ; Polyunsaturated fatty acid ; Stunned myocardium
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 16 (1984), S. 12 
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 16 (1984), S. 73 
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 16 (1984), S. 73 
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 26 (1994), S. 949-958 
    ISSN: 0022-2828
    Keywords: Cardiomyocytes ; Heart ; Hypoxia ; Metabolism ; Mitochondia, LDH ; Trimetazidine
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 83 (1988), S. 77-86 
    ISSN: 1435-1803
    Keywords: myocardial metabolism ; fatty acid oxidation ; fatty acid blockers ; long-chain acyl esters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fatty acid metabolites (long-chain esters of CoA and carnitine) which collect in ischemic myocardium can form amphiphiles capable of disrupting subcellular performance. It is important to document the role of these amphiphiles in intact tissue. D-Octanoylcarnitine was chosen because of its previously described effects on inhibiting palmitoylcarnitine transferasc (PCT-II) inin vitro andin vivo liver preparations. This inhibition will shift tissue levels of CoA and carnitine intermediates and thus alter amphiphile levels. The compound's actions in cardiac muscle are unknown. Dose response curves were developed in intact hearts to test the influence of D-octanoylcarnitine at pharmacological concentrations. Measurements were obtained in working, extracorporeally perfused, swine hearts. Drug was administered either systemically (IV) or via dircct intracoronary (IC) infusions into the left anterior descending coronary circulation. Excess fatty acids were provided to ensure adequate fatty acid substrate for oxidation. Coronary flow was controlled at aerobic levels. Systemic administration of D-octanoylcarnitine (0.8–6.8 mM) resulted in transient peripheral hypotension which caused correlative decreascs in14CO2 production from labeled palmitate. Infusion of D-octanoylcarnitine (0.5–3.9 mM) IC did not cause appreciable hypotension and was not associated with suppression of fatty acid oxidation. No build-up of carnitine esters was noted in treated hearts but acyl CoA levels were reduced (p〈-0.002). This latter finding was modestly related to increasing dose schedule of the compound in the IC group. The lack of suppression in fatty acid oxidation argues against significant inhibition of PCT II and lessens the attractiveness of using D-octanoylcarnitine in intact myocardium to selectively bloock fatty acid utilization at this locus.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 89 (1994), S. 293-307 
    ISSN: 1435-1803
    Keywords: Heart ; stunning ; mitochondria ; oxidation ; energetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of cardiac stunning on the oxidation of fatty acids and the oxidative phosphorylation in mitochondria was investigated. Rat hearts were perfused for 15 min according to the working mode with a Krebs-Henseleit buffer containing glucose (11 mM). The hearts were then maintained in normoxic conditions (C group) or subjected to a 15-min global no-flow normothermic ischemia followed by a 30-min reperfusion (R group). Throughout the perfusion, the aortic and coronary flows, and the heart rate and oxygen consumption were monitored. At the end of the perfusion procedure, a bolus of 1-14C palmitate was injected in the coronary arterial bed to evaluate the fatty acid oxidation. Two sub-populations of mitochondria were isolated from each heart by either mechanical (ME mitochondria) or enzymic (EE mitochondria) extraction and their respiration properties were evaluated. Furthermore, the mitochondrial energy production (ATP and creatine phosphate) was assessed. During ischemia, the aortic flow was suppressed and recovered only to approximately 50% of the preischemic value during reperfusion. This mechanical stunning was associated with an important reduction of the stroke volume (−37%,p〈0.01) and a slight decrease in heart rate (−20%,p〈0.001). At the end of reperfusion, the beta-oxidation rate constituted 55±1.7% of the cell palmitate and was similar to that assessed in the C group. The oxygen consumption was decreased to 216±31.0μL O2/min/gww and the venous O2 concentration increased to 5.1±0.572 μL O2/mL (instead of 2.9±0.342 μL O2/mL in the C group), although due to large SD, only the latter was statistically significant. A decrease in metabolic effeciency (42±14.4 vs 106±16.8 mL/μL O2 in the C group) and an increase in palmitate oxidation to oxygen consumption ratio (77±10.1 vs 47.6±4.25 % beta-oxidized palmitate/μL O2 in the C group) were observed. This increased fatty acid contribution in the oxidation metabolism could be responsible for some oxygen wasting and could contribute to decrease the energy available for the contraction despite the normal cardiac oxygen uptake. Furthermore, the respiration parameters of the mitochondria were similar in the C and R groups when glutamate (20 mM) or palmitoylcarnitine (25 μM) were used as substrate. ME mitochondria of R group displayed a reduced rate of ATP production (118±29.5 vs 180±14.5 nmoles/min/mg proteins in the C group) without altered creatine phosphate production. The presence of calcium in the medium (10−5 M) provoked a decrease in ATP production. These effects were not observed with EE mitochondria. Thus, a decreased energy production resulting from a substrate effect and/or a decreased mitochondrial phosphorylative capacity could be associated with the mechanical stunning.
    Type of Medium: Electronic Resource
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