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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 89 (1994), S. 29-38 
    ISSN: 1435-1803
    Keywords: Hypoxia ; glycerol ; lipolysis ; heart ; catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Factors controlling hypoxia-induced myocardial glycerol release were studied in isolated, perfused rat hearts. A constant coronary flow rate 10 ml g−1 min−1 was maintained. The perfusion buffer was gassed with O2−N2 mixtures containing 5% CO2. The O2∶N2 ratios were normoxia 95∶0, hypoxia 30∶65, and severe hypoxia 10∶85 (v/v). Glycerol and lactate release were stimulated during a 30-min period of either hypoxia or severe hypoxia but remained constant during normoxia. Tissue glycerol-3-phosphate levels were increased after 30 min hypoxia compard with after a similar period of normoxic perfusion (p〈0.01) and further increased after severe hypoxia (p〈0.01 vs hypoxia). β-Adrenoceptors remained sensitive to isoprenaline during hypoxia, demonstrated by an increase in glycerol release over a 30-min period of isoprenaline infusion from 897±317 to 1771±307 nmol g−1 wet weight (p〈0.05). The isoprenaline-induced increase in glycerol release during hypoxia was inhibited by both atenolol and timolol (1×10−5M). In contrast, β-adrenoceptor blockade using these drugs failed to reduce glycerol release induced by either hypoxia or severe hypoxia. Both drugs attenuated the rise in glycerol-3-phosphate during hypoxia. Chronic denervation by pretreatment with 6-hydroxydopamine reduced hypoxia-stimulated glycerol release by only 30%. Thus, a major part of hypoxia-induced glycerol release is mediated by non-adrenergic mechanisms. The results of this study bring into question the validity of the use of glycerol production during hypoxia as a reliable measure of myocardial lipolysis.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 86 (1991), S. 11-20 
    ISSN: 1435-1803
    Keywords: noradrenaline release ; ischaemia ; uptake1 ; presynaptic receptors ; adenosine ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of severity and duration of acute myocardial ischaemia on left stellate ganglion stimulation-induced noradrenaline (NA) overflow were studied in the retrogradely perfused, innervated rat heart. A 10-min period of ischaemia induced by a coronary flow reduction of 100% (0 ml/g/min), 95% (0.24 ml/g/min) and 90 % (0.48 ml/g/min) reduced neuronal NA overflow to 24 ± 4% (p 〈 0.01), 62 ± 6% (p 〈 0.05) and 70 ± 6% (p 〈 0.05) of the normoxic control values, respectively. During low-flow ischaemia, a progressive decline in neuronal NA overflow was found in hearts subjected to 95 flow reduction, but not to 90% flow reduction. The effect of ischaemia on presynaptic control of NA release was also examined. After 10 min of stop-flow ischaemia, the α-adrenergic antagonist phentolamine (1 μM) and the adenosine receptor antago-nist 8-phenyltheophylline (10 μM) failed to restore neuronal NA overflow to pre-ischaemic levels (from 24 ± 4% without drug to 23 ± 4% or 41 ± 10%, respectively, NS). In contrast, after 60 min of low-flow ischaemia (95% flow reduction), phentolamine and 8-phenyltheophylline largely restored neuronal NA overflow to normoxic control values (from 32 ± 3% without drug to 61 ± 11% (p 〈 0.05) or 79 ± 11 (p 〈 0.01), respectively). During prolonged low-flow ischaemia (95%), the neuronal NA reuptake inhibitor desipramine (0.1 μM) doubled NA overflow induced by nerve stimulation, suggesting an effective neuronal reuptake during these conditions. In conclusion, the severity of ischaemia critically affects neuronal NA release and its controlling mechanisms. Thus, heterogeneity of myocardial ischaemia may lead to gradients in NA release and myocardial adrenergic stimulation.
    Type of Medium: Electronic Resource
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