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  • 1
    Electronic Resource
    Electronic Resource
    The long-term effects of metoprolol and epanolol on tissue-type plasminogen activator and plasminogen activator inhibitor 1 in patients with ischaemic heart disease (1994)
    Springer
    European journal of clinical pharmacology 46 (1994), S. 279-282 
    Details
    ISSN: 1432-1041
    Keywords: Metoprolol ; Epanolol ; Ischaemic heart disease ; tissue-type plasminogen activator ; plasminogen activator inhibitor type 1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract This double-blind, randomized parallel group study investigated the effect of 6 months β-adrenoceptor antagonist therapy with either metoprolol (β1-selective without intrinsic sympathomimetic activity [ISA]) or epanolol (β1-selective with ISA) on markers of endogenous fibrinolysis in 20 patients with chronic stable angina receiving concurrent treatment with nifedipine. Neither drug had an effect on tissue-type plasminogen activator or plasminogen activator inhibitor type 1 (PAI-1). A significant correlation between fasting insulin and PAI-1 has previously been described and was confirmed in this study. The group treated with metoprolol showed a significant rise in fasting insulin after 6 months with no change in PAI-1. This suggests that the previously described link between these two may not be causal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00192563
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  • 2
    Electronic Resource
    Electronic Resource
    NORADRENALINE RELEASE FROM THE RAT HEART DURING ANOXIA: EFFECTS OF CHANGES IN EXTRACELLULAR SODIUM CONCENTRATION AND INHIBITION OF SODIUM UPTAKE MECHANISMS (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Anoxic perfusion of the isolated rat heart releases noradrenaline in the absence of sympathetic nerve fibre stimulation.2. Anoxic noradrenaline release is enhanced by reducing the extracellular Na+ concentration, consistent with the proposal that such release occurs by carrier-mediated efflux.3. Release is also enhanced by lignocaine but inhibited by amiloride and ethylisopropylamiloride, suggesting that sodium entry into adrenergic nerve terminals during anoxia occurs by Na+/H+ (and possibly Na+/Ca2+) exchange.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01375.x
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  • 3
    Electronic Resource
    Electronic Resource
    SEX DIFFERENCES IN THE PARASYMPATHETIC NERVE CONTROL OF RAT HEART (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. As it has been shown that oestrogen enhances the cholinergic muscarinic activity in the central nervous system, we studied sex differences in the responses to parasympathetic nervous stimulation in the rat heart using in vivo and in vitro preparations.2. In in situ perfused, innervated hearts, stimulation of bilateral vagus nerves (15 Hz with 1 μmol/L physostigmine) inhibited sympathetic nerve stimulation (5 Hz) induced noradrenaline release to a greater extent in female than in male rats (54 ± 5 vs 72 ± 5% of control). Similarly, vagus nerve stimulation at 1–20 Hz reduced heart rate (HR) more in females than males, and this sex difference became more marked in the presence of physostigmine. The chronotropic effect of vagal stimulation was attenuated after ovariectomy but potentiated after castration when compared with sham-operated controls. In contrast, the muscarinic agonist methacholine reduced neural NA release and HR equally well in both sexes.3. In anaesthetized rats, reduction in HR and mean arterial pressure by vagus nerve stimulation (1–20 Hz) was more pronounced in females than in males after inhibition of acetylcholinesterase with physostigmine.4. The results indicate that activation of parasympathetic nerve leads to greater presynaptic and postsynaptic effects in female than in male rat hearts, presumably due to a higher level of acetyl-choline release following nerve activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02545.x
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  • 4
    Electronic Resource
    Electronic Resource
    Reduced neuronal noradrenaline overflow in the ischaemic rat heart: Importance of the severity of coronary flow reduction (1991)
    Springer
    Basic research in cardiology 86 (1991), S. 11-20 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF02193867
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  • 5
    Electronic Resource
    Electronic Resource
    Hypoxia-stimulated glycerol production from the isolated, perfused rat heart is mediated by non-adrenergic mechanisms (1994)
    Springer
    Basic research in cardiology 89 (1994), S. 29-38 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00788675
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