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  • 1
    Electronic Resource
    Electronic Resource
    The effects of ethanol and lead, alone and in combination, on the severity of arrhythmias induced by coronary artery occlusion, and by noradrenaline, in anaesthetised rats (1986)
    Springer
    Archives of toxicology 59 (1986), S. 56-60 
    Details
    ISSN: 1432-0738
    Keywords: Ethanol ; Lead ; Ischaemia ; Induced arrhythmias ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to investigate whether chronic (3 or 10 months) administration, via the dinking water, of lead (25 ppm) and/or ethanol (25% v/v) altered the susceptibility of the heart to arrhythmias induced either by coronary artery occlusion or noradrenaline infusion in pentobarbitone-anaesthetised male Sprague-Dawley rats. The cardiac effects of acute intravenous infusions of ethanol (17, 33 and 66 mg kg−1 min−1) were also measured. Chronic exposure to ethanol and/or lead in the drinking water had no marked effect on the severity of arrhythmias occurring within the initial 30 min of coronary artery occlusion. In control rats and in those administered ethanol and/or lead for 10 months, noradrenaline (16 μg kg−1 min−1 given IV 1 h post-occlusion for a 15-min period) induced a similar number of ectopic beats during the infusion period, although these arrhythmias persisted beyond the infusion period in treated animals only. There was a significant accummulation of lead in the bone but not in the blood of lead-treated rats. Blood ethanol concentrations varied considerably between animals, ranging from 0 to 319 mg%. Ethanol (66 mg kg−1 min−1) given acutely and yielding a blood concentration of 174 mg % had a slight antiarrhythmic effect in this model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00263959
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  • 2
    Electronic Resource
    Electronic Resource
    NORADRENALINE SENSITIVITY AND CALCIUM FLUXES IN ARTERIES FROM RABBITS WITH PERINEPHRITIS HYPERTENSION (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 17 (1990), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Contractions of isolated vascular and cardiac preparations taken from rabbits with perinephritis (one kidney, one wrapped) hypertension were compared with those of preparations from control operated animals.2. Significantly increased sensitivity to noradrenaline, which acts on α1-adrenoceptors, was found in mesenteric arterial rings but not in aortic rings. The degree of hypersensitivity was the same in the presence and absence of cocaine, suggesting that there is no increase in uptake of noradrenaline into adrenergic nerves in this model of hypertension. In contrast to these agonist-induced contractions, no increased sensitivity was found to potassium chloride, suggesting that hypersensitivity is specific for receptor mediated rather than membrane potential mediated effects.3. No hypersensitivity to noradrenaline was found in the isolated left or right atria, which suggests that the hypertension is associated with changes in excitation–contraction coupling in blood vessels but not in cardiac muscle.4. Hypertension increased basal 45Ca uptake in the mesenteric artery but not in the aorta. However, there was no significant difference between preparations from normotensive and hypertensive rabbits in 45Ca uptake or efflux stimulated by noradrenaline or KCl.5. Increased basal 45Ca uptake could contribute to the increased sensitivity to noradrenaline found in the mesenteric artery in rabbit perinephritis hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1990.tb01354.x
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  • 3
    Electronic Resource
    Electronic Resource
    Nitric oxide mediates the anti-adrenergic effect of adenosine on calcium current in isolated rabbit atrioventricular nodal cells (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 452-457 
    Details
    ISSN: 1432-2013
    Keywords: Key words Adenosine ; Nitric oxide ; Rabbit heart ; AV nodal cells ; Anti-adrenergic ; Calcium current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to determine if adenosine exerts an anti-adrenergic effect on rabbit isolated atrioventricular (AV) nodal cells and, if so, the dependence of this effect on nitric oxide (NO) production. Inward Ca current, I Ca, was measured in AV nodal cells, enzymatically isolated from rabbit hearts. Isoprenaline (0.1 μM) increased I Ca from 676 ±59 to 1102 ±86 pA (n =25). This isoprenaline-induced increase in I Ca(178 ±15% of control) was abolished in the presence of 10 μM adenosine (I Ca100 ±2% of control, n =9, P 〈0.05). This effect of adenosine was completely blocked by the A1 receptor antagonist CPDPX (8-cyclopentyl l, 3-dipropylxanthine, 0.1 μM). In cells pre-treated with the NO synthase inhibitor, L-nitro-arginine methyl ester (L-NAME, 1 mM) the isoprenaline-induced increase in I Ca(208 ±39% of control, n =7) was not reduced by the addition of 10 μM adenosine (195 ±32% of control). Co-incubation of cells in L-NAME with L-arginine (1 mM, the endogenous substrate of NO synthase) restored the adenosine-induced attenuation of I Ca. In these cells, isoprenaline increased I Ca (157 ±7% of control, n =6), and, following addition of adenosine (10 μM) I Ca was reduced to 107 ±8% (P 〈0.05). The NO-releasing agent SIN-1 (3-morpholino-sydnonimine, 100 μM), inhibited I Ca augmented by isoprenaline (n =5). It is concluded that adenosine exerts an anti-adrenergic effect on the AV node via A1 receptors to attenuate a catecholamine-stimulated increase in I Ca and that this action involves the intracellular production of NO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050019
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  • 4
    Electronic Resource
    Electronic Resource
    Nitric oxide mediates the anti-adrenergic effect of adenosine on calcium current in isolated rabbit atrioventricular nodal cells (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 452-457 
    Details
    ISSN: 1432-2013
    Keywords: Adenosine ; Nitric oxide ; Rabbit heart ; AV nodal cells ; Anti-adrenergic ; Calcium current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to determine if adenosine exerts an anti-adrenergic effect on rabbit isolated atrioventricular (AV) nodal cells and, if so, the dependence of this effect on nitric oxide (NO) production. Inward Ca current,I Ca, was measured in AV nodal cells, enzymatically isolated from rabbit hearts. Isoprenaline (0.1 μM) increasedI Ca from 676 ± 59 to 1102 ± 86 pA (n = 25). This isoprenaline-induced increase inI Ca, (178 ± 15 % of control) was abolished in the presence of 10 μM adenosine (I Ca 100 ± 2 % of control,n = 9, P 〈 0.05). This effect of adenosine was completely blocked by the A1 receptor antagonist CPDPX (8-cyclopentyl 1, 3-dipropylxanthine, 0.1 μM). In cells pre-treated with the NO synthase inhibitor,l-nitro-arginine methyl ester (l-NAME, 1 mM) the isoprenaline-induced increase inI Ca(208 ± 39 % of control,n = 7) was not reduced by the addition of 10 μM adenosine (195 ± 32% of control). Co-incubation of cells inl-NAME withl--arginine (1 mM, the endogenous substrate of NO synthase) restored the adenosine-induced attenuation ofI Ca. In these cells, isoprenaline increasedI Ca (157 ± 7% of control,n = 6), and, following addition of adenosine (10 μM)I Ca was reduced to 107 ± 8% (P 〈 0.05). The NO-releasing agent SIN-1 (3-morpholino-sydnonimine, 100 μM) inhibitedI Ca augmented by isoprenaline (n = 5). It is concluded that adenosine exerts an anti-adrenergic effect on the AV node via A, receptors to attenuate a catecholamine-stimulated increase inI Ca and that this action involves the intracellular production of NO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02207285
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    Paper (German National Licenses)
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