Get Adrenergic System and Ventricular Arrhythmias in Myocardial PDF

By D. E. Knight, H. Von Grafenstein, D. J. Maconochie (auth.), Priv.-Doz. Dr. J. Brachmann, Prof. Dr. A. Schömig (eds.)

ISBN-10: 364274317X

ISBN-13: 9783642743177

ISBN-10: 3642743196

ISBN-13: 9783642743191

This ebook offers new points on electrophysiological mechanisms and catecholaminergic contributions within the atmosphere of acute and protracted myocardial ischemia. detailed emphasis is put on the total scope from easy molecular and mobile mechanisms to experimental versions of shut scientific proximity. a few the world over unique scientists current their most recent findings during this major study region in the perimeter of heart problems which keeps to steer mortality information in such a lot industrialized international locations. Contents of this booklet hide, as well as different topics, free up and uptake of catecholamines in ischemia, rules of receptors, adrenergic contribution to ventricular arrhythmias and mechanisms of ischemic malignant arrhythmias in addition to underlying alterations in membrane currents and the electrophysiological reaction to beta-adrenergic blocking off medications. as well as unique contributions, a couple of editorial chapters are integrated for conclusions and destiny improvement in those components.

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Extra resources for Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction

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Langer SZ (1981) Presynaptic regulation of the release of catecholamines. Pharmacol Rev 32:337-362 61. Dahlof C, Dahlof P, Lundberg JM (1986) urAdrenoceptor-mediated inhibition of nerve stimulation-evoked release of neuropeptide Y (NPY)-like immunoreactivity in the pithed guinea-pig. Eur J Pharmacol 131 :279-283 62. Lundberg JM, Stjiime L (1984) Neuropeptide Y depresses the secretion of 3H-noradrenaline and the contractile response evoked by field stimulation in the rat vas deferens. Acta Physiol Scand 120:477-479 63.

85 mM) or absence of extracellular calcium from the perfusion buffer (for details see Fig. 2). Noradrenaline and NPY were determined by HPLC [71] and RIA [55, 78], respectively. In each group n = 4-6 Neuropeptide Y and Sympathetic Transmission 29 neuron NA NPY ATP+---_I~ (energy depletion) $j=? "- -/ I l. :- AO \ Na +--- NA '\ )-J NPY uptake 1 non-exocytotic DOPEG release \ "- - - /~'\ NA I NPYj synaptic cleft NA------------~~ U postsynaptic effects Fig. 6. Non exocytotic noradrenaline (NA) release from cardiac postganglionic sympathetic nerve fibres.

DART Introduction Activation of the sympatho-adrenal system during the early stages of myocardial infarction has been inferred both from associated physiological changes [1, 2] and from measurements of elevated plasma [3, 4] and urinary [5] catecholamine concentrations. Such observations have been made in man, as well as in anaesthetised and in conscious experimental animals. Furthermore, the finding of a sinus tachycardia preceding serious ventricular arrhythmias [6] and the beneficial effect of beta-adrenoceptor blockade on sudden death in survivors of myocardial infarction [7] both suggest that the autonomic nervous system plays a role in determining the outcome of myocardial ischalemia in man.

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Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction by D. E. Knight, H. Von Grafenstein, D. J. Maconochie (auth.), Priv.-Doz. Dr. J. Brachmann, Prof. Dr. A. Schömig (eds.)


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