The intracellular and extracellular changes associated with ischaemia--effects of catecholamines in arrhythmogenesis.
Beta sympathetic stimulation and the beta-adrenergic agonists exert a variety of electrophysiologic effects which contribute to the genesis of ischaemia-related arrhythmias. These are both primary, most likely related to enhancement of the slow calcium current, and secondary, resulting from changes in the metabolism of the ischaemic myocardium as reflected in the accumulation of ions and other end products of metabolism in the extracellular space. In addition, the regional influence of these changes may contribute to the ionic and electrical inhomogeneities. Further studies are needed to define more precisely the factors responsible for the enhanced arrhythmogenicity attributed to beta-adrenergic stimulation.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D002118:Calcium / Q000378:metabolism; D002395:Catecholamines / Q000494:pharmacology*; D003327:Coronary Disease / Q000150:complications* / Q000378:metabolism; D004594:Electrophysiology; D005110:Extracellular Space / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D007473:Ion Channels / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D013552:Swine; D013997:Time Factors
D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D007473:Ion Channels; D011188:Potassium; D002118:Calcium