Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

Role of calcium ions in reperfusion arrhythmias: Relevance to pharmacologic intervention

Role of calcium ions in reperfusion arrhythmias: Relevance to pharmacologic intervention Calcium ions may play a role in reperfusion arrhythmias, as suggested by 1) evidence favoring excess internal recycling of calcium during the reperfusion period; 2) electrophysiologic studies in Purkinje fibers and guinea pig papillary muscle in which calcium-dependent delayed after-depolarizations (DADs) have been found; 3) identification of the transient inward current as the basic mechanism underlying DADs; 4) the influence of cyclic adenosine monophosphate (cAMP) in the ischemic period on reperfusion electrophysiologic abnormalities; and 5) calcium oscillations in reoxygenated myocytes. More direct evidence for the role of calcium lies in the concordance between the factors influencing DADs and those associated with reperfusion arrhythmias, as well as the role of an elevated extracellular Ca2+ in causing reperfusion ventricular fibrillation. However, a role for Ca2+ does not necessarily imply that calcium antagonist drugs will be antiarrhythmic in this situation; rather there is no good evidence that these agents are antiarrhythmic unless they have a protective effect in the ischemic period. The anti-arrhythmic role of alpha1-adrenergic blocking drugs remains controversial; in isolated hearts they work in high concentrations, not through specific receptor antagonism. Beta-blocking drugs have no established place in the therapy of reperfusion arrhythmias. The role of lidocaine and other sodium channel blockers is also controversial. In isolated preparations, lidocaine can be antiarrhythmic and can inhibit DADs. Mexiletine, another sodium channel blocker, can inhibit reoxygenation and reperfusion arrhythmias as well as DADs, all in therapeutic concentrations (10 μM). Such drugs may indirectly inhibit sodium-calcium exchange, which is one of the mechanisms underlying the formation of DADs and, hence, a potential site of pharmacologic inhibition of reperfusion arrhythmias. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cardiovascular Drugs and Therapy Springer Journals

Role of calcium ions in reperfusion arrhythmias: Relevance to pharmacologic intervention

Opie, L.; Coetzee, W.
Cardiovascular Drugs and Therapy , Volume 2 (5) – May 8, 2004
Download PDF
14 pages

Loading next page...
 
/lp/springer-journals/role-of-calcium-ions-in-reperfusion-arrhythmias-relevance-to-0kAg8ZnjoA

References (93)

Publisher
Springer Journals
Copyright
Copyright
Subject
Medicine & Public Health; Cardiology
ISSN
0920-3206
eISSN
1573-7241
DOI
10.1007/BF00054202
Publisher site
See Article on Publisher Site

Abstract

Calcium ions may play a role in reperfusion arrhythmias, as suggested by 1) evidence favoring excess internal recycling of calcium during the reperfusion period; 2) electrophysiologic studies in Purkinje fibers and guinea pig papillary muscle in which calcium-dependent delayed after-depolarizations (DADs) have been found; 3) identification of the transient inward current as the basic mechanism underlying DADs; 4) the influence of cyclic adenosine monophosphate (cAMP) in the ischemic period on reperfusion electrophysiologic abnormalities; and 5) calcium oscillations in reoxygenated myocytes. More direct evidence for the role of calcium lies in the concordance between the factors influencing DADs and those associated with reperfusion arrhythmias, as well as the role of an elevated extracellular Ca2+ in causing reperfusion ventricular fibrillation. However, a role for Ca2+ does not necessarily imply that calcium antagonist drugs will be antiarrhythmic in this situation; rather there is no good evidence that these agents are antiarrhythmic unless they have a protective effect in the ischemic period. The anti-arrhythmic role of alpha1-adrenergic blocking drugs remains controversial; in isolated hearts they work in high concentrations, not through specific receptor antagonism. Beta-blocking drugs have no established place in the therapy of reperfusion arrhythmias. The role of lidocaine and other sodium channel blockers is also controversial. In isolated preparations, lidocaine can be antiarrhythmic and can inhibit DADs. Mexiletine, another sodium channel blocker, can inhibit reoxygenation and reperfusion arrhythmias as well as DADs, all in therapeutic concentrations (10 μM). Such drugs may indirectly inhibit sodium-calcium exchange, which is one of the mechanisms underlying the formation of DADs and, hence, a potential site of pharmacologic inhibition of reperfusion arrhythmias.

Journal

Cardiovascular Drugs and Therapy – Springer Journals

Published: May 8, 2004

There are no references for this article.