Effect of α-adrenergic blockade on arrhythmias induced by acute myocardial ischemia and reperfusion in the dog

BOLLI, R; Fisher, D.; Taylor, Addison A.; Young, Jordann K.; Miller, R. Christopher

doi:10.1016/s0022-2828(85)80142-5

Cited by 9 publications

(9 citation statements)

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“…In another study, Aubry et al [20] found that prazosin (50 ~g/kg) reduced both the incidence of immediate ventricular fibrillation and the severity of delayed ventricular ectopy when reperfusion was performed after a 40-minute anterior descending occlusion. In contrast to these results, Bolli et al [21] found no effect of either prazosin (1 mg/kg) or phentolamine (5 mg/kg) on immediate reperfusion arrhythmias after a 25-minute occlusion of the left anterior descending coronary artery.…”

Section: Discussionmentioning

confidence: 79%

The duration of coronary occlusion influences adrenergic contributions to reperfusion ventricular arrhythmias

Euler

Scanlon

1988

Cardiovasc Drug Ther

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To study the role of the adrenergic nervous system in the genesis of nonlethal reperfusion arrhythmias, the proximal left anterior descending coronary artery was occluded for either 1 or 3 hours in 48 open-chest dogs anesthetized with alpha-chloralose. Heart rate was controlled (90 to 110 beats/min) by bilateral vagotomy and continuous right vagal stimulation. Dogs were treated with either saline, timolol (0.1 mg/kg), or prazosin (0.5 mg/kg) 15 minutes prior to reperfusion. Reperfusion after 1 hour of occlusion in saline-treated dogs evoked sustained polymorphic ventricular tachycardia (204 +/- 9 beats/min) that reverted to sinus rhythm by 15 minutes of reperfusion. The maximum rate of ventricular tachycardia was significantly reduced by both prazosin and timolol. Both drugs also caused about a 50% reduction in the total number of ectopic beats in the first 10 minutes of reperfusion. With a 3-hour occlusion, reperfusion in saline-treated dogs caused sustained polymorphic ventricular tachycardia (135 +/- 15 beats/min) which persisted for several hours. Neither timolol nor prazosin significantly altered the ventricular ectopic rate in these dogs. Furthermore, bilateral stellate transection, left stellate stimulation, isoproterenol (0.5 mg/kg), or methoxamine (100 ug/kg) all failed to alter the ventricular ectopic rate in the saline-treated dogs. Ventricular ectopy induced by reperfusion after a 1- or 3-hour occlusion was overdriven in all dogs by rapid atrial pacing. The results suggest that the nature of reperfusion-induced ventricular ectopy is highly dependent upon the preceeding duration of coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 79%

The duration of coronary occlusion influences adrenergic contributions to reperfusion ventricular arrhythmias

Euler

Scanlon

1988

Cardiovasc Drug Ther

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“…A great number of drugs, among them many antiarrhythmics, have been tested for their efficacy against arrhythmias following myocardial ischemia and reperfusion [32][33][34], However, neural effects of these drugs were not considered in a majority of studies, although earlier experiments demonstrated that several antiarrhythmic agents and certain p-blockers entering the brain might exert their beneficial effects, at least in part, over a mod ulation of efferent CSNA through the central nervous system [35].…”

Section: Discussionmentioning

confidence: 99%

Cardiac Sympathetic Nervous Activity during Myocardial Ischemia, Reperf usion and Ventricular Fibrillation in the Dog - Effects of Intravenous Lidocaine

Aidonidis

Brachmann²,

Seller³

et al. 1992

Cardiology

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In 12 open-chest dogs, cardiac sympathetic nervous activity (CSNA) was recorded before and after occlusion of the left anterior descending coronary artery as well as during reperfusion and ventricular fibrillation (VF). In 7 control animals, CSNA did not significantly differ from preocclusion levels when determined 20 min after occlusion (+3.5 ± 1.5%, mean ± SEM) and up to 15 min following reperfusion (+1.5 ± 0.6%). However, VF was associated with a potential increase in CSNA by 106 ± 15.5%(p < 0.001). The effect of lidocaine (6 mg/kg) on cardiac sympathetic tone was examined in 5 additional animals. Lidocaine reduced control CSNA by 23 ± 4.7% (p < 0.001); subsequent ischemia and reperfusion did not substantially change the level of preocclusion activity. CSNA decreased significantly also during VF (52 ± 4.2%, p < 0.001). In conclusion, efferent CSNA was slightly altered in the course of acute myocardial ischemia and reperfusion, but significantly increased during VF. Lidocaine produced marked attenuation of CSNA in anesthetized dogs.

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“…Nonetheless, there are puzzling aspects to the reported data that do not fit in with the above simple explanation. Thus Bolli and coworkers [70] found that high concentrations of alphablocking agents did not inhibit reperfusion arrhythmias in dogs, whereas Corr and Witkowski [4] found low concentrations to be effective in reperfusion arrhythmias in cat hearts. Thus the possible specificity of alpha-blocking agents remains an open question.…”

Section: Role Of Alpha-adrenoceptor Blocking Agentsmentioning

confidence: 99%

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

Opie

Coetzee

1988

Cardiovasc Drug Ther

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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 antiarrhythmic role of alpha 1-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 microM). 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.

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Effect of α-adrenergic blockade on arrhythmias induced by acute myocardial ischemia and reperfusion in the dog

Cited by 9 publications

References 0 publications

The duration of coronary occlusion influences adrenergic contributions to reperfusion ventricular arrhythmias

The duration of coronary occlusion influences adrenergic contributions to reperfusion ventricular arrhythmias

Cardiac Sympathetic Nervous Activity during Myocardial Ischemia, Reperf usion and Ventricular Fibrillation in the Dog - Effects of Intravenous Lidocaine

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

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