Effects of allopurinol on reperfusion arrhythmias in isolated ventricles

1992 ◽  
Vol 263 (2) ◽  
pp. H341-H348
Author(s):  
G. R. Li ◽  
G. R. Ferrier
Keyword(s):  
High Gain ◽  
Conduction Delay ◽  
Conduction Time ◽  
Reperfusion Arrhythmias ◽  
Early Reperfusion ◽  
Tissue Properties ◽  
Significant Attenuation ◽  
Electrophysiological Effects ◽  
Antiarrhythmic Efficacy ◽  
Normal Tyrode Solution

Electrophysiological effects of allopurinol on arrhythmias were studied in isolated segments of guinea pig right ventricular free walls paced from endocardium. A high-gain electrocardiogram as well as transmembrane electrical activity from endo- and epicardium were recorded. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with normal Tyrode solution. Sustained or nonsustained ventricular tachycardia, bigeminy, and trigeminy with characteristics of transmural reentry occurred in early reperfusion in 75% of 20 control preparations. Arrhythmias were associated with prolongation of transmural conduction time and abbreviation of endocardial effective refractory period (ERP). Allopurinol strongly reduced the incidence of reperfusion arrhythmias (20-33%) between 10 and 100 microM, whereas either lower or higher concentrations (5 or 500 microM) were less effective (43 and 50%). Antiarrhythmic efficacy correlated with significant attenuation of reperfusion-induced transmural conduction delay (P less than 0.05 or 0.01). Allopurinol did not affect endocardial conduction times nor did it significantly alter endocardial action potential duration or ERP. Our results indicate that allopurinol exerts antiarrhythmic efficacy during reperfusion by selectively attenuating defects related to anisotropic tissue properties.

Na+/H+ exchange and reperfusion arrhythmias: protection by intracoronary infusion of a novel inhibitor

1994 ◽  
Vol 267 (6) ◽  
pp. H2430-H2440 ◽  
Author(s):  
M. Yasutake ◽  
C. Ibuki ◽  
D. J. Hearse ◽  
M. Avkiran
Keyword(s):  
Sinus Rhythm ◽  
Coronary Perfusion ◽  
The Novel ◽  
Significant Protection ◽  
Reperfusion Arrhythmias ◽  
Early Reperfusion ◽  
Intracoronary Infusion ◽  
Rat Hearts ◽  
Novel Drug ◽  
Antiarrhythmic Efficacy

Activation of sarcolemmal Na+/H+ exchange has been proposed as a causal factor in reperfusion arrhythmogenesis. To test this hypothesis, we determined the antiarrhythmic efficacy of two structurally distinct but equipotent Na+H+ exchange inhibitors, 5-(N-ethyl-N-isopropyl)amiloride (EIPA) and the novel drug, 3-methylsulfonyl-4-piperidinobenzoyl guanidine (HOE-694), in isolated rat hearts (n = 12/group) subjected to independent dual coronary perfusion. After 15 min of aerobic perfusion of both beds, flow to the left coronary bed (LCB) was terminated for 10 min; this was followed by 5 min of reperfusion. Various concentrations of each drug were selectively infused into the LCB either during the 5-min period preceding ischemia plus during reperfusion or during reperfusion alone. With the former protocol, 0.01, 0.1, 1, and 10 microM EIPA reduced the incidence of reperfusion-induced ventricular fibrillation (VF) from 92% in controls to 83, 83, 50, and 0% (P < 0.05); the number of hearts in sinus rhythm at the end of reperfusion was increased from 17 to 42, 25, 83 (P < 0.05), and 100% (P < 0.05). HOE-694, at the same concentrations, reduced VF incidence from 92% in control to 83, 58, 50, and 8% (P < 0.05); 25, 67, 75 (P < 0.05), and 100% (P < 0.05) of hearts were in sinus rhythm, compared with 17% of controls, at the end of reperfusion. Even when infused during reperfusion alone, both drugs afforded significant protection against reperfusion-induced VF, which did not differ significantly from that observed when the drugs were also given before ischemia. The similar antiarrhythmic efficacy of EIPA and HOE-694 is consistent with an arrhythmogenic role for activation of Na+/H+ exchange during early reperfusion.

P2836Melatonin prevents reperfusion arrhythmias by receptor-dependent and independent electrophysiological effects

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
K A Sedova ◽  
O G Bernikova ◽  
J E Azarov ◽  
S N Kharin ◽  
M A Vaykshnorayte ◽  
...  
Keyword(s):  
Reperfusion Arrhythmias ◽  
Electrophysiological Effects

Abstract 3071: Reversible Transmural Electrical Dyssynchrony in Pacing-Induced Congestive Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Nilesh Mathuria ◽  
Jianwen Wang ◽  
April L Gilbert ◽  
Daryl G Schulz ◽  
Mihir Naware ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Wall Thickness ◽  
Coronary Sinus ◽  
Electrical Conduction ◽  
Recovery Of Function ◽  
Conduction Delay ◽  
Conduction Time ◽  
Ventricular Dyssynchrony ◽  
Coronary Sinus Lead

Introduction: Inter and Intra-ventricular dyssynchrony can develop during congestive heart failure (CHF). We investigated transmural electrical conduction properties within the LV wall during CHF and subsequent recovery. Methods: Biventricular pacemakers were implanted in 8 normal mongrel dogs (mean weight: 38 kg), and continuous RV pacing (230 –250 bpm) was initiated to induce CHF. Echocardiography, catheterization, and LV myocardial biopsy were performed biweekly while pacing was temporarily stopped. At each catheterization, an intracardiac electrode-catheter was placed at the LV endocardium against the pacemaker coronary sinus lead tip located at the LV epicardium. Intrinsic transmural electrical conduction delay was measured by recording endocardial electrograms via the electrode-catheter and epicardial electrograms via the pacemaker coronary sinus lead, both in posterolateral LV. The conduction delay was also assessed during LV pacing via the endocardial catheter and measuring the time to the coronary sinus lead tip. Pacing was stopped in 4 dogs with CHF to allow for recovery of function. All times were corrected for heart rate. Results: All dogs developed CHF within 2– 4 wks of pacing from baseline (EF: 27±8 vs. 49±4%; LVEDP: 20±9 vs. 6±3 mmHg; QRS: 98±8 vs. 70±14 msec with no LBBB). There was no change in LV wall thickness during CHF compared to baseline (0.9 cm), while LV myocyte size increased (21.7±6.6 vs. 16.2±1.5 μm). Transmural endocardial-to-epicardial intrinsic electrical conduction time lengthened during CHF compared to baseline (35±13 vs. 10±5msec, P<0.001). In dogs recovering from CHF 2– 4 wks after cessation of pacing, intrinsic transmural endocardial-to-epicardial conduction time shortened compared to CHF (10±9 vs. 39±1ms, n=4), which was consistent with LV endocardial pacing (recovery: 47.5±6 ms; CHF: 70.7±9 ms, n=3). Conclusions: Electrical transmural dyssynchrony develops as a consequence of pacing-induced CHF, and is reversible upon recovery of cardiac function. These changes are not associated with LV wall thickness. This novel finding suggests another aspect of ventricular dyssynchrony that may not be reflected by routine noninvasive modalities and warrants further investigation.

scholarly journals Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

Circulation ◽  
2000 ◽  
Vol 101 (6) ◽  
pp. 624-630 ◽  
Author(s):  
Yukihiko Yoshida ◽  
Makoto Hirai ◽  
Takumi Yamada ◽  
Yukiomi Tsuji ◽  
Takahisa Kondo ◽  
...  
Keyword(s):  
Reperfusion Arrhythmias ◽  
Antiarrhythmic Efficacy

scholarly journals Evaluatıon Of The Effect Of Pulmonary Veın Isolatıon Treatment With Left Atrıal Catheter Ablatıon Method On Atrıal Conductıon Tımes In Patıents With Paroxysmal Atrıal Fıbrıllatıon

2021 ◽  
Author(s):  
ibrahim dönmez ◽  
fatma erdem ◽  
tolga memioğlu ◽  
emrah acar
Keyword(s):  
Pulmonary Vein ◽  
Pulmonary Vein Isolation ◽  
Doppler Echocardiography ◽  
Left Atrial ◽  
Tissue Doppler ◽  
Tissue Doppler Echocardiography ◽  
Conduction Delay ◽  
Conduction Time ◽  
Rf Ablation ◽  
Interatrial Conduction

Purpose:Atrial fibrillation(AF) causes structural, electrical, and cellular remodeling in the atrium. Evaluation of intra- and interatrial conduction time, which is measured by tissue doppler echocardiography, indicates structural and electrical remodeling in the atrium. The aim of this study was to evaluate the effect of pulmonary vein isolation applied with RF ablation therapy on intra- and interatrial conduction time and to investigate the structural and electrically remodeling after treatment. Methods:Fifty-two patients with symptomatic PAF despite at least one antiarrhythmic drug and without structural heart disease were included in the study. Two patients were excluded because of complications developed during and after the operation. Fifty patients (28 female; mean age: 51.68 ± 11.731; mean left atrial diameter: 36.79 ± 4.318) who underwent CARTO® 3D pulmonary vein isolation applied with the RF ablation system were followed-up. Intra- and the inter-atrial electromechanical delay was measured in all patients by tissue doppler echocardiography before and three months after RF ablation. Results:All intra- and interatrial conduction times were significantly decreased 3 months after RF ablation procedure(PA lateral p = 0.022; PA septum p = 0.002; PA tricuspid p = 0.019, interatrial conduction delay p= 0,012, intra-atrial conduction delay p = 0.029). Conclusion:The results of our study suggest that providing stable sinus rhythm by the elimination of the AF triggering mechanisms with RF ablation of pulmonary vein isolation may slow down,stop or even improve structural remodeling at substrate level secondary to AF even in patients who did not yet develop atrial fibrosis and permanent structural changes.

Electrophysiological effects of ethmozine in perfused rabbit hearts

1985 ◽  
Vol 63 (11) ◽  
pp. 1418-1422 ◽  
Author(s):  
Peter E. Dresel ◽  
A. Ogbaghebriel ◽  
R. Abraham
Keyword(s):  
Refractory Period ◽  
Conduction Block ◽  
Cardiac Conduction ◽  
Effective Refractory Period ◽  
Conduction Time ◽  
Coupling Interval ◽  
Cycle Lengths ◽  
Significant Change ◽  
High Concentrations ◽  
Electrophysiological Effects

His-bundle electrocardiography was used to evaluate the effects of ethmozine on cardiac conduction in isolated perfused rabbit hearts electrically driven at cycle lengths of 320 and 250 ms. There was no significant change in conduction until high concentrations of ethmozine were reached. His-Purkinje and atrioventricular (AV) nodal conduction were slowed significantly at 0.1 μg/mL and atrial conduction at 1.0 μg/mL. Conduction block occurred at 10.0 μg/mL in all the hearts treated. Effects of the drug (0.1 and 0.01 μg/mL) on conduction of extrasystoles were also studied in hearts driven at a basic cycle length of 270 ms. No significant change was observed in atrial conduction of extrasystoles throughout the coupling intervals tested at both concentrations. Ethmozine (0.01 and 0.1 μg/mL) caused slowing of His-Purkinje conduction of extrasystoles but the effect of the drug did not change as a function of the coupling interval. An interval-dependent increase in AV-nodal conduction time was observed, with the maximum slowing of conduction occurring at coupling intervals close to the effective refractory period of the AV node. AV-nodal functional refractory period was increased significantly by ethmozine (0.01 and 0.1 μg/mL). The effective refractory period was significantly increased only at the higher concentration.

scholarly journals Ischemic preconditioning: antiarrhythmic effects and electrophysiological mechanisms in isolated ventricle

1998 ◽  
Vol 274 (1) ◽  
pp. H66-H75 ◽  
Author(s):  
Jiequan Zhu ◽  
Gregory R. Ferrier
Keyword(s):  
Ischemic Preconditioning ◽  
Conduction Block ◽  
Conduction Time ◽  
Ischemia And Reperfusion ◽  
Early Reperfusion ◽  
Ventricular Tissue ◽  
Block Preconditioning ◽  
Isolated Ventricle ◽  
Premature Beats ◽  
Antiarrhythmic Effects

The objective of this study was to identify cellular electrophysiological mechanisms by which ischemic preconditioning decreases arrhythmias in an isolated ventricular tissue model of ischemia and reperfusion. Electrical activity was recorded with microelectrodes from endocardium and epicardium of paced guinea pig right ventricular free walls. Control preparations were exposed for 15 min to Tyrode solution modified to simulate selected ischemic conditions and then were reperfused for 30 min with normal solution. Preconditioned tissues were exposed to a 2- or 5-min period of simulated ischemia before this same protocol. Neither preconditioning protocol affected incidence of ventricular tachycardia (VT) in ischemia; however, the 5-min protocol significantly decreased premature beats (PVB) and transmural conduction block. Preconditioning for 5 min, but not 2 min, significantly decreased reperfusion-induced VT and PVB. Ischemic preconditioning did not change effects of ischemia or reperfusion on action potential duration, effective refractory period, or endocardial conduction time. However, preconditioning markedly attenuated depression of transmural conduction by ischemia and early reperfusion and thereby prevented conduction delays necessary for transmural reentry.

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