aconitine and Atrial-Fibrillation

To assess and compare the safety and efficacy of allapinine and quinidine bisulphate in the treatment of patients with persistent atrial fibrillation after cardioversion. Design--Prospective, randomised, open study. Patients--73 consecutive patients (men only, mean age 44 ± 11 years) with persisnent atrial fibrillation and flutter. Interventions--37 patients were randomised to allapinine (ALP) (1.5 mg/kg/d), 36 to quinidine bisulphate (QUIN) (15 mg/kg/d) with subsequent successful pharmacological or electrical cardioversion. Main outcome measures--Recurrence of atrial fibrillation or side effects.. In the ALP group 15 of the 37 patients developed atrial fibrillation up to 12 month of follow-up, while in the QUIN group 20 patients developed atrial fibrillation and 5 experienced significant side effects. Relative risk (RR) (ALP vs QUIN) 0.58 (95% CI 0.37-0.91, p < 0.02). The number needed to treat (NNT) was (-3.48) (14.2-1.97 harm). When 5 patients with significant side effects were excluded from the analysis RR was 0.62 (95% CI 0.39-1.0, p = 0.052) and NNT--(-4.1) (122.7-2.1 harm) but power of the study was too low--67%.. Allapinine is as effective as quinidine bisulphate in the long term treatment of patients with persistent atrial fibrillation after successful cardioversion but causes significantly less side effects.

Topics: Aconitine; Adult; Anti-Arrhythmia Agents; Atrial Fibrillation; Drug Monitoring; Electric Countershock; Humans; Male; Middle Aged; Quinidine; Recurrence; Time; Treatment Outcome

Echocardiographic study was performed in 24 patients with persistent atrial fibrillation (PAF) without clinical signs of circulatory failure. When treated with allapinin , all the patients with PAF showed a significant increase in heart rate (HR) and cardiac output (CO) and a decrease in total peripheral vascular resistance (TPVR). No substantial changes in the major hemodynamic parameters were found in patients with higher left ventricular dimensions; however, a significant rise in end systolic volume (ESV) was noted. There was significantly lower HR, diminished ESV, higher stroke volume and increased CO, elevated ejection fraction and TPVR with sinus rhythm. In PAF patients without apparent signs of circulatory failure, hemodynamic effects of allapinin may be accounted for by its direct vasodilatory action on the arterial bed and by its ability to affect cardiac autonomic innervation. A moderate cardiodepressive effect of the agent may be reflected by deteriorated latent signs of myocardial incompetence which are levelled off following sinus rhythm recovery.

Topics: Aconitine; Aconitum; Adult; Anti-Arrhythmia Agents; Atrial Fibrillation; Chronic Disease; Clinical Trials as Topic; Hemodynamics; Humans; Male; Middle Aged; Sinoatrial Node; Stimulation, Chemical; Tablets

The aim was to investigate the role of the α7nAChR-mediated cholinergic anti-inflammatory pathway in vagal nerve regulated atrial fibrillation (AF).18 beagles (standard dogs for testing) were used in this study, and the effective refractory period (ERP) of atrium and pulmonary veins and AF inducibility were measured hourly during rapid atrial pacing at 800 beats/minute for 6 hours in all beagles. After cessation of 3 hours of RAP, the low-level vagal nerve stimulation (LL-VNS) group (n = 6) was given LL-VNS and injection of salinne (0.5 mL/GP) into four GPs, the methyllycaconitine (MLA, the antagonist of α7nAChR) group (n = 6) was given LL-VNS and injection of MLA into four GPs, and the Control group (n = 6) was given saline into four GPs and the right cervical vagal nerve was exposed without stimulation. Then, the levels of the tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), acetylcholine (ACh), STAT3, and NF-κB proteins were measured. During the first 3 hours of RAP, the ERPs gradually decreased while the dispersion of ERPs (dERPs) and AF inducibility gradually increased in all three groups. During the last 3 hours of 6 hours' RAP in this study, the ERPs in the LL-VNS group were higher, while the dERPs and AF inducibility were significantly lower when compared with the Control and MLA groups at the same time points. The levels of ACh in the serum and atrium in the LL-VNS and MLA groups were higher than in the Control group, and the levels of TNF-α and IL-6 were higher in the Control and MLA groups than in the LL-VNS group. The concentrations of STAT3 in RA and LA tissues were higher in the LL-VNS group while those of NF-κB were lower.In conclusion, the cholinergic anti-inflammatory pathway mediated by α7nACh plays an important role in low-level vagal nerve-regulated AF.

Topics: Acetylcholine; Aconitine; alpha7 Nicotinic Acetylcholine Receptor; Animals; Atrial Fibrillation; Cardiac Pacing, Artificial; Case-Control Studies; Disease Models, Animal; Dogs; Heart Atria; Interleukin-6; Neuroimmunomodulation; NF-kappa B; Nicotinic Antagonists; Pulmonary Veins; Refractory Period, Electrophysiological; STAT3 Transcription Factor; Tumor Necrosis Factor-alpha; Vagus Nerve; Vagus Nerve Stimulation

The relationship between atrial fibrillation (AF) and flap survival has not been fully characterized. Therefore, the goal of this study was to investigate the effect of AF on survival areas of pedicled flap and survival rates of free flap in an experimental rat AF model. An aconitine-induced rat AF model was established without intubation anesthesia. Survival areas of the pedicled rectangular epigastric flap were compared between AF rats (n = 7) and control rats (n = 7), and survival rates of the free epigastric flap were compared between AF rats (n = 10) and control rats (n = 10). Animals that died during the study or in which AF was not induced were excluded from study. A total of 64 rats were assessed in this study. Atrial fibrillation was induced with a success rate of 77.8% (21/27) throughout the study. Pedicled flap survival area was significantly higher in controls (75.1 ± 9.0%; n = 7) than that in AF animals (55.7 ± 13.0%; n = 7) (P < 0.01, nonpaired Student t test). Free flap survival rates were 80% in controls and 40% in AF animals (P = 0.07, χ² test). This is the first study to develop an aconitine-induced model of AF in rats. Atrial fibrillation has a detrimental effect on survival areas of the pedicled flap and survival rates of the free flap.

Topics: Aconitine; Animals; Atrial Fibrillation; Disease Models, Animal; Plastic Surgery Procedures; Rats; Rats, Sprague-Dawley; Surgical Flaps

Lappaconitine Hydrobromide (LH, allapinin) has been included by authors of National Guidelines on Diagnosis and Treatment of Atrial Fibrillation (AF), 2012 in the number of medications recommended for use in patients with AF for rhythm control. Moreover, LH is also included into the List of Vital and Essential Medicinal Drugs (VEMD) 2015. However, LH is not mentioned in corresponding guidelines of the European Society of Cardiology (ESC). Aim of the present review was to explore evidence base underlining use of LH in the context of AF and to understand reason for LH-related discrepancy between European and domestic guidelines.. Literature search has indicated that efficacy of LH was assessed only in small open studies. None of prospective trials included more than 100 patients. For more than 25 years of presence on the market slightly more than 400 patients were administered LH in clinical studies. In the only trial, designated as randomized number of participants (only men younger than 60 years) was small and the comparator was quinidine that presently is not used for maintenance of sinus rhythm in AF. Another study referenced in domestic guidelines on management of AF was observational and not intended for comparison of antiarrhythmic activity of drugs.. Design of studies reviewed as well as their results provide insufficient evidence supporting the use of LH for maintenance of sinus rhythm in routine management of AF. At present inclusion of LH in guidelines on AF management and in the List of VEMD appears unjustified.

Topics: Aconitine; Anti-Arrhythmia Agents; Atrial Fibrillation; Evidence-Based Practice; Humans; Male; Prospective Studies

The acetylcholine receptor-operated K(+) (KACh) channel may be a novel target for atrial-specific antiarrhythmic therapy. Recently it has been demonstrated that tertiapin, a selective blocker of KACh channel, suppressed aconitine-induced atrial fibrillation (AF) in dogs. However, the precise mechanism by which the KACh-channel blocker inhibits the aconitine-induced AF remains unknown. This study was undertaken to determine the role of KACh channel in aconitine-induced AF in guinea pigs. Tertiapin terminated the aconitine-induced AF in anesthetized guinea pigs. The results of an in vitro electrophysiological experiment using atrial cells and atrial preparations suggest that aconitine might activate KACh channels in atrial cells, probably by intracellular Na(+) accumulation, and inhibition of KACh channels by tertiapin might suppress AF by producing conduction block, probably due to further decrease in the resting membrane potential. Since it has been reported that constitutively active KACh channels can be observed in atrial cells of patients with chronic AF, aconitine-induced AF may be used as an experimental model for evaluation of drug effect on chronic AF.

Topics: Aconitine; Animals; Atrial Fibrillation; Bee Venoms; Cells, Cultured; Chronic Disease; Disease Models, Animal; Dogs; Electrocardiography; Electrophysiological Phenomena; Guinea Pigs; Heart Atria; In Vitro Techniques; Membrane Potentials; Molecular Targeted Therapy; Potassium Channel Blockers; Potassium Channels; Sodium

Many studies have shown that the relationship between alcohol consumption and most cardiovascular diseases is U-shaped, with nondrinkers and heavier drinkers having higher risks than moderate drinkers. However, the association between cardiac arrhythmias and acute alcohol consumption is not well understood. We set up several experimental arrhythmia animal models to examine the effects of acute administration of ethanol on arrhythmia. The results showed 0.4, 0.8 and 1.6 g/kg ethanol consumption obviously delayed the onset time of atrial fibrillation (AF) (P < 0.05 or P < 0.01) and increased the survival rates on acetylcholine-CaCl₂-induced AF in mice. Ethanol (0.4, 0.8 and 1.6 g/kg) consumption significantly delayed the onset time of ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA) (P < 0.01), and 0.4 and 0.8 g/kg ethanol consumption increased the survival rates on CaCl₂-induced arrhythmia in rats. Ethanol (0.4 g/kg) essentially increased the cumulative dosage of aconitine required to CA (P < 0.05), and 0.8 g/kg, 1.6 g/kg ethanol reduced the cumulative aconitine dosage to induce VT, VF and CA (P < 0.05 or P < 0.01) on aconitine-induced arrhythmia in rats. Ethanol (0.4, 0.8 and 1.6 g/kg) consumption remarkably increased the cumulative dosage of deslanoside to induce ventricualr premature contraction (P < 0.01) on deslanoside-induced arrhythmia in guinea pigs. Collectively, our results indicate that low concentrations of ethanol had anti-arrhythmic effect on experimental arrhythmia, and high concentrations of ethanol may aggravated the occurrence of experimental arrhythmia.

Topics: Acetylcholine; Aconitine; Animals; Arrhythmias, Cardiac; Atrial Fibrillation; Calcium Chloride; Cardiotonic Agents; Central Nervous System Depressants; Cholinergic Agonists; Deslanoside; Disease Models, Animal; Drug Interactions; Ethanol; Guinea Pigs; Heart Arrest; Male; Mice; Mice, Inbred ICR; Rats; Rats, Sprague-Dawley; Risk Factors; Tachycardia, Ventricular; Ventricular Fibrillation; Voltage-Gated Sodium Channel Agonists

We investigated the electrophysiological and antiarrhythmic effects of a novel antiarrhythmic agent, NIP-151, and compared these effects with those of an IKr-blocker dofetilide. NIP-151 potently inhibited acetylcholine-activated K current (IKACh) with an IC50, with 1.6 nM in HEK293 cells expressing the GIRK1/4 channel, but it had little effect on IKr (IC50 = 57.6 microM). NIP-151 dose-dependently terminated AF both in vagal nerve stimulation-induced AF (at 5 and 15 microg/kg per minute) and aconitine-induced AF (at 30 and 100 microg/kg) models. This compound significantly prolonged the atrial effective refractory period (ERP), but it had no significant effects on ventricular ERP. There were no significant changes on electrocardiographic variables with NIP-151 (up to 1,000 microg/kg per minute) administration. In contrast, dofetilide had little effect in either AF model, even though this compound potently prolonged atrial ERP. Dofetilide also significantly prolonged ventricular ERP and the QT interval in anesthetized dogs, which are related to proarrhythmic risk. In conclusion, a novel antiarrhythmic agent NIP-151, which potently blocked IKACh, was highly effective in the two types of canine AF models with an atrial-specific ERP-prolonging profile. Therefore, NIP-151 might be useful for the treatment of AF with lower risk of proarrhythmia, compared with IKr blockers.

Topics: Aconitine; Action Potentials; Analysis of Variance; Animals; Anti-Arrhythmia Agents; Atrial Fibrillation; Benzopyrans; Cell Line; Dogs; Dose-Response Relationship, Drug; Electrocardiography; ERG1 Potassium Channel; Ether-A-Go-Go Potassium Channels; Female; G Protein-Coupled Inwardly-Rectifying Potassium Channels; Hemodynamics; Humans; Inhibitory Concentration 50; Male; Patch-Clamp Techniques; Phenethylamines; Potassium Channel Blockers; Rabbits; Refractory Period, Electrophysiological; Sulfonamides; Vagus Nerve; Ventricular Function, Right

Atrial fibrillation (AF) is thought to be sustained by multiple reentrant wavelets or firing foci.. The aim of this study was to compare the spectral domain characteristics in the left atrium (LA) and right atrium (RA) in two different models of AF.. Rectangular 8 x 14 electrode arrays were placed on the LA and RA of 14 anesthetized dogs. AF episodes were induced with burst pacing and aconitine in each dog. For each model, AF was induced from the RA in six dogs and from the LA in six dogs. Dominant frequencies (DFs) were obtained using the fast Fourier transform of the unipolar recordings obtained from each electrode of the array. Standard deviation (SD) was used to compute the frequency dispersion within an atrium. Regularity of the signal was quantified using an organization index (OI).. DFs were largest in the atrium where aconitine was applied. Aconitine AF had larger gradients than burst-pacing AF (5.0 +/- 4.5 vs. 0.9 +/- 1.0 Hz: P <.006). Aconitine AF when compared with burst-pacing AF had greater absolute LA-RA differences in the SD of DFs (2.3 +/- 1.9 vs. 0.2 +/- 0.2 Hz; P <.001) and in OI (0.11 +/- 0.07 vs. 0.06 +/- 0.07; P <.07).. Differences in frequency gradients and organization were observed during AF induced by burst pacing and aconitine. This suggests that different mechanisms of AF are possible and may be identified with frequency domain analysis.

Topics: Aconitine; Animals; Atrial Fibrillation; Atrial Function, Left; Atrial Function, Right; Cardiac Pacing, Artificial; Disease Models, Animal; Dogs; Electrocardiography; Fourier Analysis; Heart Atria; Heart Rate; Signal Processing, Computer-Assisted; Tachycardia, Atrioventricular Nodal Reentry

Topics: Aconitine; Animals; Atrial Fibrillation; Electrocardiography; Fourier Analysis; Heart Atria; Heart Rate; Humans; Signal Processing, Computer-Assisted; Tachycardia, Atrioventricular Nodal Reentry

Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Atrial Fibrillation; Cats; Electric Stimulation; Electrocardiography; Periodicity; Vagus Nerve

Cyclovirobuxine-D (CVB-D) was shown to produce significant and dose-dependent protective effects against atrial fibrillation induced by CaCl2-Ach in mice. On atrial fibrillation induced by aconitine, ouabain or adrenaline in isolated guinea pig atria, the effects of CVB-D were similar to those of amiodarone. CVB-D 0.3-100 mumol.L-1 was shown to depress the automaticity of the isolated guinea pig right atria. In isolated left atria, CVB-D 0.3 mumol.L-1 was found to inhibit the abnormal automaticity elicited by adrenaline, to prolong the duration of action potential and effective refractory period and to reduce excitability. At high concentration (30 mumol.L-1), CVB-D was also found to decrease the maximal velocity of depolarization (Vmax) and to elongate the conduction time of initiation. Amiodarone 0.3-30 mumol.L-1 was shown to closely resemble CVB-D in electrophysiology without effect on Vmax.

Topics: Aconitine; Action Potentials; Amiodarone; Animals; Anti-Arrhythmia Agents; Atrial Fibrillation; Calcium Chloride; Drugs, Chinese Herbal; Electrophysiology; Female; Guinea Pigs; Heart Atria; In Vitro Techniques; Male; Mice; Refractory Period, Electrophysiological

A series of the new aminoalkyl esters of chlor-, methyl- and alkoxy carbanilates was synthesized. All the compounds prepared were found to exhibit antiarrhythmic activities comparable with those of mexiletine.

Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Carbamates; Cardiac Complexes, Premature; Epinephrine; Guinea Pigs; Mexiletine; Ouabain; Rats; Tocainide

In atrial fibrillation, allapinine was shown to enhance rhythm by 7% and to increase cardiac output (p less than 0.05), as well as to slightly lower mean blood pressure and peripheral vascular resistance at rest. With exercise, both in atrial fibrillation, and sinus rhythm, there was a decrease in end-diastolic and end-systolic volumes of the left ventricle (p less than 0.05), a slight drop in ventricular ejection, that was statistically significant only with sinus rhythm (p less than 0.05). Physical exercise was not followed by an apparent additional aggravation of myocardial contractility, which makes allapinine preferable for long-term application to preserve sinus rhythm in patients without evident signs of heart failure.

Topics: Aconitine; Adolescent; Adult; Anti-Arrhythmia Agents; Atrial Fibrillation; Echocardiography; Exercise Test; Hemodynamics; Humans; Male; Middle Aged

The cardiorespiratory system was studied comprehensively in 27 patients with permanent atrial fibrillation (PAF) without the clinically marked signs of circulatory failure. After allapinine treatment 15 patients with bronchial obstruction manifestations demonstrated, in the presence of lasting PAF, a significant increase of the forced expiration capacity per s and of the maximum volumetric expiration rates. The data obtained may attest to the fact that the drug has beta-stimulating properties, confirming the reported evidence.

Topics: Aconitine; Adult; Aged; Anti-Arrhythmia Agents; Atrial Fibrillation; Bronchodilator Agents; Cardiovascular Diseases; Chronic Disease; Humans; Male; Middle Aged; Respiration; Respiratory Function Tests

The differential effect of different antiarrhythmic agents, quinidine, propranolol, verapamil and sotalol was studied on right- and left-sided aconitine-induced atrial arrhythmias in dogs. In control experiments the time required for the reversion of right aconitine-induced atrial arrhythmias to normal sinus rhythm was higher as compared to left-sided aconitine-induced atrial arrhythmias. All the drugs studied were effective in reverting atrial arrhythmias to normal sinus rhythm, and doses required for suppression of the right atrial arrhythmias as compared to the left atrial arrhythmias were significantly higher in the case of quinidine, sotalol and verapamil, but not in the case of propranolol. The differential antiarrhythmic effect of these drugs in atrial arrhythmias is discussed.

Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Atrial Fibrillation; Atrial Flutter; Dogs; Female; Male; Propranolol; Quinidine; Sotalol; Verapamil

Topics: Acetylcholine; Aconitine; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Barium; Barium Compounds; Chlorides; Female; Guinea Pigs; Heterocyclic Compounds; Iodine; Male; Mice; Ouabain; Rabbits; Rats

The concentrations of plasma cyclic nucleotides in patients with atrial fibrillation and in dogs with aconitine-induced atrial fibrillation were measured. Radioimmunoassay was used for the determination of cyclic nucleotides. The concentration of plasma cGMP in dogs with aconitine-induced atrial fibrillation was significantly elevated at 30 and 60 min after the onset of atrial fibrillation, whereas that of plasma cAMP showed no significant changes. After the injection of atropine in dogs with atrial fibrillation and with increased plasma cGMP, the plasma levels decreased to the normal level at 60 min after the conversion to sinus rhythmus. In patients with paroxysmal atrial fibrillation, a significantly increased concentration of plasma cGMP was demonstrated on attacks of atrial fibrillation compared with those with sinus rhythmus, but no significant changes of plasma cAMP levels were observed in these patients. Thus, these results showed that the enhanced parasympathetic nervous activity had been maintained by the atrial fibrillation.

Topics: Aconitine; Aconitum; Animals; Atrial Fibrillation; Cyclic AMP; Cyclic GMP; Dogs; Electrocardiography; Heart Atria; Heart Rate; Humans; Myocardium

Topics: Aconitine; Animals; Aorta; Atrial Fibrillation; Blood Flow Velocity; Blood Pressure; Coronary Circulation; Dogs; Heart Block; Metaproterenol; Myocardial Contraction; Norepinephrine

A novel benzanilide derivative, MJ 9067, has been shown to abolish experimental atrial and ventricular arrhythmiase effectively and promote the return of normal sinus rhythm in a variety of animal models. At intravenous dose levels ranging from 0.5 to 3.2 mg/kg, MJ 9067 successfully converted atrial fibrillation induced by either local application of aconitine or electrical stimulation, and ventricular tachycardia elicited by intravenous injection of ouabain or digoxin. The compound was equally effective in vagotomized or nonvagotomized dogs, and in intact cats and monkeys. The ventricular ectopic rate in conscious dogs 18 to 20 hours after two-stage ligation of a coronary artery was also markedly reduced by the drug at 2 mg/kg i.v. At antiarrhythmic dose levels, there were no undesirable effects noted on peripheral blood pressure, heart rate or the configuration of the electrocardiogram.

Topics: Aconitine; Anilides; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Blood Pressure; Cats; Digoxin; Dogs; Electric Stimulation; Electrocardiography; Female; Haplorhini; Heart Rate; Male; Ouabain; Piperidines; Saimiri; Tachycardia

Quinidine, propranolol and their combination were studied in atrial fibrillation induced by the topical application of acetylcholine or aconitine, injury-stimulation-induced atrial flutter and ventricular ectopic tachycardia produced by coronary occlusion in the dog. The effect of combination of quinidine and propranolol was significantly greater than that of the individual drug in atrial arrhythmias but not in ventricular arrhythmias. The study provides experimental support for the combined clinical use of quinidine and propranolol in the treatment of atrial arrhythmias.

Topics: Acetylcholine; Aconitine; Animals; Anti-Arrhythmia Agents; Atrial Fibrillation; Dogs; Drug Interactions; Electric Stimulation; Female; Heart; In Vitro Techniques; Male; Propranolol; Quinidine; Ventricular Fibrillation

A comparison was made between the effects of quinidine and quinine on experimental arrhythmias and on cardiac electrophysiologic parameters. Both drugs raised ventricular fibrillation thresholds, reversed aconitine-induced atrial fibrillation, decreased ouabain-induced abnormal ventricular beats, and increased atrial refractory periods and His-Purkinje conduction time. In contrast, only quinidine antagonized acetylcholine-induced atrial fibrillation. In addition, quinidine increased ventricular fibrillation thresholds and atrial refractory periods for a longer time period than quinine. These observations are discussed in terms of choosing an appropriate model for testing new compounds with suspected quinidine-like activity.

Topics: Acetylcholine; Aconitine; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Bundle of His; Cats; Dogs; Electric Stimulation; Female; Heart Ventricles; Male; Neural Conduction; Ouabain; Purkinje Fibers; Quinidine; Quinine; Refractory Period, Electrophysiological; Time Factors; Ventricular Fibrillation

Topics: Aconitine; Animals; Atrial Fibrillation; Blood Pressure; Cardiac Output; Dogs; Electric Stimulation; Heart Conduction System; Hemodynamics; Tachycardia

Topics: Aconitine; Ajmaline; Animals; Anti-Arrhythmia Agents; Atrial Fibrillation; Atrial Flutter; Blood Pressure; Dogs; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Heart Rate; Hemodynamics; Infusions, Parenteral; Vascular Resistance

Topics: Aconitine; Aconitum; Atrial Fibrillation; Humans; Microelectrodes

The topical application of aconitine nitrate to the right atrial appendage in the "intact" anaesthetized dog produced atrial flutter. Premature systoles with fixed coupling preceded the development of flutter. In early stages of the arrhythmia, atrial rate was irregularly irregular. Also, the form of flutter beats was similar to that of preceding premature systoles. The fibrillatory activity of acetylcholine described by earlier workers has been confirmed. Transient atrial dissociation was seen after intravenous injection or topical application of acetylcholine. The occurrence of fibrillation in the left atrium after focal application of acetylcholine has been demonstrated, while the right atrial appendage containing the ectopic focus induced by aconitine continued to flutter. Aconitine produced slow-rate flutter in dogs treated with atropine or hemicholinium; this flutter was easily distinguishable from the sinus tachycardia produced by these drugs, by recording the electrocardiogram from a direct atrial lead from the area treated with aconitine, but not from limb lead II. The importance of these findings in the interpretation of the mechanism of atrial flutter and fibrillation is discussed.

Topics: Acetylcholine; Aconitine; Aconitum; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Atropine; Brugada Syndrome; Cardiac Conduction System Disease; Dogs; Electric Stimulation; Electrocardiography; Heart Atria; Heart Conduction System; Pharmacology; Research; Toxicology; Vagus Nerve

Topics: Aconitine; Aconitum; Arrhythmias, Cardiac; Atrial Fibrillation; Brugada Syndrome; Cardiac Conduction System Disease; Heart Atria; Heart Conduction System

Topics: Aconitine; Aconitum; Animals; Atrial Fibrillation; Electromyography; Electrophysiological Phenomena; Electrophysiology; Microelectrodes; Rabbits

Topics: Aconitine; Aconitum; Animals; Atrial Fibrillation; Cardiovascular Diseases; Rabbits

Topics: Aconitine; Animals; Atrial Fibrillation; Carbon Dioxide; Disease; Dogs; Heart Ventricles; Humans; Hypercapnia; Parathyroid Diseases; Parathyroid Glands; Ventricular Fibrillation

Topics: Acetylcholine; Aconitine; Atrial Fibrillation; Heart; Humans

Topics: Aconitine; Arrhythmias, Cardiac; Atrial Fibrillation