aconitine has been researched along with Tachycardia* in 30 studies
1 review(s) available for aconitine and Tachycardia
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Disturbances of transmembrane ionic fluxes and their role in the pathogenesis of cardiac dysrhythmias.
Abnormalities of cardiac rhythm are due either to disorders of impulse propagation (delay or block of conduction, re-entry, circus movement, etc.), or to disturbances of impulse formation (dysfunction of ordinary pacemakers and induction of focal activity). In most instances certain disturbances of transmembrane movements of Na or K ions may be considered to be involved basically in the genesis of dysrhythmic cardiac activity. By means of intracellular recordings as well as of voltage clamp measurements and of analogical computations it is demonstrated that characteristic changes of the membrane potential might result from entirely different ionic mechanisms. Furthermore, an attempt is made to present a detailed analysis of permeability changes underlying normal pacemaker activity in Purkinje fibers as compared with the sinus node or with focal activity induced in myocardial fibers by different influences (aconitine, barium ions, stretch, and strong currents). Topics: Aconitine; Action Potentials; Animals; Calcium; Electric Conductivity; Heart Rate; Membrane Potentials; Models, Biological; Potassium; Purkinje Fibers; Sodium; Tachycardia | 1975 |
29 other study(ies) available for aconitine and Tachycardia
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A swinging rhythm.
Topics: Aconitine; Anti-Arrhythmia Agents; Electrocardiography; Humans; Tachycardia | 2023 |
Brainstem cholinergic pathways diminish cardiovascular and neuroinflammatory actions of endotoxemia in rats: Role of NFκB/α7/α4β2AChRs signaling.
Nicotine improves endotoxic manifestations of hypotension and cardiac autonomic dysfunction in rats. Here, we test the hypothesis that brainstem antiinflammatory pathways of α7/α4β2 nicotinic acetylcholine receptors (nAChRs) modulate endotoxic cardiovascular derangements. Pharmacologic and molecular studies were performed to determine the influence of nicotine or selective α7/α4β2-nAChR ligands on cardiovascular derangements and brainstem neuroinflammation caused by endotoxemia in conscious rats. The i.v. administration of nicotine (50 μg/kg) abolished the lipopolysaccharide (LPS, 10 mg/kg i.v.)-evoked: (i) falls in blood pressure and spectral measure of cardiac sympathovagal balance (ratio of the low-frequency to high-frequency power, LF/HF), (ii) elevations in immunohistochemical protein expressions of NFκB and α4β2-nAChR in medullary neurons of the nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM), and (iii) decreases in medullary α7-nAChR protein expression. These favorable nicotine influences were replicated in rats treated intracisternally (i.c.) with PHA-543613 (selective α7-nAChR agonist) or 5-iodo-A-85380 (5IA, selective α4β2-nAChRs agonist). Measurement of arterial baroreflex activity by the vasoactive method revealed that nicotine, PHA, or 5IA reversed the LPS depression of reflex bradycardic, but not tachycardic, activity. Moreover, the counteraction by nicotine of LPS hypotension was mostly inhibited after treatment with i.c. methyllycaconitine (MLA, α7-nAChR antagonist) in contrast to a smaller effect for dihydro-β-erythroidine (DHβE, α4β2-nAChR antagonist), whereas the associated increases in LF/HF ratio remained unaltered. The data signifies the importance of brainstem α7, and to a lesser extent α4β2, receptors in the nicotine counteraction of detrimental cardiovascular and neuroinflammatory consequences of endotoxemia. Topics: Aconitine; alpha7 Nicotinic Acetylcholine Receptor; Animals; Azetidines; Bradycardia; Bridged Bicyclo Compounds, Heterocyclic; Cholinergic Fibers; Dihydro-beta-Erythroidine; Endotoxemia; Hypotension; Infusions, Intraventricular; Lipopolysaccharides; Male; Medulla Oblongata; Neural Pathways; Neurogenic Inflammation; NF-kappa B; Nicotine; Pyridines; Quinuclidines; Rats; Receptors, Nicotinic; Signal Transduction; Solitary Nucleus; Tachycardia | 2019 |
[Enhanced tachycardia arrhythmia in two patients with aconitine intoxication treated with atropine].
Topics: Aconitine; Animals; Arrhythmias, Cardiac; Atropine; Humans; Male; Parasympatholytics; Tachycardia; Voltage-Gated Sodium Channel Agonists | 2017 |
[Acute Monkshood Intoxication Requiring Acute Resuscitation in Suicidal Intent].
We report about an acute monkshood intoxication requiring acute resuscitation in suicidal intent in a 56-year-old patient. The Blue Monkshood (Aconitum napellus) is considered to be the most toxic plant in Europe. All plant parts contain the highly toxic alkonoid aconitin. The lethal dose in adults is 2 - 6 mg. Intoxications are often fatal. Asymptomatic patients with suspected monkshood intoxication should also be monitored on an ICU. First signs of intoxication are paraesthesia in the mouth and throat area, abdominal cramps, nausea, vomiting and severe pain in skeletal muscle. Affected patients die within hours after ingestion due to respiratory distress and/or cardiac arrhythmia.The most important measure after oral ingestion is to achieve a rapid primary poison elimination clearance (in the case of awareness clear patients, trigger vomiting, otherwise gastric lavage under protective intubation) and the subsequent carbonation. A specific antidote is not available. The management of an intoxication consists primarily of the therapy of the rhythm disturbances in the form of magnesium and amiodarone.Strict adherence to protective measures (gloves, masks) must be strictly observed. A direct skin contact with plant parts is to be avoided as well as the potential contact with vomit or aspirate.. Wir berichten über eine akute Eisenhutintoxikation einer 56-jährigen Patientin mit Blauem Eisenhut (Aconitum napellus) in suizidaler Absicht. Der Blaue Eisenhut gilt als die giftigste Pflanze Europas. Alle Pflanzenteile enthalten das hochgiftige Alkaloid Aconitin. Die letale Dosis beim Erwachsenen beträgt 2 – 6 mg. Intoxikationen verlaufen häufig tödlich. Auch asymptomatische Patienten mit Verdacht auf Eisenhutintoxikation sollten auf einer Intensivstation überwacht werden. Erste Intoxikationszeichen sind Parästhesien im Mund- und Rachenbereich, Bauchkrämpfe, Übelkeit, Erbrechen und starke Schmerzen der Skelettmuskulatur. Betroffene Patienten versterben innerhalb weniger Stunden nach Ingestion aufgrund von Atemlähmung und/oder Herzrhythmusstörungen.Die wichtigste Maßnahme nach oraler Ingestion besteht in einer möglichst schnellen primären Giftelimination (bei bewusstseinsklaren Patienten Erbrechen auslösen, sonst Magenspülung unter Schutzintubation) und der anschließenden Kohlegabe. Ein spezifisches Antidot steht nicht zur Verfügung. Das Management einer Intoxikation besteht vor allem aus der Therapie der Rhythmusstörungen in Form von Magnesium und Amiodaron.Auf die strikte Einhaltung von Eigenschutzmaßnahmen (Handschuhe, Mundschutz) muss unbedingt geachtet werden. Ein direkter Hautkontakt mit Pflanzenteilen ist ebenso zu vermeiden wie der potenzielle Kontakt mit Erbrochenem oder Aspirat. Topics: Aconitine; Aconitum; Amiodarone; Anti-Arrhythmia Agents; Female; Glasgow Coma Scale; Humans; Middle Aged; Plant Poisoning; Resuscitation; Suicide, Attempted; Tachycardia; Therapeutic Irrigation | 2017 |
Herbal Cardiotoxicity: Can Mother Nature Hurt the Heart?
Topics: Aconitine; Anti-Arrhythmia Agents; Electrocardiography; Female; Gastric Lavage; Humans; Tachycardia | 2016 |
An Unusual Etiology for Bidirectional Ventricular Tachycardia.
Bidirectional ventricular tachycardia is a rare variety of tachycardia with a morphologically distinct presentation. The QRS axis and/or morphology alternate in the frontal plane leads. We report a patient with bidirectional ventricular tachycardia in association with aconitine poisoning. Topics: Aconitine; Adjuvants, Immunologic; Anti-Arrhythmia Agents; Diagnosis, Differential; Electrocardiography; Female; Gastric Lavage; Humans; Middle Aged; Tachycardia | 2016 |
Herb-induced cardiotoxicity from accidental aconitine overdose.
Patients who overdose on aconite can present with life-threatening ventricular arrhythmia. Aconite must be prepared and used with caution to avoid cardiotoxic effects that can be fatal. We herein describe a case of a patient who had an accidental aconite overdose but survived with no lasting effects. The patient had prepared Chinese herbal medication to treat his pain, which resulted in an accidental overdose of aconite with cardiotoxic and neurotoxic effects. The patient had ventricular tachycardia, bidirectional ventricular tachycardia and ventricular fibrillation. Following treatment with anti-arrhythmic medications, defibrillation and cardiopulmonary resuscitation, he made an uneventful recovery, with no further cardiac arrhythmias reported. Topics: Aconitine; Adult; Anti-Arrhythmia Agents; Cardiopulmonary Resuscitation; Cardiotoxicity; Drug Overdose; Drugs, Chinese Herbal; Electric Countershock; Electrocardiography; Humans; Male; Tachycardia; Tachycardia, Ventricular; Treatment Outcome; Ventricular Fibrillation | 2015 |
[Prophylactic use of VFS in patients with coronary artery disease in the perioperative coronary artery bypass grafting].
Tachyarrhythmias (TA) - dangerous postoperative complications of coronary artery bypass grafting, threatening the lives of patients and found, according to different authors, in 13-40% of cases. VFS - an antiarrhythmic drug that belongs to a class 1C, is effective in the treatment and prevention of a variety of cardiac arrhythmias. The aim of the work was to study the clinical efficacy of VFS CHD patients with a history of tachyarrhythmias during the perioperative period of coronary bypass surgery, as well as its comparison with other antiarrhythmic drug (amiodarone). Clinical efficacy was evaluated in 218 patients with coronary heart disease at baseline with a history of tachyarrhythmia (paroxysmal atrial fibrillation or premature ventricular high grade (IV and V class on classification of Lown B. and Wolf M. in the modification of Ryan M.). Shown that the VFS is more effective than amiodarone, both in paroxysmal atrial fibrillation and ventricular arrhythmias when high gradation. Topics: Aconitine; Amiodarone; Anti-Arrhythmia Agents; Chemoprevention; Comparative Effectiveness Research; Coronary Artery Bypass; Coronary Artery Disease; Female; Heart Rate; Humans; Male; Middle Aged; Perioperative Care; Postoperative Complications; Retrospective Studies; Tachycardia; Treatment Outcome | 2013 |
Cardioprotective effect of grape-seed proanthocyanidins on doxorubicin-induced cardiac toxicity in rats.
Doxorubicin (Dox) is an anthracycline antibiotic used as anticancer agent. However, its use is limited due to its cardiotoxicity which is mainly attributed to accumulation of reactive oxygen species.. This study was conducted to assess whether the antioxidant, proanthocyanidins (Pro) can ameliorate Dox-induced cardiotoxicity in rats.. Male Sprague-Dawely rats were divided into four groups. Group I was control. Group II received Pro (70 mg/kg, orally) once daily for 10 days. Group III received doxorubicin 15 mg/kg i.p. as a single dose on the 7th day and Group IV animals were treated with Pro once daily for 10 days and Dox on the 7th day. The parameters of study were serum biomarkers, cardiac tissue antioxidant status, ECG, and effect on aconitine-induced cardiotoxicity.. Cardiac toxicity of doxorubicin was manifested as a significant increase in heart rate, elevation of the ST segment, prolongation of the QT interval and an increase in T wave amplitude. In addition, Dox enhanced aconitine-induced cardiotoxicity by a significant decrease in the aconitine dose producing ventricular tachycardia (VT). Administration of Pro significantly suppressed Dox-induced ECG changes and normalized the aconitine dose producing VT. The toxicity of Dox was also confirmed biochemically by significant elevation of serum CK-MB and LDH activities as well as myocardial MDA and GSH contents and decrease in serum catalase and myocardial SOD activities. Administration of Pro significantly suppressed these biochemical changes.. These results suggest that proanthocyanidins might be a potential cardioprotective agent against Dox-induced cardiotoxicity due to its antioxidant properties. Topics: Aconitine; Animals; Antibiotics, Antineoplastic; Antioxidants; Arrhythmias, Cardiac; Biomarkers; Cardiomyopathy, Dilated; Cardiotonic Agents; Cardiotoxins; Doxorubicin; Drug Resistance; Grape Seed Extract; Heart; Male; Myocardium; Oxidative Stress; Phytotherapy; Proanthocyanidins; Rats; Rats, Sprague-Dawley; Tachycardia; Voltage-Gated Sodium Channel Agonists | 2013 |
Toxicity following accidental ingestion of Aconitum containing Chinese remedy.
Various species of Aconitum are commonly used in traditional Chinese medicine. These plants are known to contain highly potent cardiotoxins. A 22 year old Chinese male accidentally ingested a herbal liniment prepared from Aconitum with near fatal results. His ventricular tachyarrhythmias responded to standard treatment including the use of i.v. magnesium. Topics: Aconitine; Adult; Chromatography, High Pressure Liquid; Drugs, Chinese Herbal; Humans; Injections, Intravenous; Magnesium; Male; Tachycardia | 1996 |
Microwave ablation of canine atrial tachycardia induced by aconitine.
We tested the efficacy of microwave-frequency energy for ablating atrial tachycardia in eight open-chest dogs. Five other dogs served as controls. Atrial tachycardia was induced by direct application of aconitine crystals to the epicardial atrial surface or by injection of aconitine solution (0.15 mg/ml) into the right or left atrial myocardium. Atrial tachycardias (n = 15) developed at a cycle length of 253 +/- 64 msec or within 245 +/- 116 sec after topical application or injection of aconitine. Catheter ablation was attempted on 10 atrial tachycardias in 8 experiment dogs by using continuous, unmodulated microwave energy from a 915 MHz frequency signal generator via a 7F helical or whip antenna catheter. Successful ablation was defined as conversion of atrial tachycardia to sinus rhythm during delivery of microwave energy and maintenance of sinus rhythm for > 5 minutes after termination of energy delivery. All 10 atrial tachycardias were successfully ablated by 2.3 +/- 1.6 applications of microwave energy for each atrial tachycardia induced. Forward microwave power level was 50.5 +/- 8.1 W, and the duration of energy application was 25.0 +/- 27.6 seconds. Sinus rhythm resumed 9.5 +/- 9.2 seconds after the onset of microwave energy application. After a mean follow-up of 10.4 minutes, seven atrial tachycardias recurred, most likely the result of diffusion of aconitine beyond the perimeter of rhe ablation lesions. Atrial tachycardia did not recur in 3 of 3 dogs that had larger ablation lesion. Gross examination revealed 10 demarcated round or oval transmural lesions in the right or left atrium, ranging from 12.6 to 105.6 mm2 in area.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Aconitine; Animals; Catheter Ablation; Dogs; Evaluation Studies as Topic; Female; Heart Atria; Male; Microwaves; Recurrence; Tachycardia; Time Factors | 1995 |
Positive chronotropic and inotropic effects of higenamine and its enhancing action on the aconitine-induced tachyarrhythmia in isolated murine atria.
Aconitine and higenamine are the components of aconite root. We investigated the cardiac effects of these compounds on murine right and left atria and the interaction of higenamine with aconitine on the rate of spontaneously beating right atria. Higenamine increased the rate (EC50 = 38 nM) and the force of contraction (EC50 = 97 nM), the maximal responses being comparable with those of isoproterenol. The positive chronotropic effect of higenamine was antagonized by propranolol (30-300 nM) and practolol (10 nM-3 microM), but not by butoxamine (1 microM), indicating that it was a beta 1-adrenoceptor-mediated action. The positive chronotropic effect of higenamine was not changed by pretreatment with reserpine (4 mg/kg, i.p., 4 hr). Aconitine (0.16-0.25 microM) induced tachyarrhythmia in right atria was attenuated by quinidine (1 microM), atropine (8.6 microM) and AF-DX 116 (8.6 microM), suggesting that aconitine activates sodium channels and muscarinic receptors. Higenamine (2.5 nM) and dobutamine (1 nM) did not cause chronotropic effects by themselves, but enhanced the aconitine-induced tachyarrhythmia. These results indicate that higenamine is a beta 1-adrenoceptor full agonist in murine atria and that the aconitine-induced tachyarrhythmia is augmented by the beta 1-adrenergic action of higenamine. Topics: Aconitine; Adrenergic beta-1 Receptor Antagonists; Alkaloids; Animals; Cardiotonic Agents; Heart Atria; Heart Rate; In Vitro Techniques; Male; Mice; Mice, Inbred Strains; Muscarinic Antagonists; Myocardial Contraction; Tachycardia; Tetrahydroisoquinolines | 1994 |
Anti-arrhythmic profile of a garlic dialysate assayed in dogs and isolated atrial preparations.
The effects of garlic (Allium sativum L., Liliaceae) dialysate were studied on arrhythmias induced in anaesthetized dogs and on isolated left rat atria. Garlic dialysate suppressed premature ventricular contractions (PVC) and ventricular tachycardia (VT) in ouabain-intoxicated dogs as well as the ectopic rhythms induced by isoprenaline (10(-6) M) and aconitine (10(-8) M) on electrically driven left rat atria. The effective refractory period (ERP) and the sinus node recovery time (SNRT) of isolated rat atria were prolonged in a dose-dependent manner by the administration of this extract. Garlic dialysate decreased the positive inotropic and chronotropic effects of isoprenaline in a concentration-dependent manner. These last effects were increased by propranolol. The results suggest that garlic dialysate has a significant antiarrhythmic effect in both ventricular and supraventricular arrhythmias. Topics: Aconitine; Animals; Arrhythmias, Cardiac; Dialysis; Disease Models, Animal; Dogs; Dose-Response Relationship, Drug; Electric Stimulation; Electrocardiography; Female; Garlic; Heart Atria; In Vitro Techniques; Isoproterenol; Male; Myocardial Contraction; Ouabain; Plant Extracts; Plants, Medicinal; Propranolol; Rats; Refractory Period, Electrophysiological; Tachycardia | 1994 |
[Experimental study of laser ablation on lethal arrhythmias--features and effectiveness of epicardial mapping].
To find the exact location of the ventricular arrhythmogenic myocardium, we mapped activation times of local epicardial electrograms (ATLE: 16 bipolar electrodes, 2 x 2 cm2) aided by an on-line computer and guided laser ablation of lethal ventricular arrhythmias induced by aconitine. Thirty-six tests involved 12 dog hearts. Nd:YAG laser application converted ventricular tachycardias and fibrillation to sinus rhythm in all tests. Epicardial mapping results showed: Taking ECG lead II as reference, the differences among all ATLE were within 15ms, and there was no obvious conduct slow zone before drugging and after resuming sinus rhythm, even though 298 +/- 157 mm2 photocoagulation areas (n = 36) resulted from laser irradiation; During VT, the majority of ATLE were preexcited from 90 to 30 ms, and more than one breakthrough point existed, with one predominating; ATLE changed significantly after laser. The ectopic foci were located exactly by using ATLE for laser treatment. Topics: Aconitine; Animals; Dogs; Electrocardiography; Laser Therapy; Microcomputers; Tachycardia; Ventricular Fibrillation | 1992 |
[The role of transcatheter ultra high frequency ablation of experimental arrhythmia at atrioventricular junctional area].
Topics: Aconitine; Animals; Cardiac Complexes, Premature; Dogs; Electrocoagulation; Female; Male; Myocardium; Rabbits; Radiofrequency Therapy; Tachycardia | 1991 |
[The experimental ablation of ventricular tachycardia in dogs with intracoronary ethyl alcohol injection].
In 15 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated. Localized ventricular tachycardia (VT) was induced by injecting aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch. In 6 untreated control dogs, VT lasted 17.6 +/- 8.3 minutes, 3 of them degenerated into ventricular fibrillation. The VTs were eliminated in 8 of the 9 dogs (88.9%) 1.2 +/- 1.4 minutes after injection of 96% ethyl alcohol. The pathologic examination revealed that transmural myocardial necrosis was present in 7 of 9 dogs receiving alcohol injection. Fibrin or thrombus was present in the diagonal coronary branch in 5 dogs. The conclusion was that the intracoronary injection of 96% ethyl alcohol ablated aconitine-induced ventricular tachycardia effectively. This approach may become a promising new method to treat ventricular tachycardia or other arrhythmia. Topics: Aconitine; Animals; Coronary Vessels; Dogs; Ethanol; Female; Injections, Intra-Arterial; Male; Myocardium; Necrosis; Tachycardia | 1991 |
[Experimental study of laser ablation on lethal arrhythmias in dogs].
To study the effect of laser ablation on arrhythmogenic ventricular myocardium, we applied aconitine on 36 local epicardial sites of ventricles (22 in LV, 14 in RV) in 12 dogs. Severe monographic persistent VTs or VFs were induced by aconitine and then these foci were irradiated by Nd: YAG laser. RV refractoriness (RVR) and local epicardial pacing threshold (LEPT) were measured by programmed electrical stimulation (PES) before aconitine applying and after resuming sinus rhythm. That VT or VF could not be induced by PES and the heart had persistent sinus rhythm was considered success. Aconitine doses were 7.9 +/- 4.8 micrograms in LV, 3.3 +/- 1.9 micrograms in RV, P less than 0.01. The data of time from aconitine applying to the appearance of VT were 237 +/- 228 s in LV and 148 +/- 101 s in RV, P less than 0.05. VF incidence rate was 75% (27/36). All of VT, VF could be abolished by mapping-guided laser irradiation on VT foci. The mean laser energy was 1542 +/- 893 joules (n = 36). RVR and LEPT increased significantly (P less than 0.001) after tests. Results showed that: (1) Lethal ventricular arrhythmias could be induced by giving little aconitine on the ventricular epicardium; (2) Mapping-guided lasering on arrhythmogenic myocardium could eradicate VT and VF; (3) RVR and LEPT would increase greatly after ablation. Topics: Aconitine; Animals; Dogs; Electrocardiography; Female; Heart; Laser Therapy; Male; Tachycardia; Ventricular Fibrillation | 1991 |
A canine model of torsades de pointes.
Although quinidine has been reported to induce QT interval prolongation and torsades de pointes clinically, the only experimental model currently available for quinidine-induced torsades de pointes requires the concurrent use of ischemia, reperfusion and cardiac pacing of the isolated, perfused heart. Our purpose in this study was to determine the circumstances under which quinidine might elicit torsades de pointes consistently in the intact dog. We found that maintenance of therapeutic plasma quinidine concentrations, alone, did not induce the arrhythmia. Rather, arrhythmia induction required the additional application of aconitine, which induces early afterdepolarizations and triggered activity. When aconitine was applied to two epicardial sites in dogs having quinidine-induced QT interval prolongation greater than 10%, torsades de pointes occurred in 80% of instances. When QT prolongation was less than 10%, aconitine-induced torsades de pointes was seen in only 21% of animals. Our results suggest that in a previously healthy heart quinidine-induced QT prolongation is, itself, insufficient to induce torsades de pointes consistently, and two independent sites of ectopic activity are needed as well. The ectopic foci appear to modulate one another's impulse initiation or activation sequence, thereby giving rise to the classical "twisting of the points" associated with the arrhythmia. Topics: Aconitine; Aconitum; Animals; Disease Models, Animal; Dogs; Electrocardiography; Electrodes, Implanted; Heart; Quinidine; Tachycardia | 1988 |
Intracoronary ethyl alcohol or phenol injection ablates aconitine-induced ventricular tachycardia in dogs.
The hypothesis whether localized ventricular tachycardia could be ablated by myocardial necrosis induced with chemical agents injected into a coronary artery was tested. In 59 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated either occlusively or nonocclusively. Localized ventricular tachycardia was induced by injecting approximately 0.01 ml of 30 micrograms/ml of aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch in 54 dogs. In eight untreated control dogs, aconitine-induced ventricular tachycardia lasted 10.2 +/- 2.3 minutes or degenerated into ventricular fibrillation after 7.0 +/- 4.0 minutes. In the remaining 46 dogs, 1 ml of saline solution, 25, 50 or 100% ethyl alcohol or 0.94 ml (mean [range 0.4 to 2.0]) of 25% phenol at room temperature was injected into the occluded coronary artery and 1 ml of 100% ethyl alcohol at body temperature was injected into the nonoccluded coronary artery. Ventricular tachycardia was eliminated in 9 (82%) of 11 dogs receiving phenol, 7 (88%) of 8 dogs receiving 100% ethyl alcohol occlusively, 6 (75%) of 8 dogs receiving 100% ethyl alcohol nonocclusively and 6 (67%) of 9 dogs receiving 50% ethyl alcohol for an entire follow-up period of 10 to 60 minutes. However, saline solution and 25% ethyl alcohol suppressed ventricular tachycardia only transiently in 8 (53%) of 15 and 3 (60%) of 5 dogs, respectively. Left ventricular end-diastolic pressure rose from 8.0 to 11.2 mm Hg (p less than 0.05) immediately after injection of 100% ethyl alcohol in seven dogs.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Aconitine; Animals; Coronary Vessels; Dogs; Electrocardiography; Ethanol; Female; Heart Ventricles; Injections, Intra-Arterial; Male; Myocardium; Necrosis; Phenol; Phenols; Stroke Volume; Tachycardia | 1987 |
Effects of lithium on time to onset of aconitine-induced initial arrhythmia and ventricular tachycardia.
The effects of lithium on the time to onset of aconitine-induced initial arrhythmia and onset of ventricular tachycardia were determined in mice. The mice were pretreated intraperitoneally with 1.73, 3.0, 5.1 and 8.8 mEq lithium chloride/kg/day for 5 days, or 8.8 mEq LiCl/kg/day i.p. for 1, 3, 5, 7 and 10 days. Lithium prolonged the onset-time to ventricular tachycardia, and this effect was both dose and time dependent. Under these conditions, lithium pretreatment had no effect on the time to onset of aconitine-induced initial arrhythmia. The LD50 was 15.3 mEq/kg. The observed prolongation of the onset of ventricular tachycardia can be explained in part by the influence of lithium on myocardial cations and catecholamines, and the pharmacologic effect of lithium on Purkinje fibers. Topics: Aconitine; Aconitum; Animals; Arrhythmias, Cardiac; Drug Interactions; Heart Ventricles; Lethal Dose 50; Lithium; Mice; Tachycardia; Time Factors | 1979 |
Negative chronotropic and antiarrhythmic properties of atropine and other tropane analogues on isolated cat heart preparations.
Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Atropine; Bradycardia; Cats; Dose-Response Relationship, Drug; Heart Rate; Perfusion; Tachycardia; Time Factors; Tropanes | 1978 |
[Effect of electric cardiac stimulation in experimental supraventricular tachycardia].
Experimental supraventricular tachyarrhythmia was produced in dogs by the local application of aconitine on the left auricle. The effect of various types of stimulations (right auricular, right ventricular, double-delayed right auricular and right ventricular-right auricular double-delayed stimulation) was studied for the suppression of supra-ventricular (overdrive) tachyarrhythmia. It was found that the electric stimulation of the heart is an effective method of suppressing tachyarrhythmias, though there is a significant difference in the anti-arrhythmic effects of the electric stimulations of various types. For suppression of the supraventricular tachyarrhythmia caused by aconitine, delayed double-right auricular stimulation seemed to be the most effective with respect to the right ventricle. The bioelectric features of aconitine arrhythmia and the mechanism of the antiarrhythmic effect of the electric stimulation of the heart are discussed. Topics: Aconitine; Animals; Dogs; Electric Stimulation; Electric Stimulation Therapy; Electrocardiography; Female; Heart Ventricles; Male; Tachycardia | 1977 |
Antiarrhythmic properties of MJ 9067 in acute animal models.
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 | 1977 |
[Reduction of aconitine and adrenaline tachycardia by the antifibrillating substance trimepranol in the rat heart in situ and in the isolated frog heart (comparative study) (author's transl)].
Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Anura; Disease Models, Animal; Epinephrine; Phenyl Ethers; Propanolamines; Rabbits; Rats; Tachycardia | 1977 |
[Hemodynamic aspects of ventricular tachycardia suppression by means of high supraventricular frequencies (preliminary observations)].
Topics: Aconitine; Animals; Atrial Fibrillation; Blood Pressure; Cardiac Output; Dogs; Electric Stimulation; Heart Conduction System; Hemodynamics; Tachycardia | 1976 |
[Effect of ajmaline and its therapeutically used derivatives N-propylajmaline and di-monochloracetylajmaline on the functional refractory period and contractility of guinea pig atrium and aconitine arrhythmia in the rat].
1. In the isolated left atrium of the guinea pig ajmaline and di-monochloracetylajmaline (DCAA) show almost the same activity concerning prolongation of the functional refractory period. 2. In contrast to this N-propylajmaline (NPA) is much more effective than ajmaline. 3. NPA as compared to ajmaline and DCAA, however, shows a considerably smaller difference between the concentrations prolonging refractory period (I) and those decreasing contractility (II) in the guinea pig atrium (EC25). The quotient from I and II is 0.4 with NPA, 1.2 with ajmaline and 1.6 with DCAA. 4. Differences in efficacy similar to those observed in the guinea pig atrium are also found in experimental cardiac arrhythmias in the intact animal. NPA is much more effective than ajmaline regarding inhibition of extrasystoles, ventricular tachycardia and ventricular flutter due to aconitine infusion in the rat. In this experimental model DCAA shows slightly less activity than ajmaline; this difference is statistically significant. Topics: Aconitine; Aconitum; Ajmaline; Animals; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Electrocardiography; Guinea Pigs; Heart; Heart Atria; Heart Rate; In Vitro Techniques; Male; Myocardial Contraction; Rats; Tachycardia; Ventricular Fibrillation | 1975 |
The effects of manganese on aconitine-induced ventricular tachycardia.
Isolated rabbit heart with independent perfusion of a small left ventricular area was used to study the effect of manganese ions on aconitine-induced ventricular tachycardia. Manganese chloride 4 mM in Locke solution exhibited a constant preventive or suppressive effect versus aconitum-induced rhythm disorders. It is concluded that the interpretation of aconitine cardiotoxic effects on the sole basis of phase 3 modifications require further evidence, and that an increased diastolic depolarization rate may well explain, at least in this experimental model, the genesis of arrhythmias induced by this drug. Topics: Aconitine; Aconitum; Animals; Heart Rate; Heart Ventricles; Manganese; Rabbits; Tachycardia | 1973 |
STUDIES ON ACONITINE-INDUCED VENTRICULAR FIBRILLATION BY SIMULTANEOUS RECORDING OF ELECTROCARDIOGRAMS AND TRANSMEMBRANE POTENTIALS IN SITU.
Topics: Aconitine; Aconitum; Animals; Electrocardiography; Electrophysiology; Heart; Heart Block; Membrane Potentials; Rabbits; Research; Tachycardia; Tachycardia, Paroxysmal; Ventricular Fibrillation | 1964 |
Studies on auricular tachycardia caused by aconitine administration.
Topics: Aconitine; Heart; Heart Rate; Humans; Pharmaceutical Preparations; Tachycardia | 1947 |