36 results match your criteria Toxicity Antidysrhythmic


The Case of Flecainide Toxicity: What to Look for and How to Treat.

J Emerg Med 2020 Aug 11;59(2):e43-e47. Epub 2020 Jun 11.

Department of Emergency Medicine, Beaumont Health, Royal Oak, Michigan.

Background: Flecainide is a class Ic antidysrhythmic agent used to prevent and treat both ventricular and supraventricular tachycardias, including atrial fibrillation, atrioventricular nodal re-entrant tachycardia, and Wolff-Parkinson-White syndrome. Flecainide can cause serious side effects, including cardiac arrest, dysrhythmias, and heart failure. Despite its growing use, the presenting signs and symptoms of flecainide toxicity are not familiar to most clinicians. Read More

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Chloroquine, hydroxychloroquine and COVID-19.

Toxicol Commun 2020 30;4(1):40-42. Epub 2020 Apr 30.

Division of Medical Toxicology, Department of Emergency Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

The media have featured the antimalarials chloroquine (CQ) and hydroxychloroquine (HCQ) to treat coronavirus (COVID-19). Political leaders have touted their use and recommended availability to the public. These anti-inflammatory agents have substantial human toxicity with a narrow therapeutic window. Read More

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Comprehensive review of cardiovascular toxicity of drugs and related agents.

Med Res Rev 2018 07 5;38(4):1332-1403. Epub 2018 Jan 5.

Department of Pharmacology, Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic.

Cardiovascular diseases are a leading cause of morbidity and mortality in most developed countries of the world. Pharmaceuticals, illicit drugs, and toxins can significantly contribute to the overall cardiovascular burden and thus deserve attention. The present article is a systematic overview of drugs that may induce distinct cardiovascular toxicity. Read More

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Successful treatment of flecainide-induced cardiac arrest with extracorporeal membrane oxygenation in the ED.

Am J Emerg Med 2015 Oct 29;33(10):1542.e1-2. Epub 2015 Jul 29.

Department of Emergency Medicine, Michigan State University College of Human Medicine, Grand Rapids, MI, USA; Spectrum Health Hospitals, Grand Rapids, MI, USA; Grand Rapids Medical Education Partners Emergency Medicine Residency, Grand Rapids, MI, USA.

Flecainide is a class Ic antidysrhythmic agent used to prevent and treat tachydysrhythmias. Flecainide toxicity primarily causes cardiovascular and neurologic effects through sodium-channel blockade. There is scant evidence to support specific management, and recommended therapies have been extrapolated from management of other sodium-channel blocking drugs. Read More

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October 2015

Patterns of cyanide antidote use since regulatory approval of hydroxocobalamin in the United States.

Am J Ther 2014 Jul-Aug;21(4):244-9

Departments of 1Obstetrics and Gynecology and 2Medical Toxicology Service, Department of Emergency Medicine, San Antonio Military Medical Center, San Antonio, TX; 3Department of Emergency Medicine, School of Pharmacy, Concordia University, Mequon, WI; and 4Texas A & M University Health Science Center College of Medicine, Scott and White Hospital, Temple, TX.

Sodium nitrite and sodium thiosulfate are common cyanide antidotes. Hydroxocobalamin was approved for use in the United States in 2006. Our objective was to determine the frequency of antidote use as reported to the US poison centers from 2005 to 2009 and describe which antidotes were used in critically ill cyanide toxic patients. Read More

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A case of near-fatal flecainide overdose in a neonate successfully treated with sodium bicarbonate.

J Emerg Med 2013 Apr 13;44(4):781-3. Epub 2012 Sep 13.

New York University School of Medicine and Bellevue Hospital, New York, New York and New York City Poison Control Center, New York, NY 10016, USA.

Background: Flecainide is a class IC antidysrhythmic primarily indicated for ventricular dysrhythmias and supraventricular tachycardia (SVT). Class IC antidysrhythmic overdose has a reported mortality of 22%, and death results from dysrhythmias and cardiovascular collapse. We report a near-fatal flecainide overdose in an 18-day-old treated successfully with sodium bicarbonate. Read More

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A life-threatening flecainide overdose treated with intravenous fat emulsion.

Pacing Clin Electrophysiol 2013 Mar 8;36(3):e87-9. Epub 2012 Aug 8.

Department of Emergency Medicine, Regions Hospital, St. Paul, MN 55101, USA.

Flecainide is a Vaughan Williams Class Ic antidysrhythmic associated with PR, QRS, and QTc prolongation on the electrocardiogram and development of life-threatening cardiac toxicity in overdose. The cornerstone of treatment is fluid resuscitation and the administration of magnesium and sodium bicarbonate. We report a case of flecainide overdose associated with life-threatening hemodynamic compromise successfully treated with intravenous fat emulsion (IFE) therapy. Read More

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Mechanisms of amiodarone and desethylamiodarone cytotoxicity in nontransformed human peripheral lung epithelial cells.

J Pharmacol Exp Ther 2011 Feb 15;336(2):551-9. Epub 2010 Nov 15.

Department of Pharmacology and Toxicology, Queen’s University, Kingston, Ontario, Canada.

Amiodarone (AM) is a potent antidysrhythmic agent that can cause potentially life-threatening pulmonary fibrosis, and N-desethylamiodarone (DEA), an AM metabolite, may contribute to AM toxicity. Apoptotic cell death in nontransformed human peripheral lung epithelial 1A (HPL1A) cells was assessed by annexin V-fluorescein isothiocyanate (ann-V) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), and necrotic cell death was assessed by propidium iodide (PI) staining. The percentage of cells that were PI-positive increased more than six times with 20 μM AM and approximately doubled with 3. Read More

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February 2011

The effect of amiodarone pretreatment on survival of mice with cocaine toxicity.

J Med Toxicol 2005 Dec;1(1):11-8

Medical Toxicology Fellow, Rocky Mountain Poison and Drug Center and Denver Health Medical Center, Denver, CO.

Introduction: Cocaine is a common drug of abuse and use has been associated with ventricular dysrhythmias. Published guidelines suggest that amiodarone is the first line antidysrhythmic for ventricular tachycardia and fibrillation. However, the effects amiodarone in the setting of cocaine toxicity are unknown and unstudied. Read More

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December 2005

Cardiotonic and antidysrhythmic effects of oleanolic and ursolic acids, methyl maslinate and uvaol.

Phytomedicine 2004 Feb;11(2-3):121-9

Department of Human Physiology University of Durban-Westville, Durban, South Africa.

The cardiotonic and antidysrhythmic effects of four triterpenoid derivatives, namely oleanolic acid (OA), ursolic acid (UA), and uvaol (UV), isolated from the leaves of African wild olive (Olea europaea, subsp. africana) as well as methyl maslinate (MM) isolated from the leaves of Olea europaea (Cape cultivar) were examined. The derivatives showed low toxicity on brine shrimp test. Read More

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February 2004

Evaluation of the antidysrhythmic effects of delta- and kappa-opioid receptor agonists and antagonists on calcium chloride-, adrenaline- and ischemia/reperfusion-induced arrhythmias in rats.

Methods Find Exp Clin Pharmacol 2004 Jan-Feb;26(1):31-8

Department of Pharmacology, Faculty of Health Sciences, University of Durban-Westville, Durban, South Africa.

This study was undertaken to evaluate the involvement of delta- and kappa-opioid receptors in both ischemia- and reperfusion-induced arrhythmias, and to elucidate some of the plausible mechanisms conferring antidysrhythmic effects on opioid delta- and kappa-receptor agonists and antagonists. Different models of arrhythmia (calcium chloride [CaCl(2)]-, adrenaline-, and ischemia/reperfusion-induced arrhythmias) were employed. The following opioid agonists, antagonists and blockers were used in the study: [D-Ala(2), D-Leu(5)]enkephalin (DADLE), a selective delta-receptor agonist; trans-3,4-Dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]benzeneacetamide (U-50488H), a selective kappa-receptor agonist; Naltriben Methanesul-fonate (NTB), a selective delta(2)-antagonist with kappa-receptor agonist-like activity; natrindole, a non-selective delta(1)- and delta(2)-receptor antagonist; nor-binaltorphimine dehydrochloride (nor-BNI), a selective kappa-receptor antagonist; chelerythrine, a selective protein kinase C inhibitor, and glibenclamide, a selective blocker of ATP-sensitive K channel. Read More

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Differential effects of pirfenidone on acute pulmonary injury and ensuing fibrosis in the hamster model of amiodarone-induced pulmonary toxicity.

Toxicol Sci 2003 Sep 27;75(1):169-80. Epub 2003 Jun 27.

Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada K7L 3N6.

Pulmonary toxicity, including fibrosis, is a serious adverse effect associated with the antidysrhythmic drug amiodarone (AM). We tested the potential usefulness of pirfenidone against AM-induced pulmonary toxicity in the hamster model. Intratracheal AM administration resulted in pulmonary fibrosis 21 days posttreatment, as evidenced by an increased hydroxyproline content and histological damage. Read More

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September 2003

Attenuation of amiodarone-induced pulmonary fibrosis by vitamin E is associated with suppression of transforming growth factor-beta1 gene expression but not prevention of mitochondrial dysfunction.

J Pharmacol Exp Ther 2003 Jan;304(1):277-83

Department of Pharmacology and Toxicology, Faculty of Health Sciences, Queen's University, Kingston, Ontario, Canada.

Amiodarone (AM) is an efficacious antidysrhythmic agent that can cause numerous adverse effects, including potentially life-threatening pulmonary fibrosis. The current study was undertaken to investigate potential protective mechanisms of vitamin E against AM-induced pulmonary toxicity (AIPT) in the hamster. Three weeks after intratracheal administration of AM (1. Read More

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January 2003

Induction of c-jun and TGF-beta 1 in Fischer 344 rats during amiodarone-induced pulmonary fibrosis.

Am J Physiol Lung Cell Mol Physiol 2001 Nov;281(5):L1180-8

Department of Pharmacology and Toxicology, Faculty of Health Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6.

Amiodarone (AM) is an antidysrhythmic agent with a propensity to cause pulmonary toxicity, including potentially fatal fibrosis. In the present study, the potential roles of c-Jun and transforming growth factor (TGF)-beta 1 in AM-induced inflammation and fibrogenesis were examined after intratracheal administration of AM (1.83 micromol/day on days 0 and 2) or an equivalent volume (0. Read More

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November 2001

Effects of vitamin E on cytotoxicity of amiodarone and N-desethylamiodarone in isolated hamster lung cells.

Toxicology 2001 Sep;166(3):109-18

Department of Pharmacology and Toxicology, Botterell Hall Room 535, Queen's University, Ont., K7L 3N6, Kingston, Canada.

Amiodarone (AM) is a potent and efficacious antidysrhythmic agent that can cause potentially life-threatening pulmonary fibrosis. Vitamin E has been demonstrated to decrease AM-induced pulmonary fibrosis in vivo in hamsters. In the present in vitro study, we investigated the effects of vitamin E on cell death induced by AM and its primary metabolite, N-desethylamiodarone (DEA), in freshly isolated hamster lung cells. Read More

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September 2001

Disruption of mitochondrial function and cellular ATP levels by amiodarone and N-desethylamiodarone in initiation of amiodarone-induced pulmonary cytotoxicity.

J Pharmacol Exp Ther 2001 Sep;298(3):1280-9

Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.

Amiodarone (AM), a potent antidysrhythmic agent, can cause potentially life-threatening pulmonary fibrosis. In the present investigation of mechanisms of initiation of AM lung toxicity, we found that 100 microM AM decreased mitochondrial membrane potential in intact hamster lung alveolar macrophages and preparations enriched in isolated alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells, following 2 h of incubation. This was followed by a drop in cellular ATP content (by 32--77%) at 4 to 6 h, and 30 to 55% loss of viability at 24 h. Read More

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September 2001

Effects of dietary vitamin E supplementation on pulmonary morphology and collagen deposition in amiodarone- and vehicle-treated hamsters.

Toxicology 1999 Apr;133(2-3):75-84

Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.

Amiodarone (AM) is a potent antidysrhythmic agent that is limited in clinical use by its adverse effects, including potentially life-threatening AM-induced pulmonary toxicity (AIPT). The present study tested the ability of dietary supplementation with vitamin E (500 IU d,1-alpha-tocopherol acetate/kg chow) to protect against pulmonary damage following intratracheal administration of AM (1.83 micromol) to the male golden Syrian hamster. Read More

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Amiodarone-induced disruption of hamster lung and liver mitochondrial function: lack of association with thiobarbituric acid-reactive substance production.

Toxicol Lett 1998 Sep;98(1-2):41-50

Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.

Amiodarone (AM) is an efficacious antidysrhythmic agent that is limited clinically by numerous adverse effects. Of greatest concern is AM-induced pulmonary toxicity (AIPT) due to the potential for mortality. Mitochondrial alterations and free radicals have been implicated in the etiology of AM-induced toxicities, including AIPT. Read More

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September 1998

Antioxidant and pharmacodynamic effects of pyridoindole stobadine.

Gen Pharmacol 1998 May;30(5):627-38

Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava, Slovak Republic.

1. The review summarizes the most important data known so far on chemistry, pharmacodynamics, toxicology and clinics of the investigational agent, pyridoindole stobadine. 2. Read More

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[Amiodarone and the lung].

Rev Port Cardiol 1996 Oct;15(10):745-51

Serviço de Cardiologia do Hospital de Pulido Valente, Lisboa.

The pulmonary toxicity induced by amiodarone is one of the major complications that can limit the use of this potent antidysrhythmic agent. The authors perform a bibliographical revision concerning the toxic effects of amiodarone in the lung, pathogenesis, clinical, radiologic and pathologic features, diagnostic problems, risk factors and prognostic data. Read More

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October 1996

Evaluation of reactive oxygen species involvement in amiodarone pulmonary toxicity in vivo and in vitro.

J Biochem Toxicol 1996 ;11(3):147-60

Department of Pharmacology, Queen's University, Kingston, Ontario, Canada.

Amiodarone (AM) is an effective antidysrhythmic agent, restricted in use by the development of adverse effects, including potentially fatal AM-induced pulmonary toxicity (AIPT). Although the pathogenesis of AIPT is unknown, an oxidant mechanism has been proposed. The present study evaluated the role of reactive oxygen species (ROS) in AM-induced toxicity. Read More

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Effects of gallium chloride on changes in action potentials and contraction in guinea pig ventricular muscle.

Anticancer Res 1996 Jan-Feb;16(1):327-32

Laboratorie de Pharmacologie Fondamentale, Faculté de Médecine, Besançon, France.

The electrophysiological effects of gallium chloride (Ga ) and its activity on arrhythmias induced by digitalis were investigated in guinea pig papillary muscle. KCl microelectrodes were used to record transmembrane electrical activity from Purkinje cells from the papillary muscle of guinea pig hearts during superfusion and electrical stimulation in vitro at 37 degrees C. Myocardial contractility was continuously monitored. Read More

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Mechanisms in the pathogenesis of amiodarone-induced pulmonary toxicity.

Can J Physiol Pharmacol 1995 Dec;73(12):1675-85

Department of Pharmacology and Toxicology, Queen's University, Kingston, ON, Canada.

Although amiodarone is a highly efficacious antidysrhythmic agent, the drug produces numerous adverse effects. The most critical of these is pulmonary toxicity because of the potential for mortality. This review examines the experimental model systems used to study amiodarone toxicity, summarizes the current state of knowledge regarding the processes involved in amiodarone-induced pulmonary toxicity (AIPT), and includes a discussion of potential future directions. Read More

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December 1995

Role of the vagus nerve in the antidysrhythmic effect of dexmedetomidine on halothane/epinephrine dysrhythmias in dogs.

Anesthesiology 1995 Nov;83(5):992-9

Department of Anesthesiology, Osaka University Faculty of Medicine, Japan.

Background: Dexmedetomidine, an alpha 2-adrenergic agonist, can prevent the genesis of halothane/epinephrine dysrhythmias through the central nervous system. Because stimulation of alpha 2 adrenoceptors in the central nervous system enhances vagal neural activity and vagal stimulation is known to inhibit digitalis-induced dysrhythmias, dexmedetomidine may exert the antidysrhythmic property through vagal stimulation. To address this hypothesis, the effect of dexmedetomidine in vagotomized dogs was examined and compared with that in intact dogs. Read More

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November 1995

A case of amiodarone-associated pulmonary toxicity.

Korean J Intern Med 1995 Jul;10(2):155-9

Department of Internal Medicine, Anatomical Pathology, College of Medicine, Soon Chun Hy ang University, Seoul, Korea.

Amiodarone is an iodinated benzofuran derivative that represents a new and extremely effective therapy for certain life-threatening refractory cardiac arrgythmia. There are numerous side effects associated with amiodarone therapy, including corneal microdeposits. Skin reactions and others. Read More

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Resistance of the hamster to amiodarone-induced pulmonary toxicity following repeated intraperitoneal administration.

Toxicol Lett 1994 Oct;74(1):51-9

Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.

Amiodarone is an effective antidysrhythmic agent, restricted in use by the development of pulmonary toxicity. Several in vivo animal models have been used to study amiodarone-induced pulmonary toxicity. Intratracheal administration of amiodarone to the hamster has been used as a model for the critical amiodarone-induced pulmonary fibrosis (AIPF). Read More

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October 1994

Comparison of the in vivo pulmonary toxicity of amiodarone and des-oxo-amiodarone in the hamster.

Toxicol Appl Pharmacol 1994 Aug;127(2):275-81

Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.

Amiodarone (AM) is an effective antidysrhythmic agent, the use of which is limited because of the drug's potential for causing life-threatening pulmonary fibrosis. Oxidative stress involving keto oxygen-derived free radical formation has been postulated to be responsible for initiating AM-induced pulmonary toxicity (AIPT). We have investigated whether des-oxo-amiodarone (DOAM), which has a methylene group in place of the keto oxygen group of AM, causes pulmonary fibrosis in an experimental animal. Read More

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[Preparation and pharmacologic profile of derivatives of alkoxyphenylcarbamic acid with potential effects on the cardiovascular system].

Cesk Farm 1993 Dec;42(6):260-4

Katedra farmakológie a toxikológie Farmaceutickej fakulty Univerzity Komenského, Bratislava, SR.

In a systematic study of the relationship between the chemical structure and beta-adrenolytic activity, eleven derivatives of the 4-alkoxysubstituted phenylcarbamic acids were prepared. The beta-adrenolytic efficiency of the compounds was studied in the isolated spontaneously beating guinea-pig atria and expressed as pA2 values against isoprenaline tachycardia. Negative chronotropic and antidysrhythmic activity were also evaluated. Read More

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December 1993

Amiodarone-induced injury of human pulmonary artery endothelial cells: protection by alpha-tocopherol.

J Pharmacol Exp Ther 1990 Sep;254(3):1107-12

Department of Internal Medicine, Indiana University School of Medicine, Indianapolis.

Amiodarone is a potent antidysrhythmic drug that is associated with severe pulmonary toxicity. The mechanism of amiodarone pulmonary toxicity is poorly understood. To investigate the possible involvement of oxygen-derived metabolites in amiodarone-induced injury, 51Cr-labeled human pulmonary artery endothelial (HPAE) cells were incubated with amiodarone for 18 hr in the presence of various antioxidants and in hypoxic and hyperoxic conditions with cell injury quantified by 51Cr release, expressed as cytotoxic index. Read More

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September 1990