aconitine and Heart-Arrest

Severe intoxications after ingestion of monk's hood are rare in childhood. We report a case of fatal intoxication in a 20 months old child. There is no specific therapy available. A review of the literature is added.

Topics: Aconitine; Brain; Brain Edema; Female; Gastric Mucosa; Heart Arrest; Humans; Infant; Plant Poisoning

Remote ischemic postconditioning (RIPost) has been shown to reduce the ischemia-reperfusion injury of the heart and brain. However, the protection mechanisms have not yet been fully elucidated. We have observed that RIPost could alleviate the brain injury after cardiac arrest (CA). The aim of this study was to explore whether α7 nicotinic acetylcholine receptor (α7nAChR) mediates the neuroprotection of RIPost in a rat model of asphyxial CA.. Asphyxial CA model was induced by occlusion of the tracheal tube for 8 min and resuscitated later. RIPost produced by three cycles of 15-min occlusion and 15-min release of the right hind limb by a tourniquet was performed respectively at the moment and the third hour after restoration of spontaneous circulation. The α7nAChR agonist PHA-543613 and the antagonist methyllycaconitine (MLA) were used to investigate the role of α7nAChR in mediating neuroprotective effects.. Results showed that α7nAChR was decreased in hippocampus and cortex after resuscitation, whereas RIPost could attenuate the reduction. The use of PHA-543613 provided neuroprotective effects against cerebral injury after CA. Furthermore, RIPost decreased the levels of neuron-specific enolase, inflammatory mediators, the number of apoptotic cells, and phosphorylation of nuclear factor-κB while increased the phosphorylation of signal transducer and activator of transcription-3. However, the above effects of RIPost were attenuated by α7nAChR antagonist methyllycaconitine.. Neuroprotection of RIPost was related with the activation of α7nAChR, which could suppress nuclear factor-κB and activate signal transducer and activator of transcription-3 in a rat asphyxial CA model.

Topics: Aconitine; alpha7 Nicotinic Acetylcholine Receptor; Animals; Asphyxia; Bridged Bicyclo Compounds, Heterocyclic; Disease Models, Animal; Heart Arrest; Hippocampus; Humans; Hypoxia, Brain; Ischemic Postconditioning; Male; Neuroprotection; NF-kappa B; Quinuclidines; Rats; Signal Transduction; STAT3 Transcription Factor; Treatment Outcome

Aconitine belongs to the Aconitum alkaloids and is a natural toxic substance. Aconitine has been used as a traditional medicine in East Asian culture. Today, aconitine is still in use with or without a prescription, in the Republic of Korea. Here we present a case report of accidental death due to acute aconitine poisoning. An 81-year-old woman ingested liquid that had been heat extracted from the root of the Aconitum plant; she presented to the emergency room 1 h after ingestion. Her electrocardiogram showed irregular ventricular arrhythmias including ventricular tachycardia; she progressed to cardiac arrest. Cardiopulmonary resuscitation and anti-arrhythmic drugs were administered, but the patient did not survive. An autopsy was performed 2 days postmortem. Toxicological analysis was performed, and aconitine was detected by liquid chromatography tandem mass spectrometry. The antemortem blood concentration of aconitine was 39.1 ng/ml and the concentrations of aconitine in the postmortem cardiac blood, peripheral blood, cerebrospinal fluid (CSF), pericardial fluid, and urine were 21.1 ng/ml, 28.6 ng/ml, 6.8 ng/ml, 24.1 ng/ml, and 67.4 ng/ml, respectively. This is the first forensic case report of an aconitine poisoning death in the Republic of Korea with quantitative measurement of aconitine in the antemortem blood and various postmortem body fluids. To the best of our knowledge, this is the first report of the detection of aconitine in the CSF. These data about the distribution of aconitine in the antemortem blood and various postmortem body fluids is helpful for future aconitine poisoning death cases.

Topics: Aconitine; Aconitum; Aged, 80 and over; Chromatography, Liquid; Female; Heart Arrest; Humans; Medicine, East Asian Traditional; Pericardial Fluid; Republic of Korea; Tandem Mass Spectrometry

Taurine-magnesium coordination compound (TMCC) exhibits antiarrhythmic effects in cesium-chloride-and ouabain-induced arrhythmias; however, the mechanism underlying these effects on arrhythmia remains poorly understood. Here, we investigated the effects of TMCC on aconitine-induced arrhythmia in vivo and the electrophysiological effects of this compound in rat ventricular myocytes in vitro. Aconitine was used to induce arrhythmias in rats, and the dosages required to produce ventricular premature contraction (VPC), ventricular tachycardia (VT), ventricular fibrillation (VF), and cardiac arrest (CA) were recorded. Additionally, the sodium current (I

Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Calcium Channels, L-Type; Electrophysiological Phenomena; Female; Heart Arrest; Heart Ventricles; Ion Channels; Magnesium Compounds; Male; Myocytes, Cardiac; Patch-Clamp Techniques; Rats; Rats, Wistar; Sodium Channels; Taurine

Two people out of three who accidentally ate boiled aconite leaves died in 2012. This was a typical case of aconite poisoning in Japan: Aconite (Aconitum spp.) was mistakenly collected instead of Anemone flaccida, an edible wild plant. The leaves of these plants are quite similar to each other. Chemical analyses of the aconite plant left at the scene suggested intake of a fatal amount of aconitine alkaloids by each person. The collector, who died, had missed the botanical differences between the two plants, even though he owned a wild plant guidebook. A. flaccida should be collected with its flowers in order to aid positive indentification and avoid aconite poisoning.

Topics: Aconitine; Aconitum; Adult; Aged; Chromatography, High Pressure Liquid; Fatal Outcome; Female; Heart Arrest; Humans; Male; Middle Aged; Plant Leaves; Shock, Cardiogenic; Tachycardia, Ventricular; Tandem Mass Spectrometry

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

Topics: Aconitine; Aconitum; Aged, 80 and over; Emergency Service, Hospital; Heart Arrest; Humans; Male; Tachycardia, Ventricular

Antiarrhythmic properties of taurhythman were demonstrated on experimental models of ventricular (early occlusion and calcium chloride-induced) and atrioventricular (aconitine-induced) arrhythmias. The preparation reduced or prevented episodes of paroxysmal tachycardia and ventricular fibrillation, decreased the incidence of arrhythmias, and increased the lethal dose (LD) of arrhythmogenic agents. By its efficiency, taurhythman was superior to procainamide and comparable to lidocaine.

Topics: Aconitine; Alkanesulfonic Acids; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Cardiotonic Agents; Disease Models, Animal; Heart Arrest; Lidocaine; Male; Procainamide; Rats; Tachycardia, Paroxysmal; Ventricular Fibrillation

To compare the effects of oxysophoridine (Oxy) and sophoridine (Sop) on experimental arrhythmias and myocardial physiologic properties.. Arrhythmias were induced by drugs and myocardial ischemia. Physiologic properties were determined on isolated heart atria.. Oxy 500 mg.kg-1 (1/6 LD50) decreased the incidence of ventricular arrhythmias induced by aconitine (P < 0.01), increased the threshold dose of ouabain-induced ventricular premature (VP, P < 0.05), ventricular tachycardia (VT, P < 0.05), ventricular fibrillation (VF, P < 0.01), and cardiac arrest, (P < 0.01). After i.v. Oxy 500 mg.kg-1 into the rats with ligation of left anterior descending coronary artery, the total numbers of ectopic beats were decreased (P < 0.05), the incidence of VF was lowered, and the duration of VT was shortened (P < 0.01). Oxy 250 mg.kg-1 (1/13 LD50) i.v. shortened the duration of arrhythmias induced by BaCl2 (P < 0.01) and delayed the onset of arrhythmias induced by chloroform-epinephrine (P < 0.05). Oxy produced dose-dependent positive inotropic effects in the isolated left atrial of guinea pigs, increased the concentration of epinephrine to elicit automaticity in left atria, decreased slightly the excitability, and prolonged the functional refractory period. Sop produced the similar effects on arrhythmias as Oxy.. Oxy produced the similar anti-arrhythmic effects as Sop did at the equivalent effective dose.

Topics: Aconitine; Alkaloids; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Barium Compounds; Chlorides; Female; Guinea Pigs; Heart Arrest; Male; Matrines; Mice; Myocardial Contraction; Myocardial Ischemia; Ouabain; Quinolizines; Rabbits; Rats; Rats, Wistar; Refractory Period, Electrophysiological

Crebanine (Cre) iv 5 mg/kg could convert BaCl2-induced arrhythmia into sinus rhythm in rats, and could significantly increase the tolerant dose of aconitine to produce ventricular fibrillation (VF) and cardiac arrest (CA) in rats. The drug could also decrease the incidence of VF and CA by CaCl2 in rats and by chloroform in mice, but had no protective effects on ouabain-induced arrhythmias in guinea pigs.

Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Aporphines; Arrhythmias, Cardiac; Barium; Barium Compounds; Chlorides; Female; Guinea Pigs; Heart Arrest; Male; Mice; Ouabain; Rats; Rats, Wistar; Ventricular Fibrillation

LG 6-101 (1-[3-(2-methoxy-3-(2-methylpropylamino)-propoxy)-4-methyl- 2-thienyl]-3-phenyl-1-propanon hydrochloride; MW: 426.02) and LG 6-102 (2-(2-methoxy-3-propylamino-propoxy)-3-phenyl-propiophenon hydrochloride; MW: 391.92) are two new antiarrhythmic substances. They are structurally related to propafenone which is a widely used class Ic-antiarrhythmic drug. In man the oral bioavailability of propafenone is only about 5-40%. Therefore the development of compounds with similar mode of action but higher oral bioavailability seems to be meaningful. Both, LG 6-101 and LG 6-102 proved to be effective in isolated auricles and in experimental animals after intravenous administration. In the present study we tested the antiarrhythmic effects of LG 6-101 and LG 6-102 in rats after oral administration. Animals were treated with LG 6-101 (16, 32, 64, 128, 256 mg kg-1 bodyweight), LG 6-102 (4, 8, 16, 32, 64 mg kg-1 bodyweight) and propafenone (32, 64, 128, 256 mg kg-1 bodyweight) by gavage twice daily during 4 days. Both, LG 6-101 and LG 6-102 showed strong antiarrhythmic effects against arrhythmias induced on the fifth day by infusion of aconitine (10 micrograms kg-1 min-1). LG 6-102 was significantly more effective against cardiac arrest caused by infusion of aconitine (P less than or equal to 0.05) than LG 6-101. Both substances had good effects on the delay of ventricular premature beats.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aconitine; Administration, Oral; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Biological Availability; Heart Arrest; Male; Propafenone; Rats; Rats, Inbred Strains