RESUMO
Aconite poisoning was examined in five patients (four males and one female) aged 49 to 78 years old. The electrocardiogram findings were as follows: ventricular tachycardia and ventricular fibrillation in case 1, premature ventricular contraction and accelerated idioventricular rhythm in case 2, AIVR in case 3, and nonsustained ventricular tachycardia in cases 4 and 5. The patient in case 1 was given percutaneous cardiopulmonary support because of unstable hemodynamics, whereas the other patients were treated with fluid replacement and antiarrhythmic agents. The main aconitine alkaloid in each patient had a half-life that ranged from 5.8 to 15.4 h over the five cases, and other detected alkaloids had half-lives similar to the half-life of the main alkaloid in each case. The half-life of the main alkaloid in case 1 was about twice as long as the half-lives in the other cases, and high values for the area under the blood concentration-time curve and the mean residence time were only observed in case 1. These results suggest that alkaloid toxicokinetics parameters may reflect the severity of toxic symptoms in aconite poisoning.
Assuntos
Aconitina/farmacocinética , Aconitum , Arritmias Cardíacas/induzido quimicamente , Medicamentos de Ervas Chinesas/farmacocinética , Ritmo Idioventricular Acelerado/induzido quimicamente , Aconitina/análogos & derivados , Aconitina/sangue , Aconitina/intoxicação , Aconitina/urina , Idoso , Área Sob a Curva , Arritmias Cardíacas/fisiopatologia , Biotransformação , Cromatografia Líquida de Alta Pressão , Medicamentos de Ervas Chinesas/intoxicação , Eletrocardiografia , Feminino , Meia-Vida , Humanos , Masculino , Pessoa de Meia-Idade , Índice de Gravidade de Doença , Taquicardia Ventricular/induzido quimicamente , Espectrometria de Massas em Tandem , Toxicologia/métodos , Fibrilação Ventricular/induzido quimicamente , Complexos Ventriculares Prematuros/induzido quimicamenteRESUMO
The actions of maitotoxin were studied using cultured brainstem cells and adrenal chromaffin cells. Maitotoxin induced a profound increase in the Ca2+ influx into cultured brainstem cells after a brief lag period. The maitotoxin-induced Ca2+ influx was suppressed by various voltage-dependent Ca2+ channel blockers such as Co2+, Mn2+, verapamil and diltiazem. Maitotoxin-catecholamine release in brainstem cells initiated to increase after a lag period of about 1 min and the increase continued even at 4 min after treatment, while in the adrenal chromaffin cells the release started after an about 1-min lag period to attain a maximum within first 2-min and gradually decrease thereafter. These results suggest that maitotoxin acts on Ca2+ channels to increase the Ca2+ influx, accompanied by enhancement of catecholamine release in the brainstem cells with a different temporal profile from that in the adrenal chromaffin cells.
