PubMed · 2415276
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R L Himsworth. 1985. Hyperthyroidism with a low iodine uptake.. https://doi.org/10.1016/s0300-595x(85)80040-2
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A selective and sensitive assay for amiodarone N-deethylation activity in human liver microsomes by high-performance liquid chromatography (HPLC) with UV detection is reported. The extraction of desethylamiodarone from incubation samples was performed by means of an original solid-phase extraction (SPE) procedure using a polymeric reversed-phase sorbent (Oasis HLB). The method was validated for the determination of desethylamiodarone with respect to specificity, linearity, precision, accuracy, recovery, limit of quantitation and stability. Amiodarone N-deethylation activity from low to high substrate concentrations using human liver microsomes was precisely determined without a concentration step. This method is applicable to the study in vitro of the metabolism of amiodarone.
Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option.
To investigate whether amiodarone induces apoptosis in cells of the L-132 human lung epithelial cell line, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, 4,6-diamidino-2-phenylindole staining, DNA fragmentation assay, reverse transcription-polymerase chain reaction, and casapse-3 enzyme assay were performed. Through morphological and biochemical analyses, it was demonstrated that L-132 cells treated with amiodarone exhibit several features of apoptosis. In addition, it was shown that amiodarone increases the mRNA levels of bax and caspase-3. Based on the results, amiodarone appears to activate specific intracellular death-related pathways, including possibly the bax-dependent caspase-3 activation pathway, and thus induce apoptosis in human lung epithelial cells.