Effect of Amiodarone on Rat’s Isolated Tracheal Smooth Muscle

Background: Amiodarone is considered the most effective agent to treat supraventricular and ventricular arrhythmia and prevent atrial fibrillation. The blockade of the potassium channel to elongate the refractory period of the myocardium is widely known. Its peculiar pharmacokinetics and toxicity cause some problems to clinicians. The effect on the myocardium, thyroid gland, and lung has been well explored. However, the effect of amiodarone on the tracheal smooth muscle is not well investigated. Methods: We studied the effectiveness of amiodarone on rat's isolated tracheal smooth muscle as our preparation. The following assessment of amiodarone were performed: (1) effect on the tracheal smooth muscle resting tension; (2) effect on contraction induced by 10-6 M methacholine as a parasympathetic mimetic; (3) effect on electrically induced tracheal smooth muscle contractions. Results: The addition of amiodarone at a low dose made no difference to the resting tension of trachea smooth muscle. At 10-4 M of amiodarone, temporary tracheal smooth muscle contraction was detected. When the concentration of amiodarone increased to 3 x 10-4 M, the tracheal smooth muscle relaxed following the brief contraction. For the electrical stimulation and 10-6 M methacholine-induced contraction tests, the amiodarone elicited no scientific change on trachea smooth muscle contraction with increasing concentration. Conclusion: In the animal model, amiodarone doesn't change physiologic mechanism of trachea smooth muscle at therapeutic concentration.