Vagally Induced Block and Delayed Conduction as a Mechanism for Circus Movement Tachycardia in Frog Atria

• Published in: Circulation research Vol. 64; no. 2; pp. 213 - 226
• Main Authors: Rosenshtraukh, Leonid V, Zaitsev, Alexey V, Fast, Vladimir G, Pertsov, Arcady M, Krinsky, Valentin I
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01.02.1989; Lippincott
• Subjects: Animals; Biological and medical sciences; Biomechanical Phenomena; Cardiac dysrhythmias; Cardiology. Vascular system; Electric Stimulation; Electrophysiology; Heart; Heart Atria; Heart Block - etiology; Heart Conduction System - physiopathology; In Vitro Techniques; Medical sciences; Rana temporaria; Tachycardia - physiopathology; Time Factors; Vagus Nerve - physiology; Cartography; Atrium; Arrhythmia; Amphibia; Cardiovascular disease; Stimulation; Salientia; Activation; In vitro; Electrodiagnosis; Vertebrata; Experimental disease; Vagus nerve; Paroxysmal atrial tachycardia; Rana temporaria
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.64.2.213

Episodes of tachycardia induced by strong vagal stimulation in spontaneously beating isolated atria of frog (Rana temporaria) were studied with multielectrode mapping technique. These episodes were inducible in 19 of 39 preparations. The arrhythmia started several seconds after cessation of vagal stimulation strong enough to cause sinus arrest, without electrical stimulation of the myocardium. The arrhythmia consisted of two to 20 beats (6±4, mean±SD, n=42) with a cycle length of 100-500 msec. Recording from 32 sites with spatial resolution of 1-2 mm showed that the arrhythmia was due to intra-atrial circus movement. The estimated perimeter of the reentrant circuit ranged from 6 to 20 mm. In circuits of the minimal size, the average conduction velocity along the circuit was as low as 2-3 cm/sec. Paroxysms of the tachycardia were always preceded by vagally induced nonuniform depression of conduction, with some areas of atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner, their unblocking being significantly (p<0.05) delayed after inhibition of tissue cholinesterase by proserine. The reentrant tachycardia was initiated when a sinus impulse arrived during certain phase of the unblocking. Unlike the well-known mechanism of reentrant excitation, which is based on inhomogeneous refractoriness and critically timed extrabeat(s), the circus movement in our model depended on vagally induced conduction block and could be launched by a single sinus impulse.