Auricular Fibrillation Induced and Maintained in Animals by Acetylcholine or Vagal Stimulation

Abstract

With the technical assistance of Robert D. Campo Animals pretreated with appropriate closes of anticholinesterase agents develop auricular flutter and fibrillation following injection of acetylcholine or vagal stimulation. Depression of normal sinoauricular nodal function facilitates induction of fibrillation. During fibrillation, additional injections of acetylcholine, or vagal stimulation, increase the rate of fibrillation. Atropine in small closes reverts the fibrillation to normal sinus rhythm.T HE production of auricular fibrillation by acetylcholine is well recognized. 1This type of fibrillation is not constant in occurrence and is transient. The present report describes a method for consistently producing auricular fibrillation of extended duration by the use of acetylcholine or vagal stimulation in animals treated with anticholinesterase agents. The report describes a means of regulating the rate of fibrillation, the role of normal sino-auricular node function in the initiation of the fibrillating state, and the abolition of fibrillation by atropine. METHODSThirty-four dogs, four goats and six monkeys were used. Three types of experiments were conducted. The first type used animals anesthetized with chloralose (50 mg./Kg.) in which conventional electrocardiograms were obtained. The second type of experiment used the anesthetized animal under artificial, positive pressure respiration with the chest open ut the sternal midline, and in which action potentials were obtained from electrodes applied directly to the myocardium. The third type of experiment was conducted on unanesthetized animals with normal respiration in which direct cardiac electrodes had been previously implanted using thiopental anesthesia.The preparation of the animals for the first and second type of experiments is a well established procedure. Our method for the preparation of animals for the third type of experiment is as follows:From the Physiology Division, Chemical Corps Medical Laboratories, Army Chemical Center, Maryland.Received for publication February 21, 1955.The animal was anesthetized with sodium thiopental (20 to 25 mg. per Kg.). Suitable incisions were made for insertion of a femoral vein polyethylene cannula and for a tracheal cannula. Both vagi were exposed in the neck. The right vagus was sectioned and shielded electrodes were fixed to the distal stump. The anterior two-thirds of the fourth left rib were exposed and subperiosteally resected. The parietal pleura was incised and positive pressure respiration was started. The pericardium was incised parallel and just anterior to the left phrenic nerve exposing the left auricle and half of the left ventricle. Two spring steel, shielded electrodes were clipped about 5 mm. apart to the upper mid surface of the left auricle. Two additional electrodes were clipped about 5 mm. apart to the mid portion of the left ventricle. The pericardium and pleura were then closed around the lead-in wires with sutures. The lungs were re-expanded and the skin incision closed. Artificial respira...

RR Interval Dynamics Before Atrial Fibrillation in Patients After Coronary Artery Bypass Graft Surgery

“…[11][12][13][14]38 Vagal modulation manifests as rapid oscillation in heart rate, especially as quantified by pNN50 and rMSDD. 29 Thus, the high RR interval variations observed in the high RR interval variability group are consistent with heightened vagal tone, perhaps reflex in origin, as a result of sustained perioperative sympathetic activation or accentuated antagonism.…”

“…8 -10 Autonomic nervous system perturbations may enhance vulnerability to atrial arrhythmias. 5,[11][12][13][14] Analysis of HRV has been used to probe autonomic mechanisms of ventricular tachycardia and fibrillation and to identify patients at risk for ventricular arrhythmias. [15][16][17][18][19][20] Preliminary investigations in primarily nonsurgical populations have suggested that risk for AF may be identified with measurement of HRV, but whether the onset of postoperative AF is preceded by autonomic dysfunction is not clear.…”

Direction-dependent conduction abnormalities in a canine model of atrial fibrillation due to chronic atrial dilatation

“…Various animal models of AF have been developed to study AF substrate. Parasympathetic stimulation (either with direct vagal nerve stimulation or circulating cholinergic agents) results in shortening of atrial refractoriness and sustained AF (10,16). Prolonged rapid atrial pacing (RAP) leads to shortening of refractoriness and sustained AF (18,30).…”

Vagal Stimulation Prior to Atrial Rapid Pacing Protects the Atrium From Electrical Remodeling in Anesthetized Dogs.

“…6,19,20 Yue et al showed that atrial rapid pacing reduced transient outward currents (Ito) and L-type Ca 2+ currents (ICa), and that the reduced ICa abbreviated APD and decreased accommodation to changes in rate. 21 It is well known that vagal tone is one of the most important factors in the induction of AF [9][10][11][12][13][14][15] and this induction of AF by VS might be caused by nonuniform shortening of the atrial ERP; 9-11 it may also increase ERP dispersion. 11 Cardiac vagal tone declines with age, 22,23 the smaller tachycardiac response to isometric exercise in older humans is associated with an inability to decrease cardiac vagal tone below an already reduced baseline level.…”