Sustained Left Ansae Subclaviae Stimulation for a 5-hour Period Inhibits Cesium-induced Ventricular Arrhythmogenesis in Rabbits

• Published in: Journal of molecular and cellular cardiology Vol. 30; no. 11; pp. 2237 - 2245
• Main Authors: Iwao, Tetsu, Ito, Morio, Takahashi, Naohiko, Saikawa, Tetsunori, Sakata, Toshiie
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.11.1998
• Subjects: Action Potentials; Animals; Autonomic Nervous System - physiopathology; Cesium; Early afterdepolarizations; Electric Stimulation; Left ansae subclaviae, Desensitization; Male; Rabbits; Time Factors; Ventricular arrhythmias; Ventricular Fibrillation - chemically induced; Ventricular Fibrillation - physiopathology; Ventricular arrhythmias; Early afterdepolarizations; Left ansae subclaviae, Desensitization
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1006/jmcc.1998.0784

The acute stimulation of the left ansae subclaviae (LAS) augments cesium chloride (Cs)- induced early afterdepolarizations (EADs) and ventricular arrhythmias. However, the effect of sustained cardiac sympathetic nerve stimulation on Cs-induced arrhythmogenesis remains to be elucidated. Three protocols were used. In protocol A, seven rabbits received continuous LAS stimulation for 5 h (study group), and were then given bolus injections of Cs at 5-min intervals (initial dose 1.5 mmol/kg, followed by repetitive doses 1 mmol/kg). Another eight rabbits received the same dose of Cs after a 5-h observation period without LAS stimulation (control group). The effects of 2 h of LAS stimulation were also assessed in five rabbits of each group. In protocol B, a bolus injection of Cs (1 mmol/kg) was administered during atrial pacing (cycle length: 250 ms) after a 5-h period with (study group, n=5) or without (control group, n=5) LAS stimulation, and the amplitude of Cs-induced EADs was measured. In protocol C, a bolus injection of isoproterenol (0.05 mg/kg) was given after a 5-h period with (study group, n=5) or without (control group, n=5) LAS stimulation to assess the sensitivity to β-adrenergic stimulation. In protocol A, the cumulative doses of Cs required for the induction of ventricular tachycardia (VT) and fibrillation (VF) were significantly greater in the study group than in the control group (4.4±0.1v2.8±0.3 mmol/kg for VT,P<0.05; 5.8±0.3v4.1±0.4 mmol/kg for VF,P<0.05). However, 2 h of LAS stimulation did not influence the cumulative doses of Cs required for the induction of VT and VF. In protocol B, the amplitude of Cs-induced EADs was significantly lower in the study group than in the control group. In protocol C, the increase in rate-pressure product by isoproterenol was significantly less in study than in control groups (3492±612v6504±829,P<0.05). These results suggest that sustained LAS stimulation exerts a protective effect against Cs-induced arrhythmogenesis in the rabbit heart, which may be partially explained by desensitization to the β-adrenergic stimulation.