This paper discusses the law of atrial electrical activity propagation (the timing of signal and the conduction velocity) under the sinus rhythm before and after AF caused by high-frequency electrical stimulation. The paper analyzes how different doses of acetylcholine affect the conductivity of the atrial cells of dogs. This result can also help the diagnoses and treatment of human's AF.
Acetylcholine ; pharmacology ; Animals ; Dogs ; Epicardial Mapping ; Heart Atria ; cytology ; drug effects ; physiopathology ; Mechanotransduction, Cellular

BACKGROUNDRenin-angiotensin-aldosterone system has been demonstrated to be associated with both congestive heart failure (CHF) and atrial fibrillation (AF). This study investigated the effects of spironolactone, a kind of aldosterone antagonist, on atrial electrical remodeling and fibrosis in CHF dogs induced by chronic rapid ventricular pacing.

METHODSTwenty one dogs were randomly divided into sham-operated group, control group, and spironolactone group. In control group and spironolactone group, dogs were ventricular paced at 220 beats per minute for 6 weeks. Additionally, spironolactone at 15 mg x kg(-1) x d(-1) was given to dogs 1 week before rapid ventricular pacing until pacing stopped. Transthoracic and transoesophageal echocardiographic examinations were performed to detect structural and functional changes of the atrium. Swan2 Ganz floating catheters were used to measure hemadynamics variances. Atrial effective refractory period (AERP), AERP dispersion (AERPd), intra- and inter-atrium conduction time (CT) and intra-atrium conduction velocity (CV) were determined. The inducibility and duration of AF were also measured in all groups. Finally, atrial fibrosis was quantified with Masson staining.

RESULTSAERP did not change significantly after dogs were ventricular paced for 6 weeks. However, AERPd, intra- and inter-atrium CT increased significantly, and CV decreased apparently, which was negatively correlated to the atrial fibrosis (r = -0.74, P < 0.05). Simultaneously, left atriums were enlarged and cardiac hemadynamics worsened in pacing dogs. Although spironolactone could not affect cardiac hemadynamics effectively, it can obviously improve left atrial ejection fraction (P < 0.05). Spironolactone treatment did not alter AERP duration, but this medicine dramatically decreased AERPd (P < 0.05), shortened intra- and inter-atrium conduction time (P < 0.05), and increased atrium CV. Moreover, spironolactone decreased the inducibility and duration of AF (P < 0.05), as well as atrial fibrosis (P < 0.01) induced by chronic rapid ventricular pacing.

CONCLUSIONSpironolactone contributes to AF prevention in congestive heart failure dogs induced by chronic rapid ventricular pacing, which is related to atrial fibrosis reduction and independent of hemadynamics.

Animals ; Atrial Fibrillation ; prevention & control ; Cardiac Volume ; Collagen ; analysis ; Dogs ; Heart Atria ; drug effects ; pathology ; physiopathology ; Heart Failure ; drug therapy ; pathology ; physiopathology ; Hemodynamics ; drug effects ; Spironolactone ; therapeutic use

Treatment of rabbits with thyroxine 1 mg/kg daily for three to six days produced a hyperthyroid state as evidenced by increase in the heart rate and PBI. The hyperthyroid animals exhibited a significant shortening of the atrial refractory period. Beta adrenergic receptor blocking agents, propranolol (l0(-6)M pronethalol (5 X 10(-5)M) or MJ-1999 (5 X 10(-4)M), completely blocked the shortening of the atrial refractory period produced by the treatment with thyroxin, and with norepinephrine. Consequently, the shortening of the atrial refractory period of rabbits treated with thyroxin appears to bs mediated through stimulation of the beta adrenergic receptor in the heart. From these results, it may be concluded that the stimulation of the beta adrenergic receptor plays an important role in the alteration of cardiac function found in hyperthyroidism, and that the beta adrenergic blocking agents may be useful in treatment of the cardiac complications of hyperthyroidism.
Adrenergic beta-Antagonists/pharmacology ; Animals ; Female ; Heart Atria/*drug effects/physiopathology ; Hyperthyroidism/chemically induced/*physiopathology ; Male ; Rabbits ; Sympatholytics/*pharmacology ; Thyroxine