BackgroundThere are four fat fads(FP) on the surface of the atria, in which the auto-nomic ganglionated plexi(GP) are embedded . The bilateral vagal nerves converge on these four fat pads before they innervate the atria. There are many basic and clinical evidence that activity of the autonomic nerve has great effect on the onset and maintaince of atrial fibrillation ( Af) . It was previously demonstrated that electrical stimulation of autonomic ganglia at the pulmonary vein ( PV) - atrial junction could convert PV ectopic beats into atrial fibrillation. Vagal stimulation can shorten the atrial effective refractory period (AERP) and impulse wave length , increase the AERP variation. Hai'ssagurre reported that the paroxysmal Af was initiated by the ectopic beat from the pulmonary vein and the ablation of these ectopic beats can prevent the recurrence of Af. We make the hypothesis that a hyperactive state of the GP, located at the base of each of the PVs, can induce focal firing from the PV and also provide the substrate for that focal ectopic beat to be converted into Af, which is very useful for the establishment of Af animal model.ProtocolTwenty male mongrel dogs were anesthetized with Na - pentobarbital (30mg/kg) administered intravenously. A 50 - 100mg amount was injected in order to maintain the anesthesia if necessary. These dogs were divided into 2 groups randomly (10 for Ach group and 10 for carbachol group). The right lateral thoracotomy and pericardiotomy were made to expose the fat pad ( FP) between right pulmonary vein (PV) and right atrium ( RA ). A needle was insertedin the fat pad for the injection of acylcholine and carbachol. Several octapolar e-lectrode catheters were attached by sutures to contact the right superior pulmonary vein(RSPV) and right atrium, left atrium. The measurements were made of refractory periods using programmed premature stimulation in the right atrium both before and after the administration (Ach group: lOmM acylcholine 0. 5ml; carbachol group: 10mM carbachol 0. 5ml) . The longest coupling period during which the block occurred was recorded as the effective refractory period. Programmed premature stimulations were delivered at 2x, 4x, lOx, 20x threshold at coupling intervals starting at 150 msec down to refractoriness and the ERP was recorded at each level. If the Af occurred, the following data were recorded 1: the difference between the longest and shortest coupling period during which Af occurred. (the difference was used for the measurement of the Af inducibility, recorded as WOV). 2; the longest duration of Af and the f wave frequency. All values are expressed as mean å¤ SD. Statistical analysis was performed using coupling t test for comparison of ERP, WOV, the longest duration of Af, f wave frequency before and after administration of Ach or carbachol. A p value of <0.05 was considered significant.ResultsThe major results from the experiment were: the shortened atrial ERP, the widened WOV , the prolonged duration of Af and the increased p wave frequency were observed obviously after the administration of Ach and carbachol. In the Ach group: the ERPs in the RA were 116.3 17.8ms, 102.3 22.7ms, 91.7 21.9ms, 80 23ms respectively when the stimulations were delivered at 2x, 4x, 10x, 20x threshold without the Ach administration. After Ach administra0 tion, the atrial ERPs were shortened to 103. 8 26. lms(p >0.05) ,94.7 21. 9ms(p<0. 05),74. 3 20ms(p<0. 01),65. 5 17. 8ms(p <0. 05). Before the Ach injection, all induced Afs were short paroxysmal Afs with the duration of 9.7 6sec, the average Af cycle length of 122 9ms; and after the injection, the duration of Af was prolonged to 596.7 281sec(p <0.01) ; the average Af cycle length was shortened to 76 32ms (p <0. 05). In the carbachol group,before administration the duration of Af was 10.4 8sec, and the average Af cycle length was 120 8ms;after the administration, an Af with very high frequency of f wave and long duration was induced. The duration of Af was prolonged to 2364 1169sec ( p < 0. 01) ,... |