| Objective: Sinus node dysfunction(SND) is one of the most frequently encountered arrhythmia in clinical practice.Patients with SND offent occure atrial fibrillation(Af), atrial fllute(Af), atrial premature beat (APB) , atrial tachycardia(AT) et al.At present,the domestic and foreign research workers make a lot of scientific researches on the mechanisms that Af maintains.But they do not make scientific researches on mechanisms that rabbits of SND develops atrial fibrillation(Af). Therefor,knowledge of the electrophysiological subtrates of SND with Atrial arrhythmia are still unsatisfactory. The aim of the study is to establish a model of rabbit with SND for the study of electrophysiologic characteristics of the atrium and to investigate the electrophysiologic mechanisms of rabbites with SND to develop atrial fibrillation(Af) and atrial tachycarsia(AT).Methods:The model of rabbits with SND was established in 30 rabbits using radiofrequence ablation method(ablated the sinus node region of the rabbits).We study electrophysiologic characteristics of the atrium of rabbits before and after SND.Two bipolar silver wire electrodes were made by ourselve and recored epicardium electrograms . The proximal electrodes of the two bipolar silver wire electrodes were placed in the high right atrium and the right atrial electrogrames were recorded by the other of the bipolar silver wire electrodes,whereas the implulse was delivered by the other of the bipolar silverwire electrodes. The stimulation was performed with square impuises,0.3 ms duration and twice threshoid,deliverd by programmable stimulator.The recording were filtered at 30-100Hz using BL-410 biological signal collection and amplification system.At a drive cycl length of 200 ms,atrail effective refractory periods(ERP),the duration of atrial activation (A\ and A2) and atrial latency (S1-A1 and S2-A2) were measured on the right atrium.Wavelength index(WLI) was calculatedf( WLI=ERP/A2).Results: The rabbits with SND ocured electrophiologic dchanging. Our study showed that A1 , A2 width were notable lentheningin 2h , 4h, 6h and 7d after SND compared with before SNDCA,: 65, 47 + 5. 30ms VS 79. 93+ 5. 69ms , 84. 37 + 5. 93ms, 85. 53+ 4. 13ms , 85. 93 + 3. 66ms; A2 65. 33+ 5. 39ms VS 79.60+ 6.42ms, 85.13+ 6.30ms , 85. 73 + 5. 72ms , 86.87 + 5.50 ,P 0. 001) , but there were not difference in Ih compared before SND (A,: 65.47+ 5.30ms VS 66. 53 + 4. 87ms P>0. 05 ; A2 65.33+ 5.39ms VS 66.40 6. 18ms). WLI was significantly shortening in 1h ,2h , 4h, 6h and 7d after SND compared before SND(1.86+ 0.23 VS 1.80 + 0.25, 1.42 + 0.18 , 1. 20 + 0. 15, 1. 18 + 0. 15, 1. 17 + 0. 18, P < 0.001). ERP was significantly shortening in 2h , 4h, 6h and 7d after SND compared with before SND(120. 33+ 9. 28ms VS 112. 33 + 10. 06ms, 101. 67+ 9. 13ms, 101.33 + 9.00ms ,100. 67 + 9. 44ms, P< 0. 001), but there were not difference (120. 33 + 9. 28ms VS 118. 33 10. 85ms, P>0. 05) in 1 h compared before SND. In contrast, We did not find significant statistical differences regarding S1-A1 and S2-A2 beforeand after SND .Conclusion: In our study ,the rabbits with SND showed remarkable prolonged conduction slowing abnormalities and a lower latent vulnerability index(WLT) and shorter ERP than rabbits of before SND . Reentry is more likely when refractoriness and wavelength is short ,and conduction velocity is slow .These chang is nescessary to develop Af and AF.Therefor, atrial ERP and WLI shortening , A1 , A2 width lengthening ,at least in part, explained the tendency of rabbits with SND to develop Af, AT as a part of its natural history .Atrial electrophysiologic disturbances was an important mechanisms of rabbits with SND to develop Af and AT during natural course..On the otherhand,The study alsi showed the brady arrhythmia also induced atrial electrical remodeling .Therefore ,clinic doctors treat the patientswith sick sinus syndrome as posibble as early,so that advoid that atrial electrical reodeling induces atrial arrhythmia.
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