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作 者:刘丽娟[1] 郑东诞[1] 李树彬[1] 潘德茂[2] 王强[1] 张玮[1] 高修仁[1]
机构地区:[1]中山大学附属第一医院黄埔医院心内科,广东广州510700 [2]中山大学附属第一医院黄埔医院急诊科,广东广州510700
出 处:《中山大学学报(医学科学版)》2009年第6期723-727,共5页Journal of Sun Yat-Sen University:Medical Sciences
基 金:广东省自然科学基金(06021342)
摘 要:【目的】建立兔左心房高频起搏心房颤动(AF)动物模型,并进行电生理特性研究。【方法】16只健康新西兰兔随机分为:对照组和起搏组两组。两组均在左心房外膜缝合固定一起搏电极,起搏组以1 000 min-1的频率进行高频起搏;对照组不起搏。采用心外膜程序起搏技术测定心房肌的电生理特性。【结果】①起搏组3周后房颤诱发率87.5%,与对照组比较统计学有差异(P<0.01),其中持续性AF 3/8例;②起搏组经心外膜程序起搏,在高频刺激1 h、1周、3周后心房有效不应期(ERPA)均缩短,与对照组比较有显著统计学差异(P<0.01);③频率适应性方面,起搏组表现为频率适应不良,在3周时最明显,与对照组比有统计学意义(P<0.05);④起搏组3周后P波时限比对照组延长,但两者比较无统计学差别(P﹥0.05);⑤起搏组1 h至3周,ERPA缩短、相对不应期(RRPA)延长,与对照组比较统计学有差异(P<0.01)、早搏刺激的心房间传导时间(IACD)延长,与对照组比较统计学上无差别(P﹥0.05)。【结论】兔左心房高频起搏能有效建立慢性AF动物模型;主要电生理改变有:ERPA缩短、频率适应不良、P波时限延长。[ Objective ] To establish the model of atrial fibrillation (AF) by high-frequency pacing and explore the atrial electropbysiological characters in rabbits. [ Methods] Sixteen rabbits were randomly divided into pacing group and control group. A pacing electricity pole was fixed under the adventitia of left atrium in all experiment animals. The pacing group was stimulated in a frequency of 1 000 bpm and the control group underwent without pacing stimulation. The technique of programmed stimulating was used to measure eleetrophysiologieal indexes of atrial in the groups. [Results] (1)87.5% of the animals in pacing group suffered from AF under 3 weeks high frequency pacing, which was significantly higher than that of control group (P 〈 0.0t). Permanent AF was found in 3 out of 8 cases. (2)Atrial effective refractory period (ERPA) was statistically shortened in the pacing group comparing to the control group after 1 hour, 1 week and 3 weeks stimulating (P 〈 0.01, respectively). (3)The pacing group showed a significantly poor performance of frequency adaptability comparing to the control group after 3 weeks stimulating (P 〈 0.05). (4)The P-wave interval was longer in pacing group than that of the control group after 3 weeks pacing, but no significantly different was found (P 〉 0.05). (5)ERPA was obviously shortened and RRPA was significantly prolonged in the pacing group after 1 hour to 3 weeks stimulating (P 〈 0.01 ), but there was no difference significantly in inter-atrial conduction defect (IACD) between the two groups (P 〉 0.05). [ Conclusions] The animal model of chronic atrial fibrillation could be successfully established by high frequency pacing of atrial in rabbits. The apparent electrophysiological changes of this model include: the frequency inadaptability, shortening of ERPA and extension of P-wave interval.
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