目的 探讨优先消融心房无序电活动区域治疗某些类型心房颤动（房颤）的可行性。方法 实验犬17只，消融组l2只，假性消融组5只。房颤持续过程中行激动标测，发现如下激动特征之一的部位视作优先消融艳区（简称优先区）：①电激动无序性特征最为显著的部位；②平均FF间期（AFI199）最短的部位；③最早出现F波（可重复3次以上）且超前其它导联20ms以上的部位。消融终点为用术前相同诱发方法不能诱发房颤或房颤持续时间不超过lmin。结果标测发现消融组12只犬有10只存在优先区，优先区相对局限的7只犬实施单一线径消融（单线组）；优先区较为广泛的3只犬、未能保测到优先区的2只犬以及单线组未能达到消融终点的2只犬实施多线消融（多线组）。具有优先区的10只犬中8只（80%）术后即刻达到消融终点，单、多线组各4只（4/7 vs 4/7）。未标测到优先区的2只犬均未达消融终点。达到消融终点的4只犬中，3只于术后14天及处死前均未诱发出持续性房颤。假性消融对房颤的发生和持续无明显影响。结论（1）心内膜标测指导下优先消融心房无序电活动区有望在不降低成功率的同时减少心房肌损伤；（2）右房RFCA可能是根治某些类型房颤的有效方法之一。

为研究蝎毒素BmkTXKβ对家兔心房肌细胞瞬间外向钾电流（Ito）的影响，采用全细胞膜片钳技术记录应用BmkTXKβ前后的Ito电流。结果显示BmkTXKβ（1μmol/L）使心房肌细胞Ito（刺激电压为+50mV）从（13.63±0.87）pA/pF减少到（7198±0178）pA/ pF，抑制率为4114%（n=16，P<0.001）。冲洗后，Ito部分恢复至（11.18±0.82）pA/pF（n=6，P<0101，与给药后比较）。在0.01～100μmol/L范围内BmkTXKβ呈浓度依赖性地抑制Ito，IC50的均值为0.95μmol/L（n=10，P<0.01），但无频率依赖性（n=6，P>0.05）。1μmol/L的BmkTXKβ可使Ito通道的失活动力学曲线明显左移，V1/2分别为（-23.6±2.7）mV和（-35.3±3.6）mV（n=8，P<0.05），曲线斜率基本不变。同时可使Ito通道的恢复过程明显减慢，恢复曲线右移，τ值从（51.2±8.5）ms延长至（93.5 ±13.4）ms（n=9，P<0.01），但不影响其激活过程。据此推断BmkTXKβ对家兔心房肌细胞Ito具有显著的抑制作用，主要作用于失活过程，延长该通道的恢复时间。

目的 观察兔上腔静脉和下腔静脉的心肌细胞组织结构，探讨其在生理状态和心律失常中的作用。方法 选取健康的新西兰大白兔15只，取出心脏，福尔马林溶液固定。取上腔静脉、下腔静脉, 石蜡包埋, 分别作纵向和横向连续切片，HE染色。结果 发现腔静脉壁内有心肌细胞的延伸，其内穿插有平滑肌细胞。心肌分布在前壁较侧壁、后壁厚，上腔静脉壁内心肌比下腔静脉延伸长且数目多。心肌在上腔静脉壁内呈纵行、环行或斜行排列，在下腔静脉壁内呈环行或斜行排列，这些心肌与心房肌形态相似。结论 兔上腔静脉和下腔静脉壁内有心肌细胞存在, 在心房收缩时可能起到“阀门”作用，是发生心律失常的结构基础，上腔静脉和下腔静脉壁内心肌排列不同可能使两者之间存在电生理差异。

目的 探讨房室结不同层面与细胞传导有关的细胞超微形态及连接方式有无差异。方法 用家兔含房室结组织块半薄及超薄切片，光镜及透射电镜观察。结果 光镜下家兔房室结由三层细胞组成，上层细胞细长，排列不整齐；中层细胞短小，排列紊乱，下层细胞粗长，排列整齐。透射电镜下，下层细胞线粒体和肌丝丰富，可见不完整的肌节，相邻细胞间有片状润盘样结构及缝隙连接，靠近心室肌的下层细胞甚至可见较完整的肌节；中层细胞线粒体和肌丝均较少，无肌节，细胞间特化的连接复合体及润盘样结构罕见，其中可见圆形细胞，其核较大，胞桨肌丝极少，胞内空泡样结构较多；上层细胞的线粒体和肌丝较下层细胞少，肌丝排列紊乱，肌节少见，细胞间特化连接复合体较少，偶见润盘样结构。结论 家兔房室结不同层面细胞超微形态及其连接方式有明显差异。下层细胞束可能传导较快，上层细胞可能传导较慢，中层细胞可能传导最慢。

本文报道5例不同类裂复杂寇状动脉病变腔内成形术。对于位于血管分叉处的病变，采用了双导丝技术，对于引起急性心肌梗塞的高度狭窄血管采用自灌注球囊扩张，对于完金闭ZS且病变较长的血管，采用较硬的标准直头导引钢丝导入尔后逐段扩张的办法；对于术中出现的内膜剥离，采用了自灌注球褒导管行长时间低压修补。术后血管再通，残余狭窄为0～10%。因此，认为只要针对不同情况，采用不同方法，PTCA成功率可望提高。

目的探讨肺静脉内不同温度射频消融与肺静脉狭窄的关系。方法健康杂种犬30只，分成3组，经房间隔途径将温控电极导管置入肺静脉内进行消融，各组能量分别为50℃×60s，60℃×60s，70℃×60s。消融前、后均行选择性肺静脉造影，术后留养3个月，重复肺静脉造影后，处死，取心肌、肺静脉及肺组织作病理检查。结果50℃组1只犬在行房间隔穿刺时因心包填塞死亡，其余均顺利完成试验。共在肺静脉内72处行点状消融，50℃组、60℃组、70℃组分别为20、26、26处。右上肺静脉、右下肺静脉、左上肺静脉和左下肺静脉分别为13、9、27、23处。50℃组肺静脉于消融后即刻及3个月后均未见狭窄。60℃组消融后即刻发现5处狭窄，3个月后仅遗留1处狭窄。70℃组消融后即刻有12处狭窄，3个月后复查仍有7处狭窄，发生率均明显高于50℃组及60℃组。结论肺静脉内射频消融温度为50℃及印℃时较为安全，70℃时肺静脉狭窄的发生率明显上升，提示消融温度应控制在60℃以减少肺静脉狭窄的形成。

Objective To identify predictors of left atrial appendage stunning after the use of electrical cardioversion to re store sinus rhythm in patient s with non-valvular atrial fibrillation. Methods A total of 68 consecutive patients (45men, 23 women, 60.5

Recent studies have shown that rapid atrial activation causes atrial electrical remodeling (AER), hich recovers quickly following withdrawal of stimulation. The underlying mechanisms, however, are incompletely understood. The purpose of the present study, therefore, was to characterize the effect of the vagus on AER as well as define possible mechanisms of the phenomenon. Eight dogs were used in the study for 3 consecutive protocols. In the first, the dogs were subjected to atrial pacing at 800 ppm for 7 hours. Every hour, pacing was interrupted for a short time and atrial effective refractory period (AERP) was measured at 6 sites. The rapid atrial pacing was then discontinued and the electrophysiological study was repeated every hour for another 7 hours. Timedomain parameters of heart rate variability (HRV) were also computed 1 hour before pacing as well as each of 7 hours after the rapid atrial pacing protocol. The second program was performed two weeks after the first; 0.04mg/kg of atropine was administered intravenously 30min before pacing, and then 0.007mg/kg was added at each hour. Parameters of HRV were not evaluated. Finally, the 8 dogs were subjected to the third protocol 2 weeks after completion of the second; 0.2mg/kg of propranolol was given intravenously 30min before pacing, and 0.04mg/kg was added at each hour. The dispersion of AERP (dAERP) was calculated as, maximum AERP minus minimum AERP. There was a prompt decrease in AERP as the result of pacing (P＜.05), but dAERP did not change significantly. The AERP recovered quickly, and dAERP increased from 21±5.3ms to 40±7.4ms (P＜.05) after cessation of pacing. At the same time, the parameters of HRV increased (P＜.05) after cessation of pacing. The AERP increased from 128±12 ms to 135±12ms and from 127±12ms to 142±14ms (P＜.05) after vagal and autonomic blockade. However, AERP decreased during pacing (P＜.05) with vagal or autonomic blockade, but dAERP did not change significantly during or after pacing. These results suggest that vagal and autonomic blockade can not prevent AER, but a high vagal tone is associated with a high dAERP during recovery from AER, indicating that the vagus and sympathetic have a synergistic effect on the refractory period.

Objective To investigate the effect and mechanism of arsenic trioxide (As2O3) on the prevention of re steno sis after vascular injury. Methods Apoptosis induction of As2O3 on cultured rabbit vascular smooth muscle cells (VSMCs) in vitro was observed1 Thirty-two New Zealand white rabbits were randomly divided into 2-and 4-wk study groups, and their controls1 10%As2O3 at 215mg•Kg-1•d-1 or 0.9% sodium chloride was intraperitoneally infused for 3 days before left common carotid arteries were denudated with a balloon1 After denudation 2-and 4-wk animals were sacrificed for morphometry and immunohistochemical studies on carotid arteries, and for histopathology on liver and kidney. Results It was shown via cellular morphology and DNA fragments in electrophoresis that promotion of As2O3 on cultured vascular smooth muscle cell apoptosis was dependent upon its concentration and duration1 Compared with the control animals, the mean vascular intimal proliferation area s were reduced in 2-wk study animals (P<0.05) and no difference was shown in 4-wk (P>0.05), while the mean vascular luminal areas were all enlarged in both study groups (all P<0.05) 1 The downregulated bcl-2 expression (all P<0.05 in 2-and 4-wk) and the upregulatedbax expression (P<0.01 in 2-wk; P<0.05 in 4-wk) were detected by immunohistochemistry, in comparison with control group s1 Gene bcl-2 and baxprotein expression were consistent with the suppression of intimal proliferation and the enlargement of luminal areas in corresponding sections. Conclusion As2O3 induce s apoptosis of VSMCs and inhibit s experimental re steno sis effectively after artery injury, viadownregulation of bcl-2 and upregulation of baxexpre ssion.