胺碘酮治疗心房颤动

目的：研究胺碘酮治疗心房颤动的疗效。方法：用胺碘酮治疗心房颤动患者68例（阵发性心房颤动40例,持续性心房颤动28例）。结果：连续用药治疗6个月显示治疗有效率分别为92.5%、75%。治疗12个月有效率分别为85.3%、68%。结论：胺碘酮治疗心房颤动安全有效,副作用小,可作为首选药。     

胺碘酮治疗心房颤动22例

心房颤动(房颤)是一种常见的心律失常,其发生率随年龄的增长而增加。它本身通常不是一种致命性的心律失常,但在部分患者中可使病死率增高。房颤可根据持续时间、临床表现的不同而分为阵发性、持续性和永久性3型;持续性心房颤动常不能自行恢复窦性心律,可发展为永久性心房颤动。2001年3月~2005年3月我们应用胺碘酮治疗心房颤动取得了显著效果,现报告如下。1临床资料1.1一般资料本组22例心房颤动患者,男13例,女9例;年龄42~71岁,平均52岁。经体格检查、心电图、动态心电图确诊为心房颤动,入选标准:阵发性房颤15例,每周至少发作2次,每次至少持续…     

胺碘酮治疗心房颤动的临床疗效

心房颤动在基层医院非紧急情况下多数仍首选药物复律 ,但临床方法及疗效有待探讨。本文报告胺碘酮治疗非瓣膜病心房颤动的疗效和安全性。1　资料与方法1.1　病例选择　 4 9例完全排除心脏瓣膜病 ,为非瓣膜病心房颤动患者 ,男 31例 ,女 18例 ;年龄 4 2～ 76岁 ,平均 (6 0 .5±7.8)岁 ;房颤病程 0 .5～ 16年 ,左房直径 30～ 5 5ｍｍ ,平均(36 .4± 6 )ｍｍ。入选标准 :阵发性房颤 4 2例 ,每周至少发作2次 ,每次至少持续 30分钟 ,或每日发作数次 ,每次持续数分钟以上 ;持续性房颤 7例 ,房颤至少 1个月 ,但不超过 1年。1.2　方法　胺碘酮负荷量 …     

胺碘酮治疗阵发性心房颤动40例疗效观察

我院自2003年6月～2004年6月以来，采用口服胺碘酮治疗阵发性心房颤动40例，疗效满意，报告如下。     

静脉应用胺碘酮与普罗帕酮控制快速心房颤动

心房颤动为临床上常见的心律失常之一 ,对我院 1998年5月至 2 0 0 3年 2月诊治的 182例快速心房颤动患者 ,以随机对照方法研究静脉注射胺碘酮与普罗帕酮控制及转复心房颤动的效果 ,现报道如下。1　资料与方法1.1　临床资料　 182例均有突发心悸、胸闷、气急等症状 ,发病 1～ 48小时 ,并有 12导联心电图证实心房颤动 (心室率 >12 0次 /min) ,年龄 2 5～ 79岁。 182例患者随机分成两组。胺碘酮组 91例 ,其中男 5 1例 ,女 40例 ,年龄 2 6～ 79岁 ,平均(5 2 .0± 2 6 .5 )岁 ,房颤的原发疾病 :冠心病 47例 ,高血压 2 0例 ,原发性心肌病 12例 ,肺…     

胺碘酮治疗阵发性心房颤动疗效观察

胺碘酮是目前Ⅲ类抗心律失常药中唯一无逆频率依赖现象(reverse use—dependence phenomenon)的药物。笔者从1995年1月～2003年5月随机单盲对照观察110例用胺碘酮、普罗帕酮预防阵发性心房颤动(房颤)发作的疗效,报道如下。 1 资料与方法     

胺碘酮治疗阵发性心房颤动对照观察

胺碘酮是目前 类抗心律失常药中唯一无逆频率依赖现象 (reverse use- dependence phenom enon)的药物。笔者从1993年 1月至今随机单盲对照观察 110例用胺碘酮、普罗帕酮预防阵发性心房颤动 (房颤 )发作的疗效 ,报告如下。1　资料与方法1.1　一般资料　经体格检查、心电图、动态心电图 (Holter)确定为阵发性心房颤动并持续 2天以上共 110例 ,其中男 6 2例 ,女 48例 ;年龄 32～ 76 ,平均 (5 4± 11)岁。有心力衰竭、甲亢性心脏病、房室传导阻滞、严重肝、肾、肺疾病者均不入选。1.2　方法　入选患者随机分为 3组 ,安慰剂组 30例 ;胺碘酮组 4…     

静脉注射胺碘酮与普罗帕酮治疗心房颤动的临床对比观察

目的　观察静脉应用胺碘酮与普罗帕酮对阵发性快速心房颤动 (房颤 )的疗效。方法　选择 4 9例患者按就诊顺序随机分为两组 ,胺碘酮组 (2 5例 ) :胺碘酮 15 0mg+生理盐水 10ml,静脉注射 ,10分钟注射完毕 ;普罗帕酮组 (2 4例 ) :普罗帕酮 70mg +生理盐水 10ml,静脉注射 ,5～ 10分钟注射完毕。观察 10～ 2 0分钟若未转复可重复应用 ,最大累积量胺碘酮为 4 5 0mg ,普罗帕酮为 2 10mg。 结果　转复率 :胺碘酮组 76 % (19/ 2 5 ) ,普罗帕酮组 75 % (18/2 4 ) ,两组转复率比较差异无统计学意义 (χ2 =0 .0 0 4 2 ,P >0 .0 5 )。转复时间 :胺碘酮组 (4 8.1± 15 .9)分钟 ,普罗帕酮组 (38.7± 14 .9)分钟 ,两组比较差异有统计学意义 (t=2 .13,P <0 .0 5 )。结论　胺碘酮和普罗帕酮对阵发性快速房颤均有较高的转复率 ,但转复时间普罗帕酮短于胺碘酮     

静脉普罗帕酮和胺碘酮序贯应用转复阵发性心房颤动的观察

心房颤动 (房颤 )是临床最常见的心律紊乱 ,发生在 4 8小时内的房颤可无需抗凝立即进行复律 ,虽然电复律转复率高 ,但多数患者对此有恐惧心理 ,不易被接受 ,在电复律还未成为标准治疗前 ,除紧急情况外 ,药物复律仍为临床首选 ,普罗帕酮 (心律平 )和胺碘酮为常用房颤复律药物 ,本研究旨在观察静脉心律平和胺碘酮两药序贯应用转复阵发性房颤的疗效和安全性。1　资料与方法1 1　一般资料　选择 2 0 0 1年 1月至 2 0 0 2年 10月本院急诊和住院患者 ,均为发生 4 8小时内的阵发性房颤 ,1周内未用任何抗心律失常药物 ,排除急性心肌梗死、心力衰竭 (…     

Parasympathetic blockade promotes recovery from atrial electrical remodeling induced by short-term rapid atrial pacing

The purpose of the present study was to assess the influence of autonomic blockade on shortening of effective refractory period (ERP) induced by short-term rapid atrial pacing (RAP) and its recovery process. Fifteen patients (8 men, 7 women, age 52 +/- 16 years) without structural heart disease and without a history of atrial fibrillation were included in this study. All patients underwent RAP at a cycle length of 300 ms for 5 minutes, after which the ERP was measured in all patients at 1, 3, 5, 7.5, and 10 minutes following cessation of RAP. In ten patients, these RAP and measurements of ERPs were repeated after administration of propranolol (P) and subsequent administration of atropine (P + A), respectively. In the remaining five patients atropine (A) was given first and then the administration of propranolol followed (P + A). Relative to the baseline value, the ERP immediately after RAP did not differ significantly from the Control(C), P, A, or P + A (C, 79%+/- 8%; P, 82%+/- 9%; A, 80%+/- 6%; P + A, 82%+/- 13%). However, the ERP 3 minutes after cessation of RAP was significantly (P < 0.05) longer in A (93%+/- 4%) and P + A (97%+/- 5%) than that in C (86%+/- 5%) and P (86%+/- 5%). The recovery time for ERP to return to pre-RAP value was significantly shorter during A and P + A than during either C or P (C, 536 +/- 161 s; P, 503 +/- 172 s; A, 282 +/- 111 s; P + A, 291 +/- 147 s; P < 0.05). Parasympathetic blockade may promote recovery from ERP shortening induced by short-term RAP.     

Vagal stimulation promotes atrial electrical remodeling induced by rapid atrial pacing in dogs: evidence of a noncholinergic effect

Background: Atrial electrical remodeling (AER) is one of the mechanisms by which atrial fibrillation (AF) begets AF. It is known that vagal activity increases the propensity for AF. However, vagal effects on AER have not been fully investigated. Methods: Adult mongrel dogs were divided in four groups: group I, rapid atria pacing (RAP); group II, RAP plus vagal nerve stimulation (VNS); group III, RAP and VNS with atropine (0.2 mg/kg/h, intravenous), and group IV, group III plus vasoactive intestinal polypeptide (VIP) antagonist ([D‐p‐Cl‐Phe⁶, Leu¹⁷]‐VIP, 0.125 μg/kg/h). VNS was performed bilaterally through vagosympathetic trunks to achieve second‐degree AV block or sinus rate slowing of >30 beats per minute. Atrial effective refractory periods (AERPs) were determined in the coronary sinus and right atrial appendage every hour at drive cycle lengths (DCLs) 350 ms, 300 ms, and 250 ms. Results: During 5 hours RAP with or without VNS, AERP shortened progressively from baseline at both pacing sites and at all DCLs (P < 0.01). Furthermore, RAP‐induced AERP shortening was more pronounced with VNS (P < 0.01). With atropine, the AERP shortening during VNS was blunted (P < 0.01), but was still significantly more pronounced than that in group I (P < 0.05). However, VNS effect on AERP shortening was eliminated completely with the combination of atropine and VIP antagonist (P = 0.15 vs group I). Conclusion: Increased vagal activity promotes RAP‐induced AER, which could not be totally accounted for by cholinergic effect but could be blocked by the combination of atropine and VIP antagonist. Vagally released VIP may have important role in the vagal promotion of AER. (PACE 2011; 34:1092–1099)     

Enhancement of repopulation haemopoiesis by heterozygous connexin 43 stem cells seeded on wild-type connexin 43 stroma

The present paper analyses the results of competitive blood-cell repopulation experiments in which Cx43-WT (connexin 43 wild-type) host mice, whose own HSCs (haemopoietic stem cells) were deleted, were grafted with fetal liver cells: 50% Gpi-1a (glucose phosphate isomerase-1a)/Cx43-WT cells competing with 50% Gpi-1b/Cx43-WT, 50% Gpi-1b/Cx43-HZ (heterozygous) or 50% Gpi-1b/Cx43-KO (knock-out) cells. The percentages of platelets, granulocytes, red cells, B-cells and T-cells containing Gpi-1b in blood samples obtained from 22 to 186 days after grafting, and the percentages of high-proliferation-potential colony-forming cells containing Gpi-1b at 255 days after grafting, were measured. The results show that, if we wait 4 months so that we measure the percentages of Gpi-1b end-cells formed by initially resting stem cells in the graft, values in HZ mice are greater than those in WT and KO mice by 10% or more. We propose a bipolar influence model for blood formation by grafted HSCs to explain this difference and other features of the data. Influence A is a direct one: for individual HSCs, the combined effect on HSC niching and HSC proliferation of Cx43 is superior to that of the KO allele. Influence B is a demographic one: HZ foundation mice compensate by having more HSCs than WT mice. The net outcome of influences A and B is that HZ is the winner.     

甘珀酸对癫痫大鼠脑组织缝隙连接蛋白43表达的干预及其意义

目的 探讨癫痫大鼠脑组织缝隙连接蛋白43(connexin43,Cx43)表达及缝隙连接阻断剂甘珀酸(carbenoxolone,CBX)对其表达的影响.方法 健康SD大鼠64只,随机分为正常对照组、致痫组、致痫+生理盐水组(致痫+NS组)和致痫+CBX干预组(致痫+CBX组).采用免疫组化染色方法和实时荧光定量逆转录-聚合酶链反应方法分别测定氯化锂-匹罗卡品癫痫模型大鼠脑组织Cx43免疫阳性细胞数及Cx43mRNA表达水平,并观察腹腔注射CBX对Cx43表达的影响.结果 与正常对照组比较,致痫大鼠脑组织Cx43免疫阳性细胞数及其mRNA表达差异倍数在致痫1 h开始明显增多,并持续至7 d(P＜0.05).大鼠注射CBX后Cx43免疫阳性细胞数及其mRNA表达差异倍数均明显低于同一时间点致痫组和致痫+NS组(P＜0.05),海马区Cx43免疫阳性细胞数及其mRNA表达差异倍数在注射CBX 7 d后降至正常水平,而皮层区Cx43免疫阳性细胞数及其mRNA表达差异倍数在注射CBX 3 d后降至正常水平.结论 星形胶质细胞Cx43参与了癫痫发作和发展过程.CBX减少致痫大鼠脑组织Cx43表达,具有较明确的抗癫痫作用.     

Tachycardia induced electrical remodeling of the atria and the autonomic nervous system in goats

Atrial fibrillation (AF) shortens the atrial effective refractory period (AERP). To investigate the role of the autonomic nervous system during this so-called electrical remodeling of the atria (ERA) and during recovery from ERA we analyzed heart rate variability (HRV). In 12 goats atrioventricular (300:150 beats/min) pacing was performed for 24 hours, interrupted at 4, 8, 16, and 24 hours for recording of 500 atrial (AA) intervals during sinus rhythm and measurement of the AERP(430ms) at 7.4 +/- 0.6 sites. After 24 hours, pacing was stopped and the electrophysiological study and recording of the AA intervals was repeated at 4, 8, 16, and 24 hours after cessation of pacing. Time- and frequency-domain parameters were computed from each 500 AA interval recording. After 24 hours of rapid pacing the AERP had shortened significantly (147 +/- 5.6 to 102+/- 6.4 ms, P < 0.0001). No significant changes in HRV and dispersion of refractoriness (AAERP) (47 +/- 7.1 to 44 +/- 4.2 ms) were observed. After cessation of pacing, the AERP prolonged again (102 +/-6.4 to 135+/-8.8 ms, P < 0.0001) and was paralleled by a significant increase in AAERP (44 +/- 4.2 to 63+/- 7.1 ms, P = 0.01). Furthermore, HRV increased significantly. At each time point an inverse relation between the logarithmically transformed vagal parameter HF (InHF) and AERP was observed. We calculated the mean InHF for each goat using all time points and used the median value to divide the 12 goats into high and low vagal tone groups. We compared the degree of ERA and recovery from ERA for both groups. The AERP shortened 47.4 +/- 6.5 versus 43.0+/-5.0 ms (NS) for goats with high and low vagal tone, respectively. During recovery from ERA the AERP lengthened 23.6 +/- 4.0 versus 42.5 +/- 1.7 ms (P = 0.001) for goats with high and low vagal tone, respectively. Multivariate regression analysis indicated a short AERP as the single independent determinant of the inducibility of AF during ERA and recovery from ERA (P < 0.0001). During recovery from ERA, the AERP prolonged and vagal tone and AAERP increased. A high vagal tone during recovery from ERA was associated with a short AERP and an attenuated recovery of ERA.     

超声指导食道起搏电极定位建立大鼠快速心房起搏房颤模型

目的 本研究主要探讨超声指导食道起搏电极定位建立大鼠房颤模型的可行性,并比较其与食道心电图指导定位的效果与安全性差异。方法 分别通过超声及食道心电图(心房A波振幅大小及形态)指导起搏电极定位建立快速心房起搏诱导房颤模型,比较两种方法的房颤诱导成功率、平均定位耗时、起搏阈值和无关肌肉刺激(EMS)评分。结果 与食道心电图指导电极定位相比,超声指导起搏电极定位组房颤成功率更高(80% VS 60%,P<0.05),平均定位耗时更短(2.3±0.5min VS 5.3±0.9min,P<0.05),平均起搏阈值更低(0.35±0.048mV VS 0.57±0.057mV,P<0.05),且无关肌肉刺激(EMS)发生更少(11±0.8 VS 23±0.9,P<0.05)。结论 与食道心电图指导定位相比,超声指导起搏电极定位用于建立经食道快速心房起搏大鼠房颤模型更有效、安全。     

胺碘酮与利多卡因对急性乌头碱中毒所致快速性室性心律失常治疗效果的对比研究

目的 评价胺碘酮与利多卡因治疗急性乌头碱中毒所致快速性室性心律失常的疗效及安全性.方法 将130例患者分为胺碘酮治疗组68例,利多卡因治疗组62例,回顾比较两种药物对快速性室性心律失常的疗效、病死率和不良反应发生率.结果 在急性乌头碱中毒所致快速性室性心律失常的治疗中,胺碘酮组有效率97.05%(66/68),利多卡因组有效率75.81%(47/62),胺碘酮组优于利多卡因组,差异有统计学意义(P＜0.01).胺碘酮组发生不良反应7例,不良反应发生率10.29%;利多卡因组发生不良反应1例,不良反应发生率1.61%;利多卡因组不良反应发生率低于胺碘酮组,差异统计学意义(P<0.05).结论 胺碘酮是治疗急性乌头碱中毒所致快速性室性心律失常效果较好的药物,虽然不良反应发生率较高,但能通过合理使用预防,可以作为首选药物.     

快速心室起搏诱导犬心力衰竭模型成功的时限观察

目的：观察快速心室起搏诱导犬心力衰竭模型的不同起搏时限对犬心功能、肾脏血流量的影响。 方法：①实验于2004—03／2005-06在哈尔滨医科大学第一临床医学院实验外科完成。选用健康成年杂种家犬27只。随机分为3组：假手术组（n=6），起搏2周组（n=6），起搏4周组（n=7），起搏6周组（n=8）。②麻醉犬，左侧卧位，切开、悬吊心包，固定螺旋型心外膜起搏电极于右一室心尖部，连接实验用V00型埋藏式起博器，于犬背部皮下造皮囊埋置起博器，恢复1周后起搏2，4，6周（起搏2，4，6周组），起搏频率均为240次／min；假手术组埋置起博器后不起搏。③采用彩色多普勒超声诊断仪测定各组犬左心室收缩末内径、左心室舒张末内径，左心室射血分数、心排血量、收缩期室间隔厚度、舒张期室间隔厚度、收缩期左心室后壁厚度、舒张期左心室后壁厚度。计算肾脏血浆流量（π&;#215;双肾动脉内径^2&;#215;双肾动脉最大血流速度&;#215;0．57&;#215;60／4）。④组间计量资料差异比较采用单因素方差分析，两两比较用q检验，组内比较用配对t检验。 结果：起搏6周组起搏期间死亡2只，最终进入结果分析：假手术组6只，起搏2，4，6周组分别6，7，6只。①起搏4和6周组犬心排血量、左室射血分数、肾脏血浆流量明显低于假手术组和起搏2周组（P〈0．05-0．01），左心室收缩末内径、左心室舒张末内径明显大于假手术组和起搏2周组（P〈0．05—0．01）。②起搏4和6周组犬收缩期室间隔厚度，舒张期室间隔厚度、收缩期左心室后壁厚度、舒张期左心室后壁厚度明显小于假手术组和起搏2周组（P〈0．05-0．01）。起搏2周组犬收缩期左心室后壁厚度均明显小于假手术组（P〈0．05）。 结论：快速心室起搏所致的犬心力衰竭模型呈时间依赖性，起搏4周犬心功能、肾血流明显下降而生存率高。     

快速心室起搏诱导犬心力衰竭模型成功的时限观察

目的:观察快速心室起搏诱导犬心力衰竭模型的不同起搏时限对犬心功能、肾脏血流量的影响。方法:①实验于2004-03/2005-06在哈尔滨医科大学第一临床医学院实验外科完成。选用健康成年杂种家犬27只。随机分为3组:假手术组(n=6),起搏2周组(n=6),起搏4周组(n=7),起搏6周组(n=8)。②麻醉犬,左侧卧位,切开、悬吊心包,固定螺旋型心外膜起搏电极于右-室心尖部,连接实验用VOO型埋藏式起博器,于犬背部皮下造皮囊埋置起博器,恢复1周后起搏2,4,6周(起搏2,4,6周组),起搏频率均为240次/min;假手术组埋置起博器后不起搏。③采用彩色多普勒超声诊断仪测定各组犬左心室收缩末内径、左心室舒张末内径、左心室射血分数、心排血量、收缩期室间隔厚度、舒张期室间隔厚度、收缩期左心室后壁厚度、舒张期左心室后壁厚度。计算肾脏血浆流量(π×双肾动脉内径2×双肾动脉最大血流速度×0.57×60/4)。④组间计量资料差异比较采用单因素方差分析,两两比较用q检验,组内比较用配对t检验。结果:起搏6周组起搏期间死亡2只,最终进入结果分析:假手术组6只,起搏2,4,6周组分别6,7,6只。①起搏4和6周组犬心排血量、左室射血分数、肾脏血浆流量明显低于假手术组和起搏2周组(P<0.05～0.01),左心室收缩末内径、左心室舒张末内径明显大于假手术组和起搏2周组(P<0.05～0.01)。②起搏4和6周组犬收缩期室间隔厚度、舒张期室间隔厚度、收缩期左心室后壁厚度、舒张期左心室后壁厚度明显小于假手术组和起搏2周组(P<0.05～0.01)。起搏2周组犬收缩期左心室后壁厚度均明显小于假手术组(P<0.05)。结论:快速心室起搏所致的犬心力衰竭模型呈时间依赖性,起搏4周犬心功能、肾血流明显下降而生存率高。     

缝隙连接蛋白Cx32与Cx43在癫痫发病中的作用

目的:探讨缝隙连接蛋白(Cx)与癫痫之间的关系.方法:采用免疫组织化学方法测定氯化锂-匹罗卡品致痫大鼠癫痫发作后不同时间不同脑区Cx32与Cx43免疫阳性表达情况.结果:与对照组比较,致痫组大鼠海马区与皮层区Cx32和Cx43免疫阳性表达在癫痫发作1h后开始增强(Cx32免疫阳性细胞数分别为海马区16.62±4.51和皮层区14.85±3.30,均P＜0.05;Cx43免疫阳性细胞数分别为海马区18.26±4.03和皮层区18.65±4.51,均P＜0.01),24 h达到高峰(Cx32免疫阳性细胞数分别为海马区46.53±9.47和皮层区28.25±8.69,均P＜0.01;Cx43免疫阳性细胞数分别为海马区39.77±7.79和皮层区26.50±6.56,均P＜0.01),此后逐步下降.但至14 d Cx32海马区与皮层区免疫阳性细胞数分别为22.45±6.56和15.92±3.16,仍高于对照组(均P＜0.05),而Cx43在14 d的表达则有所不同:海马区免疫阳性细胞数17.54±3.77仍高于对照组(P＜0.01);皮层区表达则降至正常水平.致痫24 h时海马区Cx32和Cx43免疫阳性表达均明显高于同一时限的皮层区(均P＜0.05).结论:Cx32和Cx43参与了癫痫的发生与发展过程,反映了脑组织中神经元、星形胶质细胞之间的缝隙连接与癫痫发病机制密切相关.