离体兔心脏Langendorff逆向流下室颤与选择性心室肌电隔离

目的:研究以选择性射频消融形成心室肌电隔离区域,分析其电生理效应、室颤诱导能力,并判断该区域是否为维系心律失常、室颤存在的必要条件。方法:以单管法制备离体兔心脏逆行Langendorff灌流模型计20例。按射频消融部位分为4组(n=5),经导管作V型线性消融以形成心室肌电隔离。心室肌射频消融前后分别记录分析室颤的电生理特征和心室肌电隔离区域内外的诱导能力。结果:各组离体心脏心室肌射频消融厚度与环射频消融区域范围所占心脏表面积百分比相似(P>0.05)。仅第4组3例形成环消融区内完全电隔离;其余形成环消融区内部分电隔离。3例完全电隔离者中,均不能在环消融区内诱发出室颤(与基线相比P<0.05);而除1例外,其余均可在环消融隔离区外起搏刺激诱发出室颤(与基线相比P>0.05)。在部分电隔离者中,环消融区内只诱发出非持续性室颤;环消融隔离区外均可起搏刺激诱发出室颤(与基线相比P>0.05)。结论:离体兔心脏Langendorff灌流模型选择性心肌电隔离试验显示完全或部分电隔离可以避免在这些区域内诱导室颤或持续性室颤,但不能避免在残留心肌中诱导室颤。实验所选各心肌区域不是维系室颤存在的必要条件。     

血管紧张素Ⅱ对心室肌细胞电生理特征的影响

目的:探讨血管紧张素Ⅱ诱导心肌肥大过程中心肌细胞电生理特征性改变及意义。方法:将24只新西兰兔随机分为血管紧张素Ⅱ组和正常对照组各12只,体外培养乳兔心室肌细胞,观察10-7mol/L血管紧张素Ⅱ作用48 h心肌细胞动作电位时程、瞬时外向钾电流密度的变化,并与对照组比较。结果:血管紧张素Ⅱ组心室肌细胞膜电容较正常对照组增加38.22%(P<0.01);心室肌细胞动作电位复极达90%时限较对照组延长22.1%(P<0.01);心室肌细胞瞬时外向钾电流密度较对照组下调28.6%(P<0.05)。结论:血管紧张素Ⅱ持续刺激可引起心室肌细胞电重构,可能是导致室性心律失常发生的一个重要机制。     

肌电诱发神经肌肉电刺激治疗脑卒中肩关节半脱位

目的:观察肌电诱发的神经肌肉电刺激疗法在脑卒中肩关节半脱位中的临床疗效。方法:脑卒中肩关节半脱位患者60例,随机分为A、B、C组各20例。3组均给予常规康复治疗,B组加用神经肌肉电刺激疗法,C组加用肌电诱发的神经肌肉电刺激疗法。治疗前后分别采用双侧肩关节X线片及肩关节指诊评价复位情况;采用运动功能评定量表(FMA)中上肢部分评定上肢功能恢复情况。结果:治疗6周后,C组复位率明显高于A、B组(45%、15%、25%,P<0.05);3组FMA的分值均较治疗前明显提高,C组更高于A、B组(P<0.05)。结论:肌电诱发的神经肌肉电刺激治疗脑卒中肩关节半脱位优于单纯常规治疗方法和神经肌肉电刺激疗法。     

急性心房压力增高对心房肌电生理性质的影响

目的:探讨急性心房压力增高对心房肌电生理性质的影响及其与房性心律失常的关系。方法:12只杂种成年犬,在阻断自主神经状态下行心外膜电生理检查,分成基础对照组,单纯升压组及胺碘酮 升压组,分别测量心房不同位点的单相动作电位(MAP)及房颤诱发率。结果:与基础对照相比,单纯升压组MAPD90明显延长,MAPD90离散度(△MAPD90)增大,RT离散度(△RT)增大,房颤诱发率增加。胺碘酮 升压组MAPD90延长,但△MAPD90减小,△RT在慢频率起搏时减小,但起搏频率增快时逐渐增大,房颤诱发率虽高于对基础对照,但与单纯升压组相比无统计学差异。结论:1)急性心房压力增高后△RT增大,这可能是此时房颤诱发率增高的电生理基础;2)胺碘酮静脉制剂在房压增高时不能有效降低房颤诱发率,推测与这时△RT在快频率起搏时增大有关。     

电刺激诱发表面肌电信号的初步实验研究

目的为探索一种无创的肌电检测方法,进行有关诱发表面肌电信号的实验。方法设计了电刺激诱发表面肌电信号检测实验系统,采用恒流电刺激器刺激腓总神经,记录小腿外侧肌肉的诱发表面肌电信号。结果分别对6例正常受试者和5例重症肌无力患者进行了测试,发现电刺激引起肌肉疲劳过程中,正常受试者和重症肌无力患者诱发肌电信号的变化显著不同,首次刺激记录到的诱发肌电P1波的中角度(A1)对照组(6.45±2.57),重症肌无力组(1.79±0.72),持续刺激30s记录到的诱发肌电P1波的中幅度(A2)对照组(3.41±1.77),重症肌无力组(0.29±0.12),与对照组相比差异有显著性意义(t=4.078,4.446,P<0.05)。结论诱发肌电信号的检测分析对于研究肌肉的疲劳耐受性具有意义,该研究方法有一定的临床应用价值。     

肌电诱发神经肌肉电刺激在偏瘫康复中应用的研究

目的：观察肌电诱发的神经肌肉电刺激在改善早期偏瘫患者肢体运动和促进功能恢复方面的临床疗效：与神经肌肉电刺激疗法相比，二者的疗效是否有明显的区别。方法：选发病4周内的不能主动完成腕背伸运动的患者90例，随机分为三组。其中对照A组30例，为常规康复治疗组；对照B组30例，在常规治疗基础上，加用神经肌肉电刺激疗法；治疗组30例．在常规治疗基础上加用肌电诱发的神经肌肉电刺激疗法。治疗次数：1次，日，5次，周，15次为一疗程。测定上述患者肌肉静态及收缩时肌电值、肌力（MMT法）应用简式Fugl-Meyer功能评价表、Barthel指数评分表对患者患肢运动功能及日常生活动作能力进行评测．在疗程开始与结束时分别予以记录。结果：三组患者治疗前后的肌肉静态及收缩时肌电值、肌力及应用Fugl-Mever评价表、Barthel指数评分表进行评分的分值均有显著性提高，治疗组与对照1，2组疗效相比有明显提高（P〈0．05）。结论：肌电诱发的神经肌肉电刺激疗法是一种有效的临床康复治疗方法．可以用于偏瘫患者上肢瘫痪的肌肉的功能治疗，其疗效优于单纯常规治疗方法和神经肌肉电刺激疗法。     

肌电诱发神经肌肉电刺激对脑卒中偏瘫患者上肢运动功能的疗效

目的观察肌电诱发神经肌肉电刺激对改善早期脑卒中偏瘫患者肢体运动功能的临床疗效。方法发病4 周内、不能主动完成腕背伸运动,且患侧腕背伸时所测收缩肌电值=基础肌电值的患者60 例,分为2 组：对照组(n=30)应用神经肌肉电刺激疗法, 治疗组(n=30)应用肌电诱发的神经肌肉电刺激疗法, 共治疗4 周。治疗前后测定患者静态及收缩时肌电值, 应用简式Fugl-Meyer 运动功能评定(FMA)、Barthel 指数对患者进行评定。结果两组患者治疗后的肌肉静态及收缩时肌电值、FMA 评分、Barthel 指数评分均有显著改善(P=0.000),治疗组比对照组改善更多(P<0.05)。结论肌电诱发的神经肌肉电刺激疗法即使于发病早期,未检测到肌肉收缩肌电值变化的情况下也可以用于偏瘫患者上肢瘫痪肌肉的功能治疗,其疗效优于神经肌肉电刺激疗法。     

电刺激诱发表面肌电信号的初步实验研究

目的：为探索一种无创的肌电检测方法，进行有关诱发表面肌电信号的实验。方法：设计了电刺激诱发表面肌电信号检测实验系统，采用恒流电刺激器刺激腓总神经，记录小腿外侧肌肉的诱发表面肌电信号。结果：分别对6例正常受试者和5例重症肌无力患者进行了测试，发现电刺激引起肌肉疲劳过程中，正常受试者和重症肌无力患者诱发肌电信号的变化显著不同，首次刺激记录到的诱发肌电P1波的中角度(A1)：对照组(6．45&;#177;2．57)，重症肌无力组(1．79&;#177;0．72)，持续刺激30s记录到的诱发肌电P1波的中幅度(A2)；对照组(3．4l&;#177;1．77)，重症肌无力组(0．29&;#177;0．12)，与对照组相比差异有显著性意义(t=4．078，4．446，P&;lt;0．05)。结论：诱发肌电信号的检测分析对于研究肌肉的疲劳耐受性具有意义，该研究方法有一定的临床应用价值。     

电刺激诱发猪心室颤动模型的研究和改进

目的:探讨通过左颈静脉插入电极导线建立稳定的交流电刺激诱发心室颤动的动物模型。方法:取健康成年猪10只,体重30～40kg,腹腔及耳缘静脉注射氯胺酮、戊巴比妥钠麻醉,行气管插管、双侧颈内静脉插管、右股动脉插管,予以30～40V的交流电通过心室内电刺激诱发心室颤动。结果:电极导线插入18～22cm,室颤诱发成功率为100%,室颤3分钟后除颤均能成功并且不留任何神经系统后遗症。结论:该心室颤动模型具有满意的可重复性及可操作性,诱发室颤效果非常好,能够满足心肺脑复苏及电击除颤的实验研究。     

表面肌电触发电刺激对脑卒中偏瘫患者下肢运动功能的影响

目的 探讨表面肌电触发电刺激对脑卒中偏瘫患者下肢运动功能的影响.方法 将30例脑卒中偏瘫患者分为治疗组和对照组,每组患者15例.2组患者均给予常规康复训练,治疗组在常规康复训练的基础上给予表面肌电触发电刺激,对照组在常规康复训练的基础上给予低频电刺激.2组患者均于治疗前和治疗3个疗程后进行Brunnstrom运动功能分期、简式Fugl-Meyer(FMA)下肢运动功能评定和表面肌电图肌电积分值(iEMG)测定.结果 3个疗程结束后,2组患者Brunnstrom分期、FAM评分及iEMG较治疗前均有显著提高(P＜0.05),且治疗组各项评分均优于对照组(P＜0.05).结论 表面肌电触发电刺激对脑卒中偏瘫患者下肢运动功能的恢复有明显的促进作用.     

Electrophysiological, Rate Dependent, and Autonomic Effects of the Class III Antiarrhythmic Almokalant After Myocardial Infarction in the Pig

Ventricular arrhythmias remain a major problem, in particular in patients with left ventricular dysfunction or heart failure. In this group of patients, Class I drugs were shown to be ineffective, and they even increased mortality during chronic treatment. New antiarrhythmic agents should preferably not only have pure antiarrhythmic effects, but should also be free from adverse autonomic properties. In the present study, the electrophysiological, rate dependent and autonomic effects of intravenously administered almokalant, a new Class III antiarrhythmic drug, were investigated in nine pigs surviving a myocardial infarction. The ventricular effective refractory period (VERP) increased after almokalant (loading dose: 0.05 μmoLkg ^?1 .min^?1, continuous infusion: 0.0025 uμmol/kg^?1.min^?1) from 292 ± 25 to 308 ± 13 ms (pacing cycle length [PCL] 500 ms + 1 extrasystole [ES]), from 249 ± 19 to 261 ± 16 ms (PCL 400 ms +1ES), and from 209 ± 18 to 219 ± 18ms (PCL 300 ms +1ES). The VERPs increased most after three ES at PCL 400 ms: from 167 ± 27 to 186 ± 29 ms (P < 0.05) and at PCL 300 ms: from 159 ± 29 to 174 ± 27 ms (P < 0.05). The ventricular monophasic action potential durations (MAPD) were similarly prolonged and the ratio VERP/MAPD did not change. Prolongation of MAPD after almokalant remained present at short pacing cycle lengths. Before almokalant infusion, sustained monomorphic ventricular tachycardia (VT) was inducible in two pigs, and nonsustained VT in a third animal. After almokalant, only one pig remained inducible. Two weeks after myocardial infarction, heart rate variability and baroreflex sensitivity were reduced. Furthermore, subsequent electrophysiological testing transiently reduced these parameters of autonomic activity. During almokalant however, no changes in autonomic functions were observed after programmed stimulation. Heart rate variability decreased after myocardial infarction from 6.3 ± 2.5 ms to 5.4 ± 4,2 ms (P = NS}. After programmed stimulation, it further decreased to 2.8 ± 2.0 ms (P = 0.028). Almokalant infusion prevented autonomic deterioration: 3.3 ± 2.2 ms before stimulation and 3.3 ± 1.3 after stimulation (P = NS). In postinfarct pigs, almokalant prolongs VERP and MAPD at shorter pacing cycle lengths. The results indicate absence of reverse rate dependence and of adverse autonomic changes.     

Beneficial hemodynamic effects of nicorandil in a canine model of acute congestive heart failure: Comparison with nitroglycerin and cromakalim

Summary— Comparative hemodynamic effects of nicorandil (NCR), nitroglycerin (NTG) and cromakalim (CRM) were examined in a canine model of acute congestive heart failure (CHF). CHF was produced by injections of saponin into coronary arteries of anesthetized dogs followed by volume loading and continuous iv infusion of methoxamine. After the treatment, aortic blood flow (AoF), left ventricular d P /d t and myocardial segment shortening (SS) markedly decreased, while the left ventricular end-diastolic pressure (LVEDP), the right atrial pressure (RAP) and the systemic vascular resistance (SVR) increased. NCR ( n = 6), NTG ( n = 6) and CRM ( n = 8), which were administered iv after production of CHF, caused a comparable reduction in LVEDP. NCR and CRM profoundly increased AoF and SS but NTG did only slightly. On the other hand, NTG and NCR but not CRM significantly reduced RAP. Intracoronary NCR ( n = 8) exerted no or similar effects on SS as well as systemic hemodynamic indices to those observed with iv NCR despite distinct coronary vasodilation. These results indicate that NCR may exert beneficial hemodynamic effects in an experimental CHF mainly due to lessening both afterload and preload rather than the coronary vasodilating effect.     

Left ventricular epicardial activation increases transmural dispersion of repolarization in healthy, long QT, and dilated cardiomyopathy dogs

BACKGROUND: Benefits of cardiac resynchronization therapy (CRT) are well established. However, less is understood concerning its effects on myocardial repolarization and the potential proarrhythmic risk. METHODS AND RESULTS: Healthy dogs (n = 8) were compared to a long QT interval (LQT) model (n = 8, induced by cesium chloride, CsCl) and a dilated cardiomyopathy with congestive heart failure (DCM-CHF, induced by rapid ventricular pacing, n = 5). Monophasic action potential (MAP) recordings were obtained from the subendocardium, midmyocardium, subepicardium, and the transmural dispersion of repolarization (TDR) was calculated. The QT interval and the interval from the peak to the end of the T wave (T(p-e)) were measured. All these characteristics were compared during left ventricular epicardial (LV-Epi), right ventricular endocardial (RV-Endo), and biventricular (Bi-V) pacing. In healthy dogs, TDR prolonged to 37.54 ms for Bi-V pacing and to 47.16 ms for LV-Epi pacing as compared to 26.75 ms for RV-Endo pacing (P < 0.001), which was parallel to an augmentation in T(p-e) interval (Bi-V pacing, 64.29 ms; LV-Epi pacing, 57.89 ms; RV-Endo pacing, 50.29 ms; P < 0.01). During CsCl exposure, Bi-V and LV-Epi pacing prolonged MAPD, TDR, and T(p-e) interval as compared to RV-Endo pacing. The midmyocardial MAPD (276.30 ms vs 257.35 ms, P < 0.0001) and TDR (33.80 ms vs 27.58 ms, P=0.002) were significantly longer in DCM-CHF dogs than those in healthy dogs. LV-Epi and Bi-V pacing further prolonged the MAPD and TDR in this model. CONCLUSIONS: LV-Epi and Bi-V pacing result in prolongation of ventricular repolarization time, and increase of TDR accounted for a parallel augmentation of the T(p-e) interval, which provides evidence that T(p-e) interval accurately represents TDR. These effects are magnified in the LQT and DCM-CHF canine models in addition to their intrinsic transmural heterogeneity in the intact heart. This mechanism may contribute to the development of malignant ventricular arrhythmias, such as torsades de pointes (TdP) in congestive heart failure (CHF) patients treated with CRT.     

炙甘草汤减缓兔右心房颤所致心肌纤维化作用

目的研究炙甘草汤逆转快速起搏兔右心房（RAP）诱导心房颤动（AF）致右心耳心肌心肌纤维化的作用。方法新西兰大白兔动物模型随机分为假手术组（A组）：植入电极不行快速起搏;起搏组（B组）：行短期快速起搏兔右心房12h致AF模型;炙甘草汤水煎液阴性方组（C组）：给予炙甘草汤阴性方水煎液灌胃2次/d,连续30d后行短期快速起搏兔右心房12h致AF模型;炙甘草汤组（D组）：给予炙甘草汤水煎液灌胃2次/d,连续30d后行短期快速起搏兔右心房12h致AF模型;每组实验动物各8只。建立房颤兔模型,行兔右心耳Masson染色和免疫组化方法检测基质金属蛋白酶-9（MMP-9）蛋白表达。检测右心耳组织场电位时程（fAPD）,并观察炙甘草汤对右心耳fAPD的作用。结果成功建立快速起搏右心房诱导房颤兔模型,Masson染色显示B组和C组心肌纤维化明显增加,D组心肌纤维化减弱。MMP-9结果显示,B组和C组MMP-9呈强阳性,D组呈弱阳性。B组和C组fAPD明显缩短,差异有统计学意义（P〈0.05）。给予炙甘草汤水煎液之后,可作用于房颤兔右心耳组织fAPD导致fAPD延长（P〉0.05）。结论炙甘草汤可逆转房颤兔心肌纤维化,同时缩短fAPD的时程。     

Rate dependent effects of procainamide on the threshold current for pacing in the setting of postrepolarization refractoriness in dogs

Normally, ventricular APD exceeds the VERP. However, under specific circumstances this relation may change and can become inverse. This phenomenon of postrepolarization refractoriness may be caused by a decrease in excitability. The threshold current (TC) for pacing has never been quantified as a possible explanation for these observations. Using a MAP pacing catheter in the right ventricular apex, the rate dependent behavior of TC, VERP, and APD before and after procainamide (dose 20 mg/kg in 10 min + 5 mg/min infusion) was determined in 17 dogs with chronic complete AV block. Initially, TC was determined with 0.1 mA accuracy. Using a pacing current of at least twice TC, VERP and APD showed a similar, rate dependent shortening for PCLs 800, 575, and 350 ms. Procainamide treatment led to an equal, rate independent VERP and APD increase: no post repolarization refractoriness. Subsequently, accuracy for TC determination was increased to 0.01 mA. Comparing PCLs 800 and 250 ms, TC doubled from 0.05 +/- 0.01 to 0.10 +/- 0.09 mA during control and almost tripled from 0.06 +/- 0.02 to 0.17 +/- 0.10 mA (P < 0.05) after procainamide. Using a fixed pacing current of exactly twice TC found at 800 ms PCL during control, VERP exceeded APD after procainamide treatment at 300 and 250 ms PCL: postrepolarization refractoriness. Increasing the pacing current to twice the rate dependent TC, the relation between VERP and APD normalized: no postrepolarization refractoriness. We conclude that after procainamide, rate dependent TC increase is of major importance for the phenomenon of postrepolarization refractoriness.     

Is the Ventricular Effective Refractory Period Different When Determined by Incremental Versus Decremental Scanning?: The Effect of Pacing Cycle Length,d-Sotalol,and Levcromakalim

In tbe clinical setting, the ventricular effective refractory period (VERP) is determined by an 8-beat drive train (S1S1), followed by a premature stimulus (S2), which is decremented in subsequent drive trains until capture is lost. Variation in intertrain pauses and capturing extra stimuli disturb steady-state conditions and reduce reproducibility of values found for the VERP. To increase reproducibility, a protocol without intertrain pause and incremental scanning (IS) of S2 was developed. In anesthetized dogs with chronic AV block, determination of the VERP using IS and decremental scanning (DS) without intertrain pause was compared at 800 and 350 msec pacing cycle length (PCL). The measurements were repeated after the administration of d-sotalol to lengthen the VERP and levcromakalim to shorten the VERP. The results showed no difference between IS and DS at both PCLs with or without medication. Recurrent and abrupt rate changes were avoided daring IS, making this the protocol of choice when induction of arrhythmias is to be avoided.     

Influence of Duration of Rapid Ventricular Pacing on Ventricular Refractoriness in the Presence of Propafenone and Lidocaine

Propafenone and lidocaine have a rate dependent negative dromotropic effect on intraventricular conduction. We investigated the use dependent actions of propafenone and lidocaine on intraventricular conduction in isolated guinea pig hearts perfused by the method of Langendorff. Of primary interest was how the number of stimuli of the conditioning train (S1) might influence the ventricular effective refractory period (VERP) when refractoriness is assessed at a high pacing rate. Propafenone (0.3 μM) and lidocaine (50 μM) caused a comparable prolongation of the intraventricular conduction time during sinus rhythm. During ventricular pacing in the presence of propafenone an abrupt decrease of the pacing cycle length (220 to 120 ms) resulted in an initial peak of rate dependent prolongation of the QRS interval that subsequently decreased to a stable steady-state level. Lidocaine also induced a rate dependent increase of the intraventricular conduction time up to a steadystate level. The time constant, characterizing the changes of the intraventricular conduction time after shortening the ventricular pacing cycle length from 220 to 120 ms was significantly (P < 0.01) longer in the presence of propafenone (τ= 31 ± 4 beats; mean ± SEM; n = 11) than for lidocaine (τ= 3 ± 1; n = 10). Both drugs caused the greatest increase of tbe VERP when the number of conditioning stimuli (S1, interstimulus interval = 120 ms) was in the range of their respective time constant. However, when the number of conditioning stimuli was further increased, VERP progressively diminished. These effects may be explained by a shortening of the action potential during high rates that results in a decreased binding of propafenone to Na⁺ channels and by the direct shortening of repolarization period by lidocaine (Class IB drug).     

快速心室起搏犬心房颤动模型研究

目的建立快速起搏心室致心力衰竭犬房颤模型,研究其电生理及心房结构和功能改变。方法 15只健康杂种犬分两组:对照组6只,实验组9只[240次/min心室起搏(25±3)d]。超声心动图测定起搏前后心房面积、面积缩小分数及左心室功能,利用心内电极测定心房有效不应期、传导速度及房颤诱发情况。结果实验组7只犬完成了实验。快速心室起搏(25±3)d后,犬的收缩末期和舒张末期左、右心房面积显著增大(与起搏前比较,P<0.01),左、右心房面积缩小分数显著减小(左心房:(35.7±1.9)%和(20.7±2.7)%,P<0.01;右心房:(35.0±2.3)%和(18.0±2.3)%,P<0.01),左室射血分数从(65.3±2.1)%降至(31.6±2.8)%(P<0.01)。实验组犬左、右心房有效不应期显著延长,心房内传导速率较对照组减慢。实验组有5只犬诱发出超过30 min的房颤,平均房颤持续时间较对照组显著延长(687±290)s和(13±9)s,P<0.01)。实验组平均房颤持续时间与左、右心房面积及面积缩小分数相关(P<0.05)。结论 快速心室起搏致心衰模型能稳定地诱发出房颤,房颤持续时间与心衰引起的显著心房结构和功能异常相关。