Inhibition of Atrial Electrical Activity by Ventricular Pacing Mediated by Vagal Stimulation

In the absence of retrograde (VA) conduction, ventricular pacing does not exert any appreciable effect upon atrial electrical activity. We report three patients (2 with complete AV block and 1 with preserved AV conduction) in which, during EP study, no VA conduction was present and, in spite of that, excessive suppression (for more than 15 secs in the first patient) of sinus (atrial) electrical activity during RV pacing was observed. The sinus node suppression was reproducible in two patients. In all patients the suppression phenomenon was not observed after intravenous administration of atropine, which suggests that it was mediated by enhanced vagal tone.     

多巴酚丁胺负荷试验对诱发心肌缺血患者室壁运动异常的研究

对２９例冠心病患者作多巴酚丁胺负荷试验，应用２－ＤＥ观察在规定剂量时左心室壁运动情况，用１５个切段４级评分法计算室壁运动积分（ＷＭＳ），评估诱发在心绞痛和无心绞痛发作状态下患者左室功能不全的程度和范围。结果表明，在冠状动脉有明显的解剖和功能病变者，多巴酚丁胺负荷试验诱发的左室功能不全，在有或无心绞痛的两组患者中是相似的，但有心绞痛发作患者ＳＴ段下降较多见（５６％对２９％，Ｐ＜０．０５），且休息状态下室壁运动异常范围较广泛。     

犬左室急性心肌缺血状态下右心功能的超声应变率研究

目的 应用应变率显像(SRI)技术研究犬左室急性心肌缺血状态下对右心功能的影响.方法 10只犬,分别于冠状动脉左前降支结扎前、后10 min采集心尖四腔观图像,测量缺血前后右室壁、右房壁及三尖瓣环的收缩期应变率(SSR)、舒张早期应变率(ESR)、舒张晚期应变率(ASR)、右室射血分数(RVEF)和用导管法测肺动脉收缩压(PASP).结果 左室局部急性心肌缺血后,PASP增加(P＜0.05),RVEF降低(P＜0.05),右室壁和三尖瓣环的SSR、ESR及ASR降低(P＜0.05),右房壁SSR和ASR增加(P＜0.05).心肌缺血前,右室壁SR与右房壁SR无明显相关性,缺血后两者呈负相关.心肌缺血前后RVEF值与右室壁及三尖瓣环的SSR峰值均呈正相关.缺血后PASP分别与右室壁SSR和RVEF呈负相关.结论 左室前壁急性心肌缺血可引起右室壁舒缩功能减退和PASP增加,右房壁舒缩功能代偿性增加,三者之间有一定的相关性.     

Reflex Vascular Responses to Left Ventricular Outflow Obstruction and Activation of Ventricular Baroreceptors in Dogs

Reflex vascular responses to acute left ventricular outflow obstruction were studied in anesthetized dogs. The studies were done to compare the effects of activation of ventricular baroreceptors on vascular resistance in skeletal muscle (gracilis muscle) and skin (hindpaw); to identify afferent and efferent pathways which mediate the reflex vasodilatation; and to assess the relative contribution of ventricular baroreceptors and baroreceptors in left atrium and pulmonary vessels in responses to left ventricular outflow obstruction. The gracilis artery and the cranial tibial artery to the paw were perfused separately at constant flow. Changes in perfusion pressure to each bed reflected changes in vascular resistance. Outflow obstruction was produced by inflating a balloon in the left ventricular outflow tract for 15 s while pressures in the left ventricle and aortic arch were measured.Inflation of the balloon increased left ventricular pressure and decreased pressure in the aortic arch. Low and high levels of obstruction produced dilator responses averaging -5+/-3 (SE) and -42+/-11 mm Hg in muscle and -1+/-1 and -3+/-2 mm Hg in paw. Denervation, phentolamine, and glyceryltrinitrate caused greater dilatation in paw than did left ventricular outflow obstruction. This indicates that dilator responses in the paw were not limited by a low level of resting neurogenic constrictor tone or by a negligible dilator capacity of these vessels.Obstruction to left ventricular inflow increased left atrial pressure, but did not cause reflex vasodilatation. This suggests that low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction.Vasodilator responses to outflow obstruction were blocked by bilateral vagotomy, sectioning the sciatic and obturator nerves, and administration of phentolamine, but were not decreased by atropine or tripelennamine.The results indicate that activation of left ventricular baroreceptors produces striking vasodilatation in skeletal muscle, but only slight vasodilatation in skin. The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin. Activation of sympathetic cholinergic or histaminergic dilator pathways does not contribute to the dilatation.     

Adrenergically Mediated Ventricular Fibrillation in Probucol-Treated Dogs: Roles of Alpha and Beta Adrenergic Receptors

A high incidence of sudden death due to ventricular fibrillation (VF) has been observed in dogs under chronic treatment with probucol, a new hypocholesterolemic agent. The present study describes the cardiac electrophysiologic properties of probucol-treated dogs and characterizes the electrophysiological response of these animals to manipulation of the autonomic nervous system. There was no significant difference in the spontaneous sinus cycle length, the QT interval, refractory period of the atrium, ventricle or A-V junction between normal and probucol-treated dogs. Epinephrine produced VF with few and sometimes no preceding premature ventricular extrasystoles. Electrical stimulation of the stellate ganglion induced VF in 16/19 dogs whereas stimulation of the right stellate ganglion induced VF in 1/19 dogs. Phenylephrine induced VF in 0/19 dogs, isoproterenol in 5/19 dogs, but phenylephrine + isoproterenol induced VF in 9/11 dogs in which isoproterenol did not produce VF. alpha (phentolamine) or beta (propranolol) blockade prevented initiation of VF by epinephrine, phenylephrine + is isoproterenol, and left stellate stimulation but alpha blockade did not prevent induction of VF by isoproterenol when isoproterenol alone produced VF. In this nonischemic model, we conclude that left stellate stimulation is a far more potent initiator of VF than right stellate stimulation and that induction of VF appears to require both alpha and beta adrenergic receptor stimulation.     

定量组织速度成像评价犬急性左心缺血心肌非同步运动的实验研究

目的 探讨定量组织速度成像(QTVI)评价犬急性左心缺血时心肌非同步运动的价值.方法 健康犬18只,暴露心脏,于左冠状动脉前降支阻断前(对照组)、后(实验组)分别获取左心室12个节段的QTVI曲线,测量各位点QRS波起点至心肌收缩期峰值速度的时间(Ts),计算同一壁内3个节段Ts差值(Intra-ΔTs)以及左心室12节段Ts的最大差值(Max-ΔTs).心室间的不同步指标测量QRS波起点到主动脉瓣血流频谱起点时间(Q-A),QRS波起点到肺动脉瓣血流频谱起点时间(Q-P)及其差值(Q-AP).结果 实验组缺血节段Intra-ΔTs和Max-ΔTs较对照组明显延长(P＜0.01),而Q-A,Q-P及Q-AP较对照组无明显变化(P＞0.05).结论 犬急性左心缺血时,左室内存在明显非同步运动,但心室间无明显不同步运动.     

两维超声心动图定量检测不同程度心肌缺血时局部左心收缩功能的变化

应用两维超声心动图（ＺＤＥ）定量检测１７只开胸犬在不同程度冠状动脉左旋支（Ｌｃｘ）狭窄和心肌缺血时的局部左室收缩功能（ＲＬＶＦ）。结果显示：在静息情况下，冠脉血流量（ＣＢＦ）减少超过４０％时，２ＤＥ可检测明显的ＲＬＶＦ异常；ＣＢＦ减少８０％时，ＲＬＶＦ完全丧失。中度心肌缺血时，室壁运动异常（ＡＷＭ）的范围较局限；但严重缺血或梗塞时，ＡＷＭ的圆周范围大于Ｌｃｘ供血的心肌范围，而室壁增厚异常的圆周范围仍小于或与Ｌｃｘ供血的心肌范围基本符合。ＲＬＶＦ与ＣＢＦ减少不呈线性相关，当静息ＣＢＦ减少超过４０％时，２ＤＥ才能检测到ＲＬＶＦ异常。在定量心肌缺血时，ＲＬＶＦ异常明显早于整体左心泵功能的异常变化。     

Promotion of Ventricular Tachycardia Induction by Procainamide in Dogs with Inducible Ventricular Fibrillation Late After Myocardial Infarction

The influence of procainamide on inducible ventricular tachyarrhythmias was evaluated in 35 dogs with experimental myocardial infarction, and 9 normal dogs. Programmed stimulation was performed from the right ventricular apex via a percutaneously positioned electrode catheter, using up to five extrastimuli before and after intravenous administration of procainamide (15 mg/kg). Procainamide levels in postinfarct dogs were 8.5 +/- 0.7 micrograms/mL (range 5.3-13.6 micrograms/mL). Procainamide exerted its greatest effect in postinfarct dogs with reproducible baseline ventricular fibrillation. Six of nine dogs (P less than 0.05) with ventricular fibrillation had sustained monomorphic ventricular tachycardia (cycle length: 147 +/- 4 msec) induced after procainamide administration. This ventricular tachycardia required significantly more extrastimuli than baseline ventricular fibrillation (3 +/- 0.3 extrastimuli before vs 4 +/- 0.3 extrastimuli after procainamide). Procainamide never converted ventricular fibrillation to ventricular tachycardia in normal dogs. Procainamide had minimal effect on inducible ventricular tachycardia after myocardial infarction. Ventricular tachycardia induction was abolished in only 2 of 17 dogs despite significant prolongation of electrophysiological parameters. Ventricular tachycardia cycle length, and the number of extrastimuli required were unchanged by procainamide in this subgroup. Conclusion: Ventricular tachycardia is insensitive to the antiarrhythmic properties of procainamide in this model. In contrast, procainamide is able to convert postinfarction ventricular fibrillation to ventricular tachycardia, presumably by promoting sustained, organized reentry. This previously undescribed action is an unusual form of proarrhythmic effect, and suggests that this drug should be used cautiously in patients after myocardial infarction.     

糖耐量减低患者神经传导速度及交感皮肤反应的研究

目的:观察糖耐量减低(IGT)患者神经传导速度(NCV)和交感皮肤反应(SSR)的变化。方法:对25例IGT患者(IGT组)、32例2型糖尿病(DM)患者(DM组)及18名对照者(对照组)进行一侧肢体NCV检测和四肢SSR检测。结果:与对照组相比,IGT组(除腓神经外)各根神经NCV均有不同程度减慢,但差异均无统计学意义;DM组(除胫神经外)各根神经NCV与对照组相比差异均减慢(P<0.05)。IGT组双下肢SSR起始潜伏期与对照组相比延长(P<0.05);与对照组相比,DM组四肢SSR起始潜伏期显著延长、波幅显著降低(P<0.01)。对照组、IGT组和DM组NCV异常率分别为5.56%、28.00%、65.63%,SSR异常率分别为33.33%、72.00%、93.75%,3组间NCV和SSR异常率均有显著差异(P<0.01)。在IGT和DM组中,SSR异常率均高于NCV异常率,且无症状者亦有一定的NCV和SSR异常率。结论:IGT患者存在临床或亚临床周围神经损害,以小纤维受累为主,大纤维受累较少且局限于感觉纤维;SSR对糖代谢紊乱相关的周围神经损害的早期诊断敏感性优于NCV,但其特异性较差。     

Examining Sympathetic Nerve Activity with Microneurography during Hypnosis: Untangling the Effects of Central Command

Using microelectrode recordings of postganglionic sympatheticaction potentials, the authors studied the effects of hypnotic suggestion on sympathetic outflow targeted to skin during static handgrip exercise. All subjects performed sustained handgrip at 33% maximal voluntary contraction (MVC) for 2 minutes during 3 consecutive trials. Two subjects randomly assigned to a hypnosis condition received suggestions that the 2nd trial was more difficult and the last trial was less difficult than the first trial. Two subjects randomly assigned to the control condition received no hypnosis or suggestions about task difficulty. In the nonhypnosis condition, skin sympathetic nerve activity (SNA) increased by 6% from baseline during the 2nd trial and 13% from baseline during the 3rd trial. In the hypnosis condition, skin SNA increased by 25% during the 2nd trial (suggestion of increased difficulty) and returned to baseline during the 3rd condition (suggestion of decreased difficulty). Therefore, the impact of central command on skin SNA is suggested by these results.     

声学定量技术检测左冠分支急性闭塞再通后左心室功能的实验研究

目的应用声学定量技术探讨实验犬左冠分支闭塞再通后的左心室整体功能改变。方法对7只实验犬使用冠状动脉球囊扩张技术制作左冠分支急性闭塞及再通动物模型;应用超声声学定量技术检测急性闭塞30min再通、90min再通、300min再通的左心室收缩、舒张功能。结果左冠分支急性闭塞30min再通后与闭塞前相比,射血分数0.50±0.11vs0.48±0.10、左室峰值射血率(6.95±0.73)EDV/svs(5.93±0.67)EDV/s,P>0.05,无显著差异,左室峰值充盈率(4.55±2.85)EDV/svs(6.06±2.69)EDV/s,P<0.05;左冠分支急性闭塞90min再通后与闭塞前相比,射血分数0.44±0.18vs0.48±0.10、左室峰值射血率(4.88±1.32)EDV/svs(5.93±0.67)EDV/s,P均<0.05;左室峰值充盈率(3.86±3.15)EDV/svs(6.06±2.69)EDV/s,P<0.01;但与300min再通相比,以上测值均明显恢复。结论(1)成功制作了冠状动脉急性闭塞再通的动物模型;(2)左冠分支急性闭塞30min再通后仅有舒张功能轻度损害;而闭塞90min再通后左室收缩功能、舒张功能均有损害,但较300min再通有明显改善。     

The Effects of Ventricular Pacing on Left Ventricular Geometry,Function, Myocardial Oxygen Consumption,and Efficiency of Contraction in Conscious Dogs

The effects of ventricular pacing on left ventricular (LV) dynamic geometry, function, and myocardial oxygen consumption (MVO₂) were measured in 12 conscious dogs using sonomicrometry, micromanometry, ultrasonic flow probes, and oximetry catheters during right atrial (A-) and right ventricular (V-) pacing at 150 beats/mm. Systolic function was quantified using slopes (M_w) and volume-intercepts (V_w) of linear relationships between end-di-astolic volume (EDV) and stroke work (SW) for data obtained during vena caval occlusion. V-pacing shifted SW-EDV relationships downward (M_w decreased from 97 ± 21 to 81 ± 21 Kerg/mL) and to the right (V_w increased from 14 ± 11 to 20 ± 12 mL) in comparison with A-pacing (P < 0.05). These functional changes correlated with altered contractile geometry manifest as early shortening in the septal free wall relative to anterior-posterior dimension (increased minor axis mid-wall eccentricity at end-diastole and begin-ejection). Steady-state LV power output decreased from 802 ± 213 mW during A-pacing to 514 ± 170 mW during V-pacing (P < 0.05), while MVO₂ remained relatively unchanged during V-pacing (10 ± 3 mL O₂/min vs 11 ± 3 mL O₂/min during A-pacing, P = NS). As a result, overall LV efficiency decreased from 0.24 ± 0.08 during A-pacing to 0.16 ± 0.06 during V-pacing (P < 0.05). These data illustrate the impact of V-pacing on dynamic LV geometry and function, including impaired LV work output at all physiological levels of preload. Most importantly, the relationship between LV work output and MVO₂ is depressed during V-pacing, emphasizing the interaction between LV mechanics and pump efficiency in intact subjects. As a result, measures taken to restore normal contractile geometry might improve LV efficiency and performance when V-pacing is necessary.     

斑点追踪成像技术定量评价急性心肌梗死患者左室收缩同步性

目的 探讨二维斑点追踪成像技术定量评价急性心肌梗死患者左室同步性临床价值.方法 46例急性心肌梗死患者和40例对照者接受二维超声检查,用斑点追踪成像软件分析测量收缩期纵向应变达峰时间(tssl)、收缩期径向和环向应变达峰时间(tssr,tssc).计算左室各节段达峰时间标准差(tssl-SD,tssr-SD,tssc-SD)及节段达峰时间最大差值(tssl-dif,tssr-dif,tssc-dif),测量纵向应变延迟指数(LSDI),LSDI≥25％作为左室不同步标准.同时运用改良Simpson双平面法测量左室射血分数LVEF.结果 急性心肌梗死组同步性参数较对照组增加(P＜0.001或P＜0.05);LSDI与LVEF呈负向线性相关(r=-0.786,P＜0.001).结论 二维斑点追踪技术能准确评价左室不同步性,纵向应变延迟指数LSDI与LVEF呈线性负相关.     

三维超声探讨实验犬心尖在左室收缩功能中的作用

目的应用三维超声(3DE)评价心尖在左室收缩功能中的作用。方法本实验在14只杂种犬中进行,用电加热器对实验犬的心尖进行加热,使加热区心肌完全坏死。用3DE检测左室射血分数(LVEF);测量损伤的心肌占左室整体心肌的比例。根据加热前、后LVEF的变化评价心尖在左室收缩功能中的作用。结果心尖加热后,LVEF减低[(58.3±5.5%)及(62.8±2.8)%,P0.01];加热区收缩期应变率减低(-0.78 s~(-1)±0.46 s~(-1)及-1.83 s~(-1)±0.72 s~(-1),P0.001)。心尖加热后,心尖损伤心肌占左室整体心肌的比例为(10.2±0.4)%,且损伤心肌的范围末超过解剖学的心尖范围。结论心尖在左室收缩功能中起重要作用;心尖在左室收缩功能中的作用与左室收缩顺序开始于心尖,使心尖首先参与收缩期芹室压力的形成,并与心尖的解剖位置有关。     

应用VFM技术评价心肌梗死患者左室收缩功能的初步探讨

目的 应用血流向量成像(vector flow mapping,VFM)技术对陈旧性心肌梗死(old myocardial infarction,OMI)患者收缩期左室心腔血流流场变化情况进行测定,初步探讨VFM技术评价OMI患者左室收缩功能方面的临床应用价值.方法 选择25例临床明确诊断为OMI患者作为病例组,另选35例正常健康体检者作为对照组.在VFM成像模式下观察两组二维血流速度向量分布特点并测量收缩期峰值流速(vectory,Vs)、峰值流量(flow,Fs)及取样线上的总流量(local-line qtotal,LQs);同时观察两组二维血流速度向量模式下左室心腔血流流场结构特征,并比较两组差异.结果 病例组基底段、中间段及心尖段收缩期血流Vs、Fs及LQs测值均低于对照组(P＜0.05),以心尖段为著;两组组内比较各项指标测值均呈由基底段至心尖段逐渐递减变化趋势(P＜0.01).病例组收缩早期、中期、晚期的血流速度向量分布宽度小于对照组,不对称,而且向量分布方向不集中,心尖段改变较明显.结论 VFM技术可观察和定量分析OMI患者左室心腔内血流流场的变化情况,可为临床提供一种较准确检测OMI患者左心功能的新方法.     

多普勒超声心动图评价多巴酚丁胺对心肌梗塞患者左室舒张功能的影响

目的：评价多巴酚丁胺对心肌梗塞患者左室舒张功能有何影响。方法：在静注多巴酚丁胺的同时应用二维和多普勒超声心动图观察３３例陈旧性心肌梗塞患者的心室壁运动及心内血流。结果：在多巴酚丁胺峰值剂量时，左室等容舒张时间（ＩＶＲＴ）和心率校正后的ＩＶＲＴ（ＩＶＲＴｃ）存活心肌（ＶＭ）组比无存活心肌（ＮＭ）组明显缩短，ＶＭ组的二尖瓣口血流Ａ峰用药后比用药前明显增高。结论：本研究提示，在多巴酚丁胺注射时ＩＶＲＴ和ＩＶＲＴｃ的变化对于检测存活心肌是一项敏感的参考指标     

二维应变对室壁运动正常冠心病的应用研究

目的 应用二维应变超声心动图(2DSE)定量分析常规方法 显示室壁运动正常冠心病患者的左室收缩运动,探讨其临床应用意义.方法 采集经冠脉造影证实的38例冠心病和31例对照组患者的心尖长轴、四腔和二腔观的二维灰阶动态图像,应用二维应变软件测量左室壁各节段的收缩应变、应变率及整体长轴应变(GLS),心尖双平面Simpson 法测量左室射血分数(LVEF),比较两组参数值及分析LVEF与GLS的相关性.结果 组间比较,各项常规超声指标均无统计学差异(P>0.05),部分节段的应变、应变率及GLS有统计学差异(P<0.05或P<0.01),LVEF与GLS呈良好相关性P<0.05).结论 二维应变与应变率互为补充,对评价缺血心肌的敏感性高于常规超声心动图.     

多普勒超声心动图评价多巴酚丁胺对心肌梗塞患者左室舒张？…

目的：评价多巴酚丁胺对心肌梗塞患者左室舒张功能有何影响。方法：在静注多巴酚丁胺的同时应用二维和多普勒超声心动图观察３３例陈阳性主肌梗塞患者的心室壁运动及心内血流。结果：在多巴酚丁胺峰值剂量时，左室等容舒张时间（ＩＶＲＴ）和心率校正后的ＩＶＲＴ（ＩＶＲＴｃ）存活心肌（ＶＭ）组比无存活心肌（ＮＭ）组明显缩短，ＶＭ组的二尖瓣口血流Ａ峰用药后比用药前明显增高。结论：本研究提示，在多巴酚下胺注射时ＩＶＲＴ和