牵张家兔左心室所致的心律失常及链霉素的阻断作用

目的:研究复极末期牵张家兔左心室对心脏电活动的影响及其机制.方法:应用心室压力钳技术观察复极末期牵张刺激(120 mmHg,50 ms)对家兔心脏节律的影响,并用链霉素(500 μmol/L)对其机制进行探讨.结果:复极末期牵张刺激引起心律失常的发生(P<0.05),链霉素则抑制复极末期牵张的致心律失常作用(P<0.05).结论:利用心室压力钳技术对家兔左心室施加复极末期牵张刺激可导致心律失常的发生,而链霉素可抑制这种致心律失常作用,说明牵张激活离子通道在牵张刺激引起的心律失常中可能发挥作用.     

基于微机控制的心脏电生理刺激仪的研制

本文介绍一种新的基于微机控制的心脏电生理刺激系统。利用微机可视化界面设置各项刺激参数,然后通过串行口将所有参数传送给外接单片机系统,最后由微机启动控制单片机按照既定模式发放刺激脉冲,同时微机接收单片机反馈的当前状态参数并将其实时显示在可视化界面之上。实践表明,该系统较以往的电生理刺激仪而言功能完备,操作简单,并且监测实时,在临床心脏电生理治疗中具有很大的应用价值。     

刺激兔迷走神经引起的压抑心室纤颤作用

单个期前刺激引起急性缺血心脏能终止的心室纤颤。电刺激左侧颈迷走神经外周端可以缩短心室纤颤的持续时间。静脉注射β受体阻滞剂心得安后,刺激迷走神经对心室纤颤的作用消失。实验表示增加迷走神经的紧张性可能对终止室颤起有益作用。     

电刺激小脑顶核对主要心血管生理参数的影响

目的:本文通过研究电刺激小脑顶核对光电容积脉搏波的影响,探讨电刺激小脑顶核对于人体心血管系统产生的生理效应。方法:记录30位受试者在小脑顶核受刺激时的脉搏波数据,提取了上升支主波幅度H、上升沿斜率Slope、脉搏波波形特征量K值等5种波形特征值。对比分析在刺激中和刺激前后各特征值的变化并根据该变化描述电刺激小脑顶核所引起的生理变化。结果:电刺激小脑顶核使脉搏波呈现出灵敏的一过性变化。结论:特征值的变化反应出电刺激小脑顶核使外周血流量、外周阻力等生理参数发生了一过性的变化。     

评价狗心肌缺血性室性心律失常的电生理学方法

用冠状动脉Harris二期结扎并部分再灌注法及心肌梗塞恢复期的心脏程控刺激技术(PES),进行心电生理检查并诱发与终止室性心动过速(VT)和心室纤颤(VF),建立了狗心肌缺血/再灌注后VT/VF的在体心脏电生理学研究方法,对该方法的可靠性、实用性及其临床相关性进行了探讨。结果表明,狗心肌缺血/再灌注5～8d后用PES能可靠地、重复地诱发出VT/VF,再灌注的梗塞心肌是其电生理异常的病理基础,该方法具有较好的重复性,是一种有价值的电生理学研究方法。     

起搏器

对于心律不齐,特别是心率在每分钟30次以下者,要向心脏施以电刺激,使心跳恢复到正常,这种刺激装置叫心脏起搏器,或者简称为起搏器。为了对心脏施行电刺激,要从静脉向心室插入附有电极的导管,使用约5V,1ms的脉冲刺激,这种最简单的,给以一定周期的脉冲刺激起搏器,叫固定速度起波器。通常当自发心率恢复正常时,为了不使心率与起搏     

心电图检测的新产品

为简化心脏保健技术,以帮助医生提高诊断、治疗和监测病人。荷兰阿姆斯特丹的皇家飞利浦电子公司新近研发出PageWriter TC70十六导联全自动分析心电图机,可选择自动或手动方式,进行12导联等同步记录,以及长时间节律导联记录和周期记录。在记录常规心电图中,可自动完成节律导联的1分钟波形记录。另外,该仪器除了能进行实时记录心电波形外,还可通过“回顾”键,记录按此键之前lO秒的心电波形,让使用者能有选择地记录清晰、稳定的心电波形。     

128道心外膜电位标测系统的前置放大模块的设计

心电标测是心脏电生理机理研究的主要方法,也是临床精密诊断和对心律失常病灶进行精确定位的重要手段,特别适用于房颤等复杂心律失常电生理机制的研究.该文主要介绍了心外膜电位标测系统中的前置放大模块的设计,并根据实际需要,增加了右腿驱动电路.通过人体与动物实验检测,应用右腿驱动电路后均能得到清楚的心电波形.     

利用吸引电极记录家兔在体心脏单相动作电位的实验分析

本文分析了利用吸引电极记录家兔在体心脏单相动作电位(MAP)的实验技术。结果表明,吸引电极抽吸负压的大小是影响 MAP 记录稳定性的基本因素;电极部位的心肌出血则是引起 MAP 波形畸变的重要原因。兔心脏的心尖部位不易出血,因而是记录 MAP 的最适部位。改进的弹簧银球电极可以减少畸变波形。观察了缺血和几种特异性药物对 MAP 的影响,说明 MAP 能反映出心肌复极过程的变化,对于分析心肌的某些电生理特性有一定的实用价值。     

电压钳控制电流钳的设计

研究证明,传统膜片钳放大器在电流钳模式下记录到的快速电压信号会存在失真,且造成失真的根本原因是由于膜片钳的探头电路设计.为了克服这些缺陷重新设计了一种探头,新探头电路不仅能像传统的电压跟随器一样测量瞬态电压,而且适用于传统的电压钳工作模式.此外,一种命名为电压钳控制的电流钳技术被应用来改进传统的膜片钳放大器.用可变的低通滤波器来调整电压钳模块的响应速度,从而在实现膜电位钳位的同时准确记录快速电压信号.桥平衡电路用来消除命令电流流过串联电阻时带来的电压误差.而传统膜片钳中的快电容补偿环节则被改进用来补偿电极分布电容和探头放大器输入电容并提高电流钳模式下系统的响应速度.细胞模型实验结果表明,改进后的膜片钳放大器能够满足电生理研究中快速电位变化测量的需要.     

Mechanoelectrical excitation by fluid jets in monolayers of cultured cardiac myocytes.

Although the prevailing view of mechanoelectric feedback (MEF) in the heart is in terms of longitudinal cell stretch, other mechanical forces are considerable during the cardiac cycle, including intramyocardial pressure and shear stress. Their contribution to MEF is largely unknown. In this study, mechanical stimuli in the form of localized fluid jet pulses were applied to neonatal rat ventricular cells cultured as confluent monolayers. Such pulses result in pressure and shear stresses (but not longitudinal stretch) in the monolayer at the point of impingement. The goal was to determine whether these mechanical stimuli can trigger excitation, initiate a propagated wave, and induce reentry. Cells were stained with the voltage-sensitive dye RH237, and multi-site optical mapping was used to record the spread of electrical activity in isotropic and anisotropic monolayers. Pulses (10 ms) with velocities ranging from 0.3 to 1.8 m/s were applied from a 0.4-mm diameter nozzle located 1 mm above the cell monolayer. Fluid jet pulses resulted in circular wavefronts that propagated radially from the stimulus site. The likelihood for mechanical stimulation was quantified as an average stimulus success rate (ASSR). ASSR increased with jet amplitude and time waited between stimuli and decreased with the application of gadolinium and streptomycin, blockers of stretch-activated channels, but not with nifedipine, a blocker of the L-type Ca channel. Absence of cellular injury was confirmed by smooth propagation maps and propidium iodide stains. In rare instances, the mechanical pulse resulted in the induction of reentrant activity. We conclude that mechanical stimuli other than stretch can evoke action potentials, propagated activity, and reentrant arrhythmia in two-dimensional sheets of cardiac cells.     

Qualitative modeling of mechanoelectrical feedback in a ventricular cell

Mechanical changes in the heart muscle can influence its electrical properties through a process called mechanoelectrical feedback (MEF). This feedback can operate via changes in calcium dynamics during the cross-bridge cycle or via mechanosensitive (stretch-activated) channels. We present a four-variable ordinary differential equation (ODE) system that caricatures the electrical and mechanical activity of a ventricular cell and their mutual interactions. A three-variable excitable system with restitution properties of the FitzHugh-Nagumo type is coupled to a fourth equation which describes changes in cell length during a lightly loaded contraction. The resulting four-variable system models MEF in a cell and can be incorporated into spatially distributed models for mechanoelectric behavior during wave propagation in the cardiac tissue.     

Programmed electrical stimulation-induced arrhythmias in isolated hearts from adult and senescent rats

In isolated hearts from normal rats, we previously demonstrated an age-related increase of spontaneous ventricular arrhythmias. The aim of the present experiments was to test the possible effect of aging on ventricular arrhythmias induced by programmed electrical stimulation. Experiments were performed in isolated cardiac preparations of 6- and 24-month-old normal Wistar rat hearts. Programmed electrical stimulation (single or double premature stimuli following a stimuli train) was tested in isolated Langendorff perfused hearts during control perfusion, after left anterior descending coronary artery ligature and during global hypoxia. No significant differences were observed between adult and senescent hearts in the incidence of programmed electrical stimulation-induced ventricular arrhythmias during these three different situations. These experiments demonstrate that the cardiac "physiological" aging process is not associated with a greater propensity to programmed electrical stimulation-induced arrhythmias.     

Ventricular myosin light chain 1 is developmentally regulated and does not change in hypertension.

Cardiac myosin heavy chain (MHC) isoform distribution has been shown to undergo changes during development, in response to hormonal stimuli, and during pathologic states like hypertension. We initiated a study of myosin light chain 1 (MLC1) expression in cardiac tissue to determine whether MLC1 undergoes changes similar to those seen for MHC. We isolated a full length cDNA for the predominant MLC1 sequence in rat hearts. This gene is expressed in ventricular tissue at much higher levels than in atrial tissue. Based on its expression pattern and sequence homology, this cDNA encodes the rat ventricular MLC1 and has been named RVMLC1. RVMLC1 is expressed at very low levels in cardiac tissue during early development and is expressed abundantly after birth and in adult hearts. The expression of RVMLC1 was found not to change in the hearts of rats with renovascular hypertension.     

Mechanical efficiency of isolated in situ perfused hearts of the eel Anguilla australis

Administration of exogenous Ach to isolated in situ saline-perfused hearts of Anguilla australis via the perfusate, resulted in reduction in cardiac frequency (F). This reduction in F became significant at Ach concentrations of 10(-11) M or greater. A weak inotropic effect of Ach at the lowest concentration tested (10(-13) M) was also observed. Maximum power output of preparations was 2.94+/-0.26 mW gVM(-1). The mechanical efficiency of A. australis hearts working at 25 and 50% of maximum power under different conditions of stroke volume (SV) and F was investigated. Cardiac frequency was manipulated using a combination of temperature and Ach administration. Stroke volume was manipulated by regulating input pressure of the perfusate supplying the preparations (pre-load). Values of MEF from preparations generating flow under conditions of low F/ high SV (treated with Ach 10(-7) M) were significantly greater than under conditions of high F/ low SV (untreated). The MEF of preparations appears to be related to inotropic state. The negative inotropy and increased mechanical efficiency produced by Ach appears to be the opposite of the so-called 'oxygen-wasting' effect produced by the positive inotropic agents, the catecholamines. This effect of Ach may be related to the dependence of teleost myocardium on extracellular Ca(2+) for excitation-contraction coupling during the cardiac cycle.     

Stochastic behavior of atrial and ventricular intrinsic cardiac neurons.

To quantify the concurrent transduction capabilities of spatially distributed intrinsic cardiac neurons, the activities generated by atrial vs. ventricular intrinsic cardiac neurons were recorded simultaneously in 12 anesthetized dogs at baseline and during alterations in the cardiac milieu. Few (3%) identified atrial and ventricular neurons (2 of 72 characterized neurons) responded solely to regional mechanical deformation, doing so in a tightly coupled fashion (cross-correlation coefficient r = 0.63). The remaining (97%) atrial and ventricular neurons transduced multimodal stimuli to display stochastic behavior. Specifically, ventricular chemosensory inputs modified these populations such that they generated no short-term coherence among their activities (cross-correlation coefficient r = 0.21 +/- 0.07). Regional ventricular ischemia activated most atrial and ventricular neurons in a noncoupled fashion. Nicotinic activation of atrial neurons enhanced ventricular neuronal activity. Acute decentralization of the intrinsic cardiac nervous system obtunded its neuron responsiveness to cardiac sensory stimuli. Most atrial and ventricular intrinsic cardiac neurons generate concurrent stochastic activity that is predicated primarily upon their cardiac chemotransduction. As a consequence, they display relative independent short-term (beat-to-beat) control over regional cardiac indexes. Over longer time scales, their functional interdependence is manifest as the result of interganglionic interconnections and descending inputs.