钠离子和钾离子通道噪声扰动对神经网络 时空模式的影响

研究了钠离子和钾离子通道噪声扰动对Hodgkin-Huxley神经网络放电时空模式的影响. 发现无论钠离子通道噪声还是钾离子通道噪声扰动, 当取定一组温度、噪声强度, 随着耦合强度的增大, 神经网络放电时空斑图总能演化出螺旋波, 而且存在形成螺旋波所需的临界耦合强度. 分析发现钠离子通道噪声有利于神经网络螺旋波的形成, 而钾离子通道噪声不利于螺旋波形成. 结果还表明较低的温度能够使神经网络对噪声更加敏感. 最后, 讨论了特定参数下螺旋波与靶波之间的转化现象.     

心脏中的螺旋波和时空混沌的抑制研究

以Luo-Rudy相I心脏模型为基础,研究心脏中螺旋波和时空混沌的控制,提出了两种控制方法: (Ⅰ)通过交替改变细胞外钾离子浓度来产生平面波,再利用弱外电场辅助平面波抑制螺旋波和时空混沌; (Ⅱ)先提高细胞外钾离子浓度,然后利用外电场激发波的方式产生平面波,再用平面波去抑制螺旋波和时空混沌. 研究结果表明,只要适当选择控制参数,这两种方法都能够有效抑制螺旋波和时空混沌. 当心肌出现局部缺血时,在心肌缺血处就会出现高的细胞外钾离子浓度,在这种情况下, 可以采用电场发射波的方法来抑制心脏中的螺旋波和时空混沌.对这些控制方法的优点和控制机制做了解释.     

细胞外钾离子浓度延迟恢复对螺旋波的影响研究

在Luo-Rudy相I心脏模型中考虑了细胞外钾离子浓度的频率依赖性,并研究了细胞外钾离子浓度的延迟恢复对螺旋波动力学的影响.数值模拟结果表明,在螺旋波态下,细胞外钾离子浓度的延迟恢复会导致细胞外钾离子浓度周期振荡,其振荡周期和振幅随延迟恢复时间的增加而增加,进而导致出现呼吸螺旋波、多螺旋波共存、螺旋波做Lévy飞行式漫游、螺旋波通过不同方式消失等现象,这些结果与实验结果一致.     

用低通滤波方法终止心脏组织中的螺旋波和时空混沌

通过让心肌细胞钠离子通道的触发门变量延迟打开, 使介质具有激发延迟能力, 介质延迟激发时间随控制电压和刺激频率增加而增加, 当控制电压超过一个阈值时, 延迟激发介质具有低通滤波作用:低频波可以连续通过, 而高频波不能连续通过. 本文用Luo-Rudy相I模型研究了介质延迟激发对螺旋波和时空混沌的影响, 数值模拟结果表明: 当控制电压超过阈值时, 介质的延迟激发可有效消除螺旋波和时空混沌; 从小逐渐增大控制电压, 在钙最大电导率较小情况下, 延迟激发会导致介质激发性降低, 使螺旋波漫游幅度增大, 直至传导障碍导致螺旋波消失; 当钙最大电导率较大时, 延迟激发会导致螺旋波失稳变弱, 这样当控制电压增加到一定值时, 时空混沌可以演化成漫游螺旋波, 当控制参数被适当选取时, 观察到漫游幅度大的螺旋波漫游出系统边界消失现象, 继续增大控制电压将导致时空混沌直接消失.     

随机中毒对神经元网络时空动力学行为的影响

神经元细胞膜上的离子通道能够被一些有毒的化学物质阻断. 离子通道阻断会降低离子通道的电导率和激活通道数, 影响神经元的放电活动, 进而影响神经网络时空模式的动力学行为. 本文采用具有周期边界的近邻耦合Hodgkin-Huxley神经元网络, 数值研究了钠离子和钾离子通道随机中毒时神经网络时空模式的演化过程. 发现钠离子和钾离子通道随机中毒可以导致螺旋波破裂. 通过分析网络的放电概率, 发现钠离子通道随机中毒降低了神经网络的兴奋性, 且其对中毒的敏感程度与噪声强度有关; 钾离子通道随机中毒增强了神经网络的兴奋性. 与均匀的通道中毒相比, 随机通道中毒的神经网络具有更丰富的动力学行为. 最后, 采用无流边界条件对神经网络进行数值仿真, 得到了类似的结果. 该研究更真实地反映神经系统中毒时整体兴奋性的变化, 从另一个方面揭示离子通道中毒对网络时空行为的影响, 有利于更进一步理解离子通道在网络整体行为中的作用. 关键词： 神经网络 离子通道 随机中毒 时空动力学     

钾扩散耦合引起的心脏中螺旋波的变化

在某些情况下, 心肌细胞外的钾离子浓度是变化的, 钾离子的横向扩散会导致细胞外钾离子的聚集和产生钾扩散耦合, 用考虑钾扩散耦合的Luo-Rudy相I心脏模型研究了钾扩散耦合对螺旋波动力学的影响. 数值模拟结果表明: 当钾扩散耦合比较强时, 钾扩散耦合使细胞外钾离子浓度先升高, 然后做规则振荡, 导致螺旋波做无规则漫游; 观察到螺旋波的波臂宽度和频率随钾扩散耦合的强度增大而减小, 这样, 当钾扩散耦合足够强时, 钾扩散耦合可以消除螺旋波和时空混沌. 关键词： 钾扩散耦合 螺旋波 时空混沌     

通过抑制波头旋转消除心脏中的螺旋波和时空混沌

本文采用Luo-Rudy相I模型研究如何通过调控心肌细胞钠电流变化来控制心脏中的螺旋波和时空混沌,提出了这样的钠电流调控方案:当细胞将被激发时启动钠电流调节,若由模型方程得到的钠电流的绝对值小于钠电流控制阈值的绝对值,就让钠电流等于钠电流控制阈值,其他情况下则限制钠电流的绝对值不能高于一个给定的最大值;当膜电位上升超过-5 mV时,让钠电流自然演化.这种调节钠电流的方式保证了所有细胞几乎具有相同的钠电流幅值,从而使所有细胞具有相同的激发性,数值模拟结果表明,只要钠电流控制阈值达到一定临界值,就可以有效抑制螺旋波波头的旋转,导致螺旋波运动出系统边界而消失,以及时空混沌演化为螺旋波后消失,如果钠电流控制阈值足够大,螺旋波和时空混沌还可通过传导障碍而消失.这些结果能够为抗心律失常治疗提供新的思路.     

螺旋波动力学性质的元胞自动机有向小世界网络研究

以Greenberg-Hastings激发介质元胞自动机模型为基础,研究了有向小世界网络中重新连接概率p对螺旋波动力学行为的影响.对于在规则网络下的稳定螺旋波,施加有向小世界网络后发现:当p值较小时,原本稳定的螺旋波仍保持其稳定性.随着p的增大,先后观察到螺旋波持续漫游、螺旋波断裂以及螺旋波消失等现象.通过监测系统的激发比率,发现以上现象的产生源于介质激发性随p的增大而降低.同时还发现元胞周期的变化也与p有关. 关键词： 元胞自动机 螺旋波 激发介质 有向小世界网络     

Formation of virtual isthmus: A new scenario of spiral wave death after a decrease in excitability

Termination of rotating (spiral) waves or reentry is crucial when fighting with the most dangerous cardiac tachyarrhythmia. To increase the efficiency of the antiarrhythmic drugs as well as finding new prospective ones it is decisive to know the mechanisms how they act and influence the reentry dynamics. The most popular view on the mode of action of the contemporary antiarrhythmic drugs is that they increase the core of the rotating wave (reentry) to that extent that it is not enough space in the real heart for the reentry to exist. Since the excitation in cardiac cells is essentially change of the membrane potential, it relies on the functioning of the membrane ion channels. Thus, membrane ion channels serve as primary targets for the substances, which may serve as antiarrhythmics. At least, the entire group of antiarrhythmics class I (modulating activity of sodium channels) and partially class IV (modulating activity of calcium channels) are believed to destabilize and terminate reentry by decreasing the excitability of cardiac tissue. We developed an experimental model employing cardiac tissue culture and photosensitizer (AzoTAB) to study the process of the rotating wave termination while decreasing the excitability of the tissue. A new scenario of spiral wave cessation was observed: an asymmetric growth of the rotating wave core and subsequent formation of a virtual isthmus, which eventually caused a conduction block and the termination of the reentry.     

Two forms of spiral-wave reentry in an ionic model of ischemic ventricular myocardium

It is well known that there is considerable spatial inhomogeneity in the electrical properties of heart muscle, and that the many interventions that increase this initial degree of inhomogeneity all make it easier to induce certain cardiac arrhythmias. We consider here the specific example of myocardial ischemia, which greatly increases the electrical heterogeneity of ventricular tissue, and often triggers life-threatening cardiac arrhythmias such as ventricular tachycardia and ventricular fibrillation. There is growing evidence that spiral-wave activity underlies these reentrant arrhythmias. We thus investigate whether spiral waves might be induced in a realistic model of inhomogeneous ventricular myocardium. We first modify the Luo and Rudy [Circ. Res. 68, 1501-1526 (1991)] ionic model of cardiac ventricular muscle so as to obtain maintained spiral-wave activity in a two-dimensional homogeneous sheet of ventricular muscle. Regional ischemia is simulated by raising the external potassium concentration ([K(+)](o)) from its nominal value of 5.4 mM in a subsection of the sheet, thus creating a localized inhomogeneity. Spiral-wave activity is induced using a pacing protocol in which the pacing frequency is gradually increased. When [K(+)](o) is sufficiently high in the abnormal area (e.g., 20 mM), there is complete block of propagation of the action potential into that area, resulting in a free end or wave break as the activation wave front encounters the abnormal area. As pacing continues, the free end of the activation wave front traveling in the normal area increasingly separates or detaches from the border between normal and abnormal tissue, eventually resulting in the formation of a maintained spiral wave, whose core lies entirely within an area of normal tissue lying outside of the abnormal area ("type I" spiral wave). At lower [K(+)](o) (e.g., 10.5 mM) in the abnormal area, there is no longer complete block of propagation into the abnormal area; instead, there is partial entrance block into the abnormal area, as well as exit block out of that area. In this case, a different kind of spiral wave (transient "type II" spiral wave) can be evoked, whose induction involves retrograde propagation of the action potential through the abnormal area. The number of turns made by the type II spiral wave depends on several factors, including the level of [K(+)](o) within the abnormal area and its physical size. If the pacing protocol is changed by adding two additional stimuli, a type I spiral wave is instead produced at [K(+)](o)=10.5 mM. When pacing is continued beyond this point, apparently aperiodic multiple spiral-wave activity is seen during pacing. We discuss the relevance of our results for arrythmogenesis in both the ischemic and nonischemic heart. (c) 1998 American Institute of Physics.     

用钙离子通道激动剂抑制心脏组织中的螺旋波和时空混沌

本文以LuoRudy91模型为基础,研究心脏组织中的螺旋波和时空混沌的抑制.提出应用钙离子通道激动剂来提高慢速内行钙离子流的最大电导率—Gsi,达到抑制螺旋波和时空混沌的目的.研究结果表明:该方法可以有效抑制心脏组织中的螺旋波和时空混沌,即使系统出现含时外行钾离子流的最大电导率—GK分布不均匀,该控制方法仍然有效.对控制机理进行了分析.     

局部不均匀性对时空系统振荡频率的影响

以复金兹堡一朗道方程为模型,利用数值实验方法观察了时空系统中螺旋波斑图的演化行为,发现在局域非均匀参数条件下,系统的螺旋波可以受到该杂质区域的影响而演化成为稳定的靶波.研究表明,内传的螺旋波转换为稳定靶波的必要条件是非杂质系统和杂质系统的振荡频率相等且小于系统的固有频率,并在参数一频率空间形成一个特殊的V形区域,进一步分析表明,该V形区域具有左右对称、两侧靶波传播方向相反以及随杂质区域参数α_2的增大而向参数β_2减小方向平移等性质.     

利用短期心脏记忆消除螺旋波和时空混沌

在Luo-Rudy的心脏模型中引入了记忆效应, 该记忆效应表现为膜间电压的延迟耦合. 研究了记忆效应对螺旋波的影响, 数值模拟结果表明:心脏记忆可导致螺旋波无规则漫游;当延迟时间适当选取时, 增加记忆强度会导致螺旋波的频率减小, 如果记忆强度超过临界值, 心脏记忆效应还可以使螺旋波和时空混沌消失, 因为含时外行钾离子电流被心脏记忆过度抑制.     

具有早期后除极化现象的可激发系统中螺旋波破碎方式研究

在Greenberg-Hasting元胞自动机模型中引入了正常元胞和老化元胞,并规定只有老化元胞存在早期后除极化现象且早期后除极化可以激发其他元胞.在正常元胞和老化元胞均匀分布的情况下,研究了早期后除极化对螺旋波演化行为的影响,重点探讨了早期后除极化导致的螺旋波破碎方式.数值模拟结果表明:早期后除极化在比率约为26.4%的少数情况下不对螺旋波产生影响,在其他情况下则会对螺旋波产生各种影响,包括使螺旋波漫游、漂移、波臂发生形变以及导致螺旋波破碎和消失等.观察到早期后除极化通过传导障碍消失和通过转变为反靶波消失,早期后除极化导致螺旋波破碎有8种方式,包括非对称破缺导致的破碎、对称破缺导致的破碎、同时激发双波导致的破碎、非对称激发导致的破碎、整体传导障碍导致的破碎、整体快速破碎等.分析发现这些螺旋波破碎现象都与早期后除极化产生回火波有关,得到螺旋波破碎的总比率通常约为13.8%,但是在适当选取老化元胞密度和早期后除极化的激发下,螺旋波破碎比率可达到32.4%,这些结果与心律失常致死的统计结果基本一致,本文对产生这些现象的物理机理做了简要分析.     

时空调制对可激发介质螺旋波波头动力学行为影响及控制研究

本文首先研究了时空调制对可激发介质中周期螺旋波波头动力学行为的影响. 随着时空调制的增大, 螺旋波经历了周期螺旋波、外滚螺旋波、旅行螺旋波和内滚螺旋波的显著变化. 通过定义序参量来定量的描述由时空调制引起的螺旋波在不同态之间非平衡跃迁的临界条件, 及漫游螺旋波波头圆滚圆半径随调制参数的变化情况. 当时空调制增大到某个临界值时, 螺旋波发生了破碎; 再增加时空调制, 螺旋波则发生了衰减, 系统最终演化为空间均匀静息态. 在文中给出了螺旋波发生破碎和衰减的机理和原因. 最后将时空调制方法运用于漫游螺旋波, 实现了将漫游螺旋波控制成周期螺旋波, 或将其控制为空间均匀静息态.     

Development and transition of spiral wave in the coupled Hindmarsh--Rose neurons in two-dimensional space

The dynamics and the transition of spiral waves in the coupled Hindmarsh--Rose (H--R) neurons in two-dimensional space are investigated in the paper. It is found that the spiral wave can be induced and developed in the coupled HR neurons in two-dimensional space, with appropriate initial values and a parameter region given. However, the spiral wave could encounter instability when the intensity of the external current reaches a threshold value of 1.945. The transition of spiral wave is found to be affected by coupling intensity D and bifurcation parameter r. The spiral wave becomes sparse as the coupling intensity increases, while the spiral wave is eliminated and the whole neuronal system becomes homogeneous as the bifurcation parameter increases to a certain threshold value. Then the coupling action of the four sub-adjacent neurons, which is described by coupling coefficient D’, is also considered, and it is found that the spiral wave begins to breakup due to the introduced coupling action from the sub-adjacent neurons (or sites) and together with the coupling action of the nearest-neighbour neurons, which is described by the coupling intensity D.     

通过控制钙和钾离子流抑制心脏中的螺旋波和时空混沌

采用LuoRudy91心脏模型研究螺旋波和时空混沌的控制,提出联合使用钙通道激动剂和钾通道阻滞剂的控制策略来增大钙离子电导率和减小钾离子电导率,达到消除心脏组织中的螺旋波和时空混沌的目的.数值模拟结果表明,该方法可以有效抑制螺旋波和时空混沌,即使介质存在无扩散功能的缺陷时该方法仍有效.对控制机制做简单探讨.     

Influence of Control Parameters on the Competition Between Spiral Waves and Target Waves

In this paper we systematically investigate the influence of control parameters on the competition results between spiral waves and target waves. Driving frequency f, amplitude A and injection area n of the input signals are three important parameters and the competition results between spiral waves and target waves are influenced by these three parameters remarkably. Based on these understandings we can control spiral waves effectively by suitable combination these parameters to generate faster target waves. And the effective controllable parameter regions are also studied.     

Spiral Wave in Small-World Networks of Hodgkin--Huxley Neurons

The effect of small-world connection and noise on the formation and transitionof spiral wave in the networks of Hodgkin-Huxley neurons are investigated in detail. Some interesting results are found in our numerical studies. i) The quiescent neurons are activated to propagate electric signal to others by generating and developing spiral wave from spiral seed in small area. ii) A statistical factor is defined to describe the collective properties and phase transition induced by the topology of networks and noise. iii) Stable rotating spiral wave can be generated and keeps robust when the rewiring probability is below certain threshold, otherwise, spiral wave can not be developed from the spiral seed and spiral wave breakup occurs for a stable rotating spiral wave. iv) Gaussian white noise is introduced on the membrane of neuronsto study the noise-induced phase transition on spiral wave in small-world networks of neurons. It is confirmed that Gaussian white noise plays active role in supporting and developing spiral wave in the networks of neurons, and appearance of smaller factor of synchronization indicates high possibility to induce spiral wave.     

热敏神经元网络中螺旋波死亡和破裂的数值模拟

实验发现大脑皮层内出现螺旋波且螺旋波对神经元电信号传递有积极作用.利用细胞网络方法从对大脑皮层观察到的螺旋波进行数值模拟.以包含温度因子的热敏神经元模型在二维空间构造规则网络,研究了神经元膜片温度参数对神经元网络中螺旋波演化影响;定义了一类统计同步因子来刻画温度因子引起螺旋波相变(破裂和死亡)的临界条件.发现在规则网络下,当温度超过一定值后螺旋波会死亡和消失而导致整个网络达到均匀同步;在考虑了弱通道噪声情况下,螺旋波温度超越一定临界值则引起螺旋波的破裂.进一步分析了暂时性发烧昏迷的可能机制在于神经系统某些功能区螺旋波传播电信号的中断.