生理学双语-循环-2

1,第二节 心肌的生物电现象,2,心肌细胞,工作细胞 心室 心房,自律细胞 窦房结 房室交界 房室束 蒲肯野纤维,心肌细胞的分类,3,528.1-529.1The heart is composed of three major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized (excitatory and) conductive muscle fibers.,4,The atrial and ventricular types of muscle contract in much the same way as skeletal muscle except that the duration of contraction is much longer.,5,工作细胞,6,7,8,Conversely, the specialized excitatory and conductive fibers exhibit rhythmicity and varying rates of conduction, providing an excitatory system that controls the rhythmical beating of the heart.,9,一、工作细胞(心室肌)的跨膜 电位及形成机制,10,11,（一） 静息电位 -90mV,形成机制 钾平衡电位,12,ventricular muscle fibers have stable resting membrane potentials of about -90 millivolts (mV) . This value approaches the K+ equilibrium potential.,13,（3）2期 平台期 0mv,（5）4期 静息期 -90mv,（二）动作电位,14,AP的形成机制O期 钠内流 钠通道的激活和失活都快，开放时间短，故称 快通道。可被河豚毒阻断。,15,1期 钾离子快速外流（Ito通道）2期 钾离子外流，钙离子内流， 两种离子流平衡。,16,钙通道激活和失活都慢，称为 慢通道。可被Mn2+和多种Ca2+阻断剂（如异博定，D-600等）所阻断。,17,3期 钾离子快速外流（Ik 通道） 4期 排钠和钙，摄钾。钠钾转运是依靠钠泵，,18,Phase 0is the upstroke of the action potential.is caused by a transient increase in Na+ conductance. This increase results in an inward Na+ current that depolarizes the membrane. At the peak of the action potential, the membrane potential approaches the Na+ equilibrium potential.,19,Phase 1is a brief period of initial repolarization.Initial repolarization is caused by an outward current, in part because of the movement of K+ ions (favored by both chemical and electrical gradients) out of the cell and in part because of a decrease in Na+ conductance.,20,Phase 2is the plateau of the action potential. ,.is caused by a transient increase in Ca2+. conductance, which results in an inward Ca2+ current, and by an increase in K+conductance.During the plateau, outward and inward currents are approximately equal, so the membrane potential is stable at the plateau level.,21,Phase 3is repolarization.During phase 3, Ca2+ conductance decreases, and K+ conductance increases and therefore it predominates.,22,The high K+ conductance results in a large outward K+ current, which hyperpolarizes the membrane back toward the K+ equilibrium potential.,23,Phase 4is the resting membrane potential.is a period during which inward and outward currents are equal and the membrane potential approaches the K+ equilibrium potential.,24,Action potentials of ventricular muscle fiber are of long duration.,25,26,二、窦房结细胞的跨膜电位及形成机制529.2-530.5,27,（一） 最大复极电位 -70mv,28,（二）动作电位,1、波形,特点：(1). O期除极速度慢，幅值小。(2)无1，2期。,29,30,(3).自律细胞的动作电位在3期复极末到达最大复极电位后，膜电位开始自动除极，称为4期自动除极 。除极到达阈电位后，产生新的动作电位。,31,0期： 缓慢Ca 2+内流3期: K+外流4期： 自动除极： K+外流进行性衰减 Na+ 内流进行性增强 T型钙通道激活，钙内流增加,2、机制,32,窦房结细胞0期除极由慢通道开放所成，该动作电位称为慢反应动作电位，而窦房结细胞称为慢反应(自律)细胞。,33,1. Sinoatrial (SA) node is normally the pacemaker of the heart It does not have a constant resting potential and exhibits phase 4 depolarization, or automaticity.,34,Phase 0is the upstroke of the action potential.is caused by an increase in Ca2+ conductance. This increase causes an inward Ca2+ current that drives the membrane potential toward the Ca 2+ equilibrium potential.,35,The ionic basis for phase 0 in the SA node is different from that in the ventricles, atria, (where it is the result of an inward Na+ current).,36,Phase 3is repolarization.is caused by an increase in K+ conductance. This increase results in outward K+ current that causes repolarization of the membrane potential.,37,phase 4is slow depolarization.accounts for the pacemaker activity of the SA node (automaticity).is caused by an increase in Na+ conductance, which results in an inward Na+ current called If.,38,三、浦肯野细胞的跨膜电位及形成机制,（一） 最大复极电位 -90mv,39,（二）动作电位,1、波形除4期呈现自动除极外，其余部分与工作细胞很相似。,40,41,0期： Na+ 内流3期: K+外流4期： K+外流进行性衰减 Na+ 内流进行性增强,2、机制,42,浦肯 野细胞O期去极以钠通道开放为 其机制,因此AP为快反应动作电位，浦肯 野细胞为快反应(自律)细胞。,43,四、心肌的电生理学分类,（一）根据0期去极化速度,（二）根据4期是否自动去极化,44,快反应非自律细胞,心室肌细胞,快反应自律细胞,浦肯野细胞,慢反应非自律细胞,结区,慢反应自律细胞,窦房结细胞,45,第三节 心肌的生理特性,自律性 兴奋性 传导性 收缩性,46,一、心肌的自动节律性 535.2,组织细胞在没有外来刺激时，能自动发生节律性兴奋的特性。,（一）概念,47,组织、细胞单位时间（每分钟）内能够自动发生兴奋的次数，即自动兴奋的频率，是衡量自动节律性高低的指标。,48,其中窦房结细胞自律性最高，约为每分钟100次，浦肯野纤维最低（约每分钟25次），而房室交界和束支的依次介于两者之间。,49,一个起搏点主宰整个心脏的整体活动：心脏始终是依照当时自律性最高的部位所发出的兴奋（AP）而兴奋与收缩。,50,窦房结的 自动节律性最高，其发出的兴奋（AP）控制心脏的兴奋与收缩，窦房结是心脏的正常起搏点 。此时的心律称为窦性节律。,51,潜在起搏点 窦房结以外的自律组织，正常情况下自律性不能表现，称为潜在起搏点 。,52,在异常情况时，窦房结以外的自律组织成为起搏点，称为异位起搏点。此时心律称为异位节律。,53,抢先占领和超速抑制窦房结对潜在起搏点的控制的两种方式。,54,抢先占领,55,（二）影响自律性高低的因素,1、4期自动除极速度,2、最大复极电位与阈电位间的差距,1, 2 图4-12,56,the sinus node (also called sinoatrial or S-A node), in which the normal rhythmical impulse is generated,57,The impulse normally arises in the sinus node. In some abnormal conditions, this is not the case because other parts of the heart can exhibit rhythmical excitation in the same way that the sinus nodal fibers do; this is particularly true of the A-V nodal and Purkinje fibers.,58,The A- V nodal fibers discharge at an intrinsic rhythmical rate of 40 to 60 times per minute, and the Purkinje fibers discharge at a rate somewhere between 15 and 40 times per minute. These rates are in contrast to the normal rate of the sinus node of 70 to 80 times per minute.,59,The intrinsic rate of phase 4 depolarization (and heart rate) is fastest in the SA node and slowest in the His-Purkinje system: SA node AV node His-Purkinje,60,Thus, the sinus node controls the beat of the heartbecause its rate of rhythmical discharge is greater than that of any other part of the heart. Therefore, the sinus node is the normal pacemaker of the heart.,61,The AV node and the His-Purkinje systems are latent pacemakers that may exhibit automaticity and override the SA node if SA node is suppressed.,62,A pacemaker elsewhere than the sinus node is called an ectopic pacemaker. An ectopic pacemaker causes an abnormal sequence of contraction of the different parts of the heart and can cause significant debility衰弱 of heart pumping.,63,Another cause of shift of the pacemaker is blockage of transmission of the impulses from the sinus node to the other parts of the heart. The new pacemaker then occurs most frequently at the A-V node.,64,When A-V block occurs-that is, when the cardiac impulse fails to pass from the atria into the ventricles ,and fails to continue to beat at the normal rate of rhythm of the sinus node, a new pacemaker develops in the Purkinje system of the ventricles and drives the ventricular muscle at a new rate somewhere between 15 and 40 beats per minute.,65,After sudden A-V bundle block, the Purkinje system does not begin to emit its intrinsic rhythmical impulses until 5 to 20 seconds later because, before the blockage, the Purkinje fibers had been overdriven by the rapid sinus impulses and, consequently, are in a suppressed state. During these 5 to 20 seconds, the ventricles fail to pump blood, and the person faints after the first 4 to 5 seconds because of lack of blood flow to the brain. If the delay period is too long, it can lead to death.,66,二、心肌的传导性530.6,67,（一）心脏内兴奋的传播途径,结间束房室结,68,Action potentials originating in the sinus node travel outward into these atrial muscle fibers. In this way, the action potential spreads through the entire atrial muscle mass and, eventually, to the A-V node,69,m/s,心房肌,优势通路,结区,左右束支,蒲肯野纤维,心室肌,71,房室交界兴奋传导慢（0.1秒),称为房室延搁,使房室舒缩有序,意义重大。房室交界兴奋传导慢，易发生传导阻滞。,72,73,The velocity of conduction is somewhat more rapid in several small bundles of atrial muscle fibers, (about 1 m/sec).,74,Atrioventricular Node, and Delay of Impulse Conduction from the Atria to the VentriclesThe conductive system is organized so that the cardiac impulse does not travel from the atria into the ventricles too rapidly; this delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins. It is primarily the A - V node and its adjacent conductive fibers that delay this transmission of the cardiac impulse from the atria into the ventricles.,Atrioventricular Node, and Delay of Impulse Conduction from the Atria to the VentriclesThe conductive system is organized so that the cardiac impulse does not travel from the atria into the ventricles too rapidly; this delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins.,75,It is primarily the A - V node and its adjacent conductive fibers that delay this transmission of the cardiac impulse from the atria into the ventricles.,76,Summary of the Spread of the Cardiac Impulse Through the HeartThe cardiac impulse from SA node spreads at moderate velocity through the atria but is delayed more than 0.1 second in the A-V nodal region before appearing in the ventricular septal ,A-V bundle.,77,Once it has entered this bundle, it spreads rapidly through the Purkinje fibers to the entire endocardial surfaces of the ventricles.,78,（三）影响心肌细胞传导性的因素,1、心肌细胞的直径直径小的细胞内电阻大，产生的局部电流小，兴奋传导速度也慢。而结区细胞直径很小，传导速度也最慢。,79,2、0期去极化的速度和幅度0期去极化的速度和幅度高,传导快。反之则慢。,80,在相对不应期或超常期内出现的期前兴奋，可引起升支缓慢、幅度小的动作电位，兴奋传导因之减慢。,81,3、临近部位的兴奋性临近未兴奋部位的兴奋性高，即膜电位和阈电位的距离小，传导速度就快。,82,三、心肌的兴奋性,兴奋性,excitability,83,Excitability is the ability of cardiac cells to initiate action potentials in response to inward, depolarizing current. reflects the recovery of channels that carry the inward currents for the upstroke of the action potential.changes over the course of the action potential. These changes in excitability are described by refractory periods .,84,（一）影响兴奋性的因素,1、静息电位与阈电位的距离（1）静息电位水平：静息电位（最大复极电位）增大时，距离阈电位的差距就加大，兴奋所需的刺激阈值增大，兴奋性降低。,85,（2）阈电位水平：阈电位水平上移，则和静息电位之间的差距增大，引起兴奋所需的刺激阈值增大，兴奋性降低。,86,2、Na+通道的性状备用状态 激活状态 失活状态,（二）心肌兴奋性的周期性变化,1、有效不应期：心肌细胞发生一次兴奋后，0期开始到3期膜电位-55mV时期内，不论受多强刺激，肌膜都不会反应，这时期称为绝对不应期；膜电位由-55mV到-60mV，如果给予强刺激，可发生局部电位，但不能引起动作电位。,心肌细胞兴奋开始后，由0期开始到3期-60mV不能再产生动作电位的时期，称为有效不应期。绝大部分钠通道失活。,2、相对不应期 3期 -60mV -80mV, 阈上刺激可产生AP。兴奋性低于正常。部分钠通道已复活，其余仍处于失活状态。,3、超常 期 3期 -80mV -90mV，阈下刺激可产生AP。兴奋性高于正常。小部分钠通道仍处于失活状态。,在相对不应期和超常期出现的动作电位， 0期去极化的速度和幅度低于正常，因此传导慢。,92,1. Absolute refractory period (ARP)-begins with the upstroke of the action potential and ends after the plateau.reflects the time during which no action potential can be initiated, regardless of how much inward current is supplied.,93,2.Effective refractory period (ERP)is slightly longer than the ARP.-is the period during which a conducted action potential cannot be elicited.,94,2.Relative refractory period (RRP)RRP is the period immediately after the ERP when repolarization is almost complete. It is the period during which an action potential can be elicited, but more than the usual inward current is required.,（三）心肌兴奋性变化与收缩活动的关系,1、心肌有效不应期长，相当于整个收缩期和舒张早期，在此期间内，任何强刺激都不能使心肌发生兴奋而收缩。心肌与骨骼肌不同，不发生完全强直收缩，非常有利于泵血功能。,2、期前收缩和代偿性间歇期前收缩 心肌受异常刺激，产生提前于正常节律的收缩。之后，有一段较长的心脏舒张期，称为代偿性间歇。,100,四、心肌的收缩性,收缩性,contractility,特点:一、对细胞外液中的Ca 2+有明显依赖在一定范围内，细胞外液中的Ca 2+浓度高，兴奋时(2期)内流的钙（通过肌膜和横管） 就增高，心肌收缩就随之加强。,二、同步收缩（全或无式收缩）心脏功能上是合胞体 ， 心肌以闰盘相连，可产生同步电活动。实际是两个合胞体。,103,C. Contractilityis the intrinsic ability of the cardiac muscle to develop force at a given muscle length. is also called inotropism. It can be estimated by the ejection fraction which is normally 0.55 (55%).,104,Positive inotropic agents produce an increase in contractility. Negative inotropic agents produce a decrease in contractility.,105,1. Factors that increase contractility (positive inotropism) a. Increased heart rate When more action potentials occur per unit time, more Ca2+ enters the myocardial cells during the action potential plateaus,More Ca2+ is released from the SR(Sarcoplasmic reticulum) , and greater tension is produced during contraction.,106,b. Sympathetic stimulation (catecholamines) via 1 receptorsincreases the force of contraction by two mechanisms:(1) It increases the inward Ca2+ current during the plateau of each cardiac action potential.(2) It increases the activity of the Ca2+ pump of the SR ,more Ca2+ is accumulated and thus more Ca2+ is available for release in subsequent beats.,107,c. Cardiac glycosides (digitalis)increase the force of contraction by inhibiting Na+,K+-ATPasein the myocardial cell membrane.As a result of this inhibition, the intracellular Na+ increases, diminishing the Na+ gradient across the cell membrane.,108,Na+- Ca2+ exchange (a mechanism that extrudes Ca2+ from the cell) depends on the size of the Na+ gradient and is diminished, producing an increase in intracellular Ca2+.,109,2. Factors that decrease contractility (negative inotropism)Paras