physiology静息状态下Na驱动力

电化学驱动力=Vm-E离流inwardcurrent,如Na+,Ca2+内流)outwardcurrent,如K+外流,Cl-内流)静息状态下Na+的驱动力静息状态下K+的驱动力局部电特点性(幅度呈“等级性(传导呈衰减反应可以总类型终板电位兴奋性突触后电慢波电发生器电膜电导的电压依赖性和时间依赖性动作电位的成因，GN和G依次增大相应离子发生跨膜扩散，复极化的因素GNa减小，GK增肌细胞的收ContractionofMuscle(肌束(肌纤维/肌细胞(肌原纤维(肌节/肌小节(肌丝

InteractionswiththeProductionofbody运动单位(motor一、骨骼肌神经-肌接头的传神经-肌接头（NMJ）接头前（pre-junctional接头后膜或终板（endplate接头间（junctional神经肌接头（NMJ）*ActivationofACh-gatedionchannel(nAChR)resultsinEnd-PlatePotential(EPP)神经肌接头传递（电-化学-电过程神经神经冲动到达末梢，接头前膜去极电压门控电压门控Ca2＋通道开放、Ca2囊泡向接头前膜移动、融合破裂至接头间EPPEPP电紧张性扩布至周围肌使其达到阈电位、爆发动作电Na＋内流使终板膜去极化NMJ兴奋传递的特征是电-化学-电的过程N末梢AP→ACh＋受体→EPP→肌膜具1对1①接头前膜传来一个AP，便能引起肌细胞兴奋和收缩一次（因每次h的量，产生的EP是引起肌膜P所需阈值的倍）。②神经末梢的一次AP只能引起一次肌细胞兴奋和收缩（因终板膜上含有丰富的胆碱酯酶，能迅速水解）。影响NMJ兴奋传递的因素阻断ACh受体：箭毒(curare)和α银环蛇毒，肌松剂如驰肌碘（Flexadil三碘季胺抑制胆碱酯酶活性：有机磷，的明自身免疫性疾病：MyastheniaGravis（抗体破坏ACh受体),Lambert-Eatonsyndrome（抗体破坏N接头前膜ACh↓：肉毒杆菌二、横纹肌细胞的兴奋-收缩耦兴奋-收缩耦联的结构基Longitudinaltubularsystem：LTriad：T管+终兴奋-收缩耦联的关键离子——L型钙通道和钙通骨骼肌细胞和心肌细胞的骨骼肌细胞和心肌细胞的钙回钙瞬变（calciumtransient）引起肌肉的收缩和舒兴奋-①肌膜电兴奋的传导②肌膜和T管上L型Ca2+通道激活calciumtransient);④触发肌丝滑行，肌细胞收缩三、横纹肌的收缩和舒肌丝的分子组粗肌丝（thick肌球蛋白横桥（cross-

细肌丝（thin肌动蛋白原肌球蛋白肌钙蛋白（troponin横纹肌收缩的原理—ZZMHZA直接肌细胞收缩时①相邻Z线靠近,即肌节缩短④明带和H带变窄slidingfilamentsZZMHZAICTICT白的相互作指横桥激活、与肌动蛋白结合、耗能摆动、获能解离、复位及再结合的周期性活动过程。20200s分解横桥与结合位点结合，分解横桥与结合位点结合，头原肌球蛋白位移细肌丝上的结合位肌节缩短肌节缩短,SourcesofBacktocalciumCa2+pumpinsarcoplasmicreticulum~100%inskeletal~70%incardiacOutofthe①Na+-Ca2+exchangerincell②Ca2+pumpincellDiseasesassociatedwithabnormalregulationtheintracellularCa2+inskeletal Malignanthyperthermia:geneticdefectinryanodinereceptor,1in15,000children,1in50,000adults;Halothane/etherorsuccinylcholinestimulateCa2+releasefromSR,resultingmusclerigidityandhyperthermiaCentralcoredisease:geneticdefectinryanodinereceptor;SRreleases/leakCa2+,whichisthenaccumulatedbymitochondria,resultinginmitochondrialCa2+overloadandhencelossofmitochondriaandmuscleweaknessBrody’sdisease:geneticdefectinSRCa2+pump(SERCA):painlessmusclecramduringexerciseduetoslowedCa2+Summary:SequentialeventsmusclecontractionandThesarcolemmaisdepolarizedandtheactionpotential(AP)propagates;TheactionpotentialspreadsinsidealongtheT-tubules;APistransmittedfromT-tubuletoterminalsacsofsarcoplasmicreticulum;Calciumisreleasedfromsarcoplasmicreticulumintosarcoplasm;Calciumbindstotroponinleadingtocooperativeconformationalchangesintroponin-tropomyosinsystem;Theinhibitionofactinandmyosininteractionisreleased;Crossbridgesofmyosinfilamentsareattachedtoactinfilaments;Tensionisexertedand/orthemuscleshortensbytheslidingfilamentCalciumispumpedbackintosarcoplasmicreticulum;Crossbridgesaredetachedfromthethinfilaments;Troponin-tropomyosinregulatedinhibitionofactinandmyosininteractionisActivetensiondisappearsandtherestlengthis四、影响横纹肌收缩效能的因肌肉收缩的形等张收缩(Isotoniccontractions):肌等长收缩(Isometric肌肉长度不变，张力增等张收IsotonicForce等长ForceIsometric骨骼肌动作电位、钙瞬变（calciumtransient）单收缩、复合收缩与强直收前负荷 后负荷(After-determineslengthofcross-bridgecyclesandhencetotalnumberofcross-bridgesinteractingwiththinfilaments;肌肉的收缩性intrinsicpropertiesofmusclesandneurohumoralfactorsaffectingthoseproperties前负荷（Preload)：肌肉收缩前所承受的负荷,决定了肌肉的初长肌节最适初长（2.0-2.2m）时，粗细肌丝佳，大于最适初长时，粗细肌丝↓，肌缩速度、小于最适初长时，细肌丝可缩短距离↓→↓大部分骨骼肌的静态长度即是其最适初长，故Optimalinitiallength也称Restinglength.肌 M Optimalinitiallength(resting后负荷(Afterload)：肌肉缩短过程中所承受的后负荷为0→肌缩速度、幅度↑后负荷↑→肌缩速度、幅度↓和张力；后负荷↓→肌缩速度、幅度↑和张力↓后负荷过大，虽肌缩张力↑，但肌缩速度、幅↓，不利作功后负荷过小，虽肌缩速度、幅度↑，但肌缩张↓，也不利作功肌缩能力：是指与负荷无关、决定肌缩TypesofskeletalTypeImuscleTypeIImuscleOtherSlowMyosinisoenzymeATPaserateCa2+-pumcapacityofsarcoplasmicLong,slow,posture-Fine,skilled五、平滑肌的收缩和舒MorphologicalandfunctionalMechanismsof形态学特involuntarymuscle;innervatedbyANS;foundprimarilyinthewallsofholloworgans;Spindle-shapedcellstypicallyarrangedinNot-tubules&littlesarcoplasmic eres(soarenotstriated)butaremadeupofthick&thinmyofilaments.Thinfilamentsinsmoothmuscledonotcontaintroponin;Calciumbindstocalmodulin.Thecalcium-calmodulincomplex'activates'myosinwhichthenbindstoactin&contraction(swivellingofcross-bridges)begins.Twotypesofsmooth多个单位平滑单个单位平滑肌（内脏平滑肌visceral,orunitary,smoothfoundinthewallsofholloworgans(e.g.,smallbloodvessels,digestivetract,urinarysystem,&reproductivesystem)multiplefiberscontra aunit(b ausei pulsestravleasilyacrossgapjunctionsfromcelltocell)&,insomecases,areself-excitable(generatespontaneousactionpotentials&multiunitsmoothconsistsofmotorunitsthatareactivatedbynervousfoundinthewallsoflargebloodvessels,intheeye(adustingtheshapeofthelenstopermit modation&thesizeofthepupiltoadju