2011年10月自考《生理心理学》必背知识汇总
自学考试《生理心理学》复习要点总结10
自学考试《生理心理学》复习要点总结10第十章运动和意志行为1.神经系统引起或调节肌肉的收缩功能主要是通过类似突触结构的装置——神经肌肉接点的功能实现的。
(1)终板电位：神经肌肉接点由神经末梢一再分支并膨大而成为终板(终扣)终板与肌纤维膜以一定间隙相联系。
神经末梢兴奋时终板释放神经递质乙酰胆碱，扩散到间隙后的肌膜上与受体结合产生终板电位。
(2)终板电位的性质类似突触后电位，是缓慢的级量反应，但它却比突触后电位强很多。
所以，终板电位总能激发肌纤维发放动作电位并沿它的全长传导，引起它的受损。
(3)肌纤维的细胞质内，启动了能量供给机制，使肌纤维中的肌球蛋白和肌动朊之间的横桥发生变化，两者发生相对位移，产生肌收缩运动。
2.运动单位：脊髓运动神经元的轴突一再分支，与许多肌纤维形成神经肌肉接点，该神经元兴奋发出神经冲动使这些纤维收缩。
每个脊髓运动神经元及其所支配的骨骼肌纤维称为运动单位。
神经效应器接点：平滑肌、腺体和心肌接受植物性神经支配，植物性神经末梢和它们之间的接点统称为神经效应器接点。
①无论是形态上还是功能上神经效应器接点、神经元之间突触可以存在多种神经递质，突触后神经元接受数以千计的突触前成分，即一个神经元可与大量其他神经元形成突触，这些突触的突触后电位可能是兴奋性的或抑制性的，它们之间发生时间和空间总和导致单位发放。
②神经肌肉接点中每个纤维只接受一个神经元的有髓鞘的轴突末梢，且只释放一种神经递质——乙酰胆碱，因而只能引起一种兴奋性终板电位。
③神经效应器接点中一个效应器细胞只接受一个神经元的无髓鞘神经纤维，可能有两类神经递质中的一种——乙酰胆碱或去甲肾上腺素。
3.肌梭：是一种特殊的本体感受器，即肌肉长度变化的感受器。
肌梭是单突触反射的反射感受器。
4.脊髓运动反射：其反射中枢位于脊髓的简单运动过程，它是其他复杂反射活动的基础。
脊髓运动反射分为：单突触反射、二突触反射、多突触反射。
5.单突触反射、反射中枢及生理意义?(1)单突触反射：在反射弧结构中只由感觉神经元和运动神经元形成的单个突触的反射，就是单突触反射。
2011年自学考试生理心理学串讲笔记第三章
2011年自考生理心理学串讲笔记 2.听觉失认症：患者大脑初级听皮层（颞横回的41区）、内侧膝状体、听觉通路、听神经和耳的结构与功能无异常所见，但却不能根据语音形成语词知觉或不能分辨乐音的音调，也有患者不能区别说话人的嗓音。
词聋患者大多数左颞叶22区或42区次级听觉皮层受损所致。
乐音失认症患者，多为右颞22区、42区次级听皮层受损所致。
3.体觉失认症：顶叶皮层的中央后回（3－1－2区）躯体感觉区结构与功能基本正常，但此区与记忆功能和语言功能的脑结构间联系受损，引起皮层性触觉失认症，实体觉失认症等多种类型的体觉失认症。
实体觉失认症，多为右半球顶叶感觉区与记忆中枢间的联系障碍，引起左手触觉失认症状。
总结：从上述多种类型的失认症中得出结论——失认症是知觉障碍，不是因该感觉系统的损伤，而是由高层次脑中枢间的联络障碍所致。
证明知觉是许多脑结构和多种脑中枢共同活动的结果。
即使是以其中一种感觉系统为主的知觉，无论是视知觉、听知觉还是躯体知觉，也是这些感觉系统与注意、记忆、语言中枢共同活动的产物。
二、知觉的细胞生理学基础 1.视觉功能柱、超柱及超柱的特征提取（多模式感知细胞及生理意义） （1）功能柱：具有相同感受野并具有相同功能的视皮层神经元，在垂直于皮层表面的方向上呈柱状分布，只对某一种视觉特征发生反应，从而形成了该种视觉特征的基本功能单位，所以称之为功能柱。
功能柱是感觉的基础。
有两种功能柱理论：特征提取功能柱和空间频率功能柱。
（2）超柱：在大脑视觉皮层中，具有相同感受野的多种特征检测细胞聚集在一起，形成了对各种视觉属性综合反应的基本单元，就是超柱。
超柱是简单知觉的生理基础。
（3）多模式感知细胞：在颞-顶-枕区之间的联络皮层和额叶联络区皮层中，都存在着“多模式感知细胞”，可以对多种信息发生反应，实现着多种感觉的综合反应过程。
多模式感知细胞，是知觉的细胞生理学基础。
（4）总之，皮层中的超柱和联络区皮层多模式感知细胞，在知觉形成中具有重要作用，并可能是知觉的结构和功能单元。
自学考试《生理心理学》复习要点总结
裂脑手术：为治疗一种癫痫偶尔进行的脑手术，医生切开连接大脑两半球的胼胝体。
切开胼胝体的病人就是裂脑人。
2．杏仁核：颞叶嘴端内部的结构，包括一系列的核，是边缘系统的组成部分。
恐惧中枢——杏仁核实验证据：杏仁核毁损可阻断大鼠对天敌和新异事物的恐惧。
刺激杏仁核可引起类似恐惧样的行为表现条件化学习和记忆中枢——杏仁基底外侧核条件恐惧表达中枢——杏仁中央核海马：海马：学习和记忆的重要脑区双侧海马受损会导致空间记忆严重破坏海马损伤导致的顺行性遗忘症3. 精神药理学：研究药物对神经系统和行为的效应科学。
拮抗剂：能对抗和抑制特定神经递质的突触后效应的药物。
安慰剂：给予有机体的一种替代生理活性药物的无活性物质，可用于控制实验中的给药效应。
4. 实验毁损法：实验动物脑组织的部分移除或毁损；可以推测，动物丧失的功能即是被毁损脑区的功能。
脑毁损研究是实验毁损法的同义词。
5. 光感受器：三原色编码我们的眼睛有三种不同的感受器，分别对三种不同的色调敏感。
人们能够看到的任何一种颜色，都可以通过混合光谱上的三种颜色获得。
三种视锥细胞：红，绿，蓝。
色觉就是由这三种视锥细胞负责的三种色觉缺陷：（1）红色盲：患者不能分辨红色和绿色，他们的视敏度是正常的，说明视网膜上不缺乏红绿视锥。
他们的红视锥细胞中填充的是绿视锥细胞的视蛋白。
（2）绿色盲，也不能分辨红色和绿色。
他们的绿视锥里填充的是红视锥细胞的视蛋白。
（3）蓝色盲，他们的视网膜上缺乏蓝视锥，视敏度没有受到明显的影响。
视网膜节细胞：对立加工编码红色和绿色为一对，黄色和蓝色为一对。
于是，视网膜上有两种颜色敏感性节细胞：红-绿细胞与黄-蓝细胞。
部分颜色敏感节细胞以中心-外周的方式进行反应。
对颜色不敏感的节细胞也接收视锥细胞的传入信息，但不同波长的光对于它们来说没有差别，它们只是简单地在其感受野的中心部和外周部编码视觉信息的相对亮度，这些细胞的作用相当于“黑-白-探测器”。
视网膜节细胞对不同波长的光的反应特征取决于三种视锥细胞与两种节细胞之间的神经回路的特点。
2011年10月自考《生理心理学》必背知识汇总
2011年10月自考《生理心理学》必背知识汇总1987年以来，逐渐将受体按其发生的生物效应机制和作用加以分类，如G-蛋白依存性受体家族、电压门控受体和自感受体等。
神经细胞间信息传递的化学机制并非总是如此复杂，当那些电压门控受体与神经递质结合时，就会直接导致突触后膜的去极化，产生突触后电位。
脑重量约占全身体重的2%，但其耗氧量与耗能量却占全身的20%，而且99%利用葡萄糖为能源代谢底物，又不像肝脏、肌肉等其他组织那样，本身不具糖元贮备，主要靠血液供应葡萄糖。
第一章感觉特异感觉系统和非特异感觉系统感受阈值：即刚能引起主观感觉或细胞电活动变化的最小刺激强度。
感受器的适应：随着刺激物长时间持续作用，感受灵敏率下降，感受阈值增高，此现象称感受器的适应。
感受野：把有效地影响某一感觉细胞兴奋性的外周部位，称为该神经元的感受野。
如果把微电极插在视觉中枢的某个神经元上，记录其电活动，凡能引起其电活动显著变化的视野范围，就是该视觉神经元的感受野。
第一节视觉眼的基本功能就是将外部世界千变万化的视觉刺激转换为视觉信息，这种基本功能的实现，依靠两种生理机制，即眼的折光成像机制和光感受机制。
前者将外部刺激清晰地投射到视网膜上，后者激发视网膜上化学和光生物物理学反应，实现能量转化的光感受功能，产生是感觉信息。
眼动的生理心理学机制：通过眼外肌肉的反身活动，保证使运动着的物体或复杂物体在网膜上连续成像的机制，也就是眼动的生理心理学机制。
眼睛的随意运动有哪几种方式?它的生理心理学意义是什么?答：眼睛的运动有许多方式，当我们观察位于视野一侧的景物又不允许头动时，两眼共同转向一侧。
两眼视轴发生同方向性运动，称为共轭运动。
正前方的物体从远处移向眼前时，为使其在视网膜上成像，两眼视轴均向鼻侧靠近，称为辐合。
物体由眼前近处移向远处时，双眼视轴均向两颞侧分开，称为分散。
辐合与分散的共同特点是两眼视轴总是反方向运动，称为辐辏运动★。
辐辏运动和共轭运动都是眼睛的随意运动。
生理心理学笔记摘要
1、生理心理学研究方法：揭示脑与心理（行为）关系的研究方法有以下：比较解剖法皮层刺激法毁损皮层法一侧麻醉法一侧电休克法反应时实验分耳双听技术分视野速示刺激法眼动研究技术斯佩里的“割裂脑”法计算机技术后新工具2、PET和FMRI的原理：正电子闪射脑扫描（positrum emission tomograph,PET）是利用放射性同位素葡萄糖H3探测脑细胞的活动情况，用电子计算机控制的三维摄影机扫描，显示人在某种思维活动中同位素在脑内相应区域的分布图。
FMRI：功能性磁共振成像(functional magnetic resonance imaging），（fMRI）：当人脑因在内外刺激作用下处于功能活动状态时，脑激活区的血流、血容积及血氧消耗增加，这导致磁共振信号的差异，从而可反映相关脑区的激活状态。
3、脑激活：脑激活是指神经元和神经胶质的生物化学和生物物理学活动的快速增强。
当脑激活时，突触区域的能量需求是最高的，葡萄糖和氧的额外需求导致脑区域性血流量的增加。
4、大脑皮质机能定位：1. 第I 躯体运动区：中央前回和中央旁小叶前部2. 第I 躯体感觉区：中央后回和中央旁小叶后部3. 视区：距状沟两侧的皮质4. 听区：颞横回5. 平衡觉区：中央后回下端头面部代表区6. 味觉区：中央后回下方的岛盖部7. 运动性语言中枢：额下回的后部8. 书写中枢：额中回的后部9. 听觉性语言中枢：颞上回的后部10. 视觉性语言中枢：角回11. 嗅觉区：海马回钩附近12. 内脏运动中枢：边缘叶5、静息电位：静息电位是指细胞未受到刺激时存在于细胞膜内外两侧的电位差。
细胞膜存在着电位差。
a 、特点：1、只要细胞维持正常的新陈代谢而未受外来刺激，静息电位就稳定在某一固定水平。
2、如果规定膜外电位为零，则膜内电位在-70—-90mV之间。
b、静息电位产生的机制：1、静息电位的产生是由细胞膜本身的特性所决定的。
2、细胞内液高K+ 和A-（有机负离子的总称），细胞外液中含3、有大量的的Na+、CL-等4、静息状态下神经细胞膜对K+的通透性是Na+的50倍。
2011年10月自考《生理心理学》必背知识2
2011年10⽉⾃考《⽣理⼼理学》必背知识2绪论1.兴奋性概念：是指机体对刺激发⽣反应的能⼒。
2.兴奋：功能活动的出现或由弱到强。
3.兴奋：动作电位的出现。
兴奋性:细胞或机体对刺激发⽣动作电位的能⼒。
4. ⽐较兴奋与兴奋性：兴奋性是兴奋的前提和基础，兴奋是兴奋性的表现5.不同标本兴奋性⽐较：阈值（衡量兴奋性⾼低指标）阈值（阈强度）：能引起机体、组织或细胞产⽣兴奋（动作电位）的最⼩刺激强度。
例如在⽐较三组学⽣制作神经肌⾁标本好坏时，常可⽤阈值来衡量制作结果：第⼀组阈值为4.1V；第⼆组阈值为4.9V；第三组阈值为8.9V。
（说明什么？）※兴奋性与阈值的关系：反⽐关系6.兴奋性是⼀种能⼒，因此它可以有、⽆之分，也有⾼、低之分。
7.内环境：细胞直接⽣存的环境，亦称细胞外液。
8.稳态定义：内环境的化学成分和理化性质保持相对稳定的状态。
9.神经调节的基本⽅式：反射：在中枢神经系统参与下，机体对内、外环境变化产⽣的适应性反应。
10.神经调节的特点:迅速.精确.作⽤局限、持续时间短11.体液调节的特点：缓慢.作⽤部位⼴泛.作⽤持续时间长12.⾃⾝调节特点调节幅度⼩、灵敏度低、但有⼀定的意义13.负反馈（1）负反馈定义：指受控部分发出的反馈信息抑制或减弱了控制部分的活动。
（2）意义：由于负反馈控制具有加强或减弱的双向作⽤特点。
因此，它的作⽤在于维持稳态。
14．正反馈（1）定义：指受控部分发出的反馈信息，促进或加强控制部分的活动。
（2）意义：使整个调控系统处于⼀种不断的重复与加强状态。
较为少见。
练习题1、判断组织兴奋性⾼低最常⽤的指标是（）A 阈电位 B 反应⼤⼩ C 阈强度D兴奋程度2、正好引起神经纤维兴奋的刺激是（）A阈刺激B阈下刺激C最⼤刺激 D 阈上刺激3. 最能反映内环境状况的体液部分是（）A.细胞内液 B.脑脊液 C.⾎液 D.淋巴液4. 正常⼈体内环境的理化特性经常处于（）A.固定不变 B.相对稳定C.随机多变 D.绝对不变A.条件反射B.⾮条件反射C.两者都是D.两者都不是1.光照⼀侧瞳孔时,另⼀侧瞳孔缩⼩,属于2.看到酸葡萄引起唾液分泌,属于A.神经调节B.体液调节C.⾃⾝调节D.神经体液调节3.回⼼⾎量增加使⼼肌收缩⼒增强,属于4.胰岛素调节⾎糖浓度,属于5.见到可⼝的⾷物,引起唾液分泌,属于6.平均动脉压在⼀定范围内升降时,肾⾎流量保持相对稳定,属于7.交感神经兴奋引起肾上腺髓质激素分泌,属于8. 维持机体稳态的重要调节过程是（）A.神经调节 B.体液调节C.正反馈调节 D.负反馈调节9. 下列中不属于正反馈调节的是（）A.降压反射 B.⾎液凝固过程C.分娩过程 D.排便和排尿反射填空1．⽣理学主要从、和三个不同⽔平进⾏研究。
10月自考《生理心理学》必背知识6
10月自考《生理心理学》必背知识6
第六章记忆的生理心理学基础
1.记忆痕迹理论：①短时记忆——神经回路中生物电反响振荡;长时记忆——神经生物学基础是生物化学与突触结构形态的变化。
②1小时的时间是短时记忆痕迹转变为长时记忆痕迹的必需时间。
③长时记忆痕迹是突触或细胞的变化，有3方面含义：突触前的变化——神经递质的合成、储存、释放等环节;突触后变化——受体密度、受体活性、离子通道蛋白和细胞内信使的变化;形态结构变化——突触的增多或增大。
2.海马的记忆功能：海马是端脑内一个特殊的古皮层结构，位于侧脑室下角的底壁，形似海马而得名。
海马不仅与学习记忆有关，还参与注意、感知觉信息处理、情绪和运动等脑调节机制。
3.海马的两个记忆回路：①帕帕兹环：海马→穹窿→乳头体→乳头丘脑束→丘脑前核→扣带回→海马，这条环路是30年代就认识到的边缘系统的主要回路，称为帕帕兹环。
②三突触回路(下面)：
3.三突触回路的特性，为什幺成为长时记忆的基础?(长时程增强效应及其。
2011年10月自考《生理心理学》必背知识4
SAGE-Hindawi Access to ResearchCardiology Research and PracticeVolume2011,Article ID532620,6pagesdoi:10.4061/2011/532620Research ArticleEffect of Exercise Training on Interleukin-6,Tumour Necrosis Factor Alpha and Functional Capacity in Heart Failure Neil A.Smart,1,2Alf rsen,3,4John P.Le Maitre,5and Almir S.Ferraz61Faculty of Health Science,Bond University,QLD4229,Australia2Department of Exericse Physiology,University of New England,Armidale NSW2351,Australia3Department of Cardiology,Stavanger University Hospital,4068Stavanger,Norway4University of Bergen,Institute of Medicine,5020Bergen,Norway5Mazankowski Alberta Heart Institute,Edmonton,Alberta,Canada T6G2B76Cardiovascular Rehabilitation Section,Institute Dante Pazzanese of Cardiology,S˜a o Paulo04011-002,BrazilCorrespondence should be addressed to Neil A.Smart,n smart@Received5October2010;Revised12January2011;Accepted14January2011Academic Editor:Gregory GiamouzisCopyright©2011Neil A.Smart et al.This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use,distribution,and reproduction in any medium,provided the original work is properly cited.Background.We pooled data from four studies,to establish whether exercise training programs were able to modulate systemic cytokine levels of tumour necrosis factor-alpha(TNF-alpha)and interleukin-6(IL-6).A second aim was to establish if differences in ExT regimens are related to degree of change in cytokines and peak VO2.Methods.Data from four centres relating to training protocol,exercise capacity,and cytokine measures(TNF-alpha and IL-6)were pooled for analysis.Results.Data for106CHF patients were collated(98men,age62±10yrs,wt79±14Kg).Patients were moderately impaired(peak VO216.9±4.4mls/kg/min),with moderate LV systolic dysfunction(EF30±6.9%),78%(83)had ischaemic cardiomyopathy.AfterExT,peak VO2increased1.4±3.4ml/kg/min(P<.001),serum TNF-alpha decreased1.9±8.6pg/ml(P=.02)and IL-6was not significantly changed(0.5±5.4pg/ml,P=.32)for the whole group.Baseline and post-training peak VO2changes were not correlated with change in cytokine levels.Conclusions.Exercise training reduces levels TNF-alpha but not IL-6in CHF.However, across a heterogenic patient group,change in peak VO2was not correlated with alterations in cytokine levels.While greater exercise volume(hours)was superior in improving peak VO2,no particular characteristic of ExT regimes appeared superior in effecting change in serum cytokines.1.IntroductionInflammatory activation with increased serum cytokine levels has been described by several authors as an important factor in the progression of the syndrome of chronic heart failure(CHF)[1–3].In multifactorial analyses,elevated lev-els of tumour necrosis factor-(TNF-)alpha and interleukin-(IL-)6have been identified as prognostic heart failure markers[4–6].Cytokines act as catabolic factors involved in the pathogenesis of muscle wasting and cardiac cachexia [3,7],and increased levels of serum TNF-alpha have been identified in patients with reduced skeletal muscle cross-sectional area and peripheral muscle strength[1].There also exists a statistical significant association between elevated serum cytokine levels(especially TNF-alpha)and New York Heart Association(NYHA)functional class as well as exercise intolerance[2].Inflammatory cytokines may alter skeletal muscle histology and have a negative impact on left ventricular remodelling and cardiac contractility[2, 3,8].The inflammatory response is also associated with progression of atherosclerosis[9],oxidative stress[10],NO impairment[11],vasoconstriction,endothelial cell apoptosis [12],and adverse vascular remodelling[13].Exercise training has been documented to improve the inflammatory profile in CHF by inhibition of cytokine-chemokine production,regulation of monocyte activation and adhesion,inhibition of inflammatory cell-growth signals and growth factor production,reduction of soluble apoptosis signalling molecules[12],and attenuation of monocyte-endothelial cell adhesive interaction[14].A study of277 patients with coronary artery disease reported a significant 41%reduction in high-sensitivity C-reactive protein following exercise training[15].A recent study of four-month duration,utilizing combined endurance/resistanceTable1:Studies identified in PUBMED,MEDLINE search.Study Subjects(Control)Year Cytokines measured% VO2Mode of Exercise Adamapoulos et al.[23]122001Soluble adhesion molecules13Home bike Adamopoulos et al.[12]242002TNF-alpha,Interleukin-615Home bikeConraads et al.[16]23(12)2002TNF-alpha,Interleukin-67.5Bike and resistance training Ferraz et al.[21]#30(10)2004TNF-alpha,Interleukin-623BikeGielen et al.[2]20(10)2003TNF-alpha,Interleukin-1,6andbetaIn both serum and skeletal muscle29BikeKaravidas et al.[24]16(8)2006TNF-alpha,Interleukin-6,107.5∗Electrical stimulationLarsen et al.[22]#282001TNF-alpha,Interleukin-6,88∗Aerobic endurance training and home bikeLarsen et al.[25]252008Plasma Chromogranin A(CgA)8∗Aerobic endurance training and home bikeLaoutaris et al.[26]382007TNF-alpha,Interleukin-612Low versus high intensity inspiratory muscle trainingLeMaitre et al.[17]#462004TNF-alpha,Interleukin-63Bike and electricalstimulationNiebauer et al.[27]18(9)2005TNF-alpha Interleukin-6,e-selectin11BikeSmart[28]#222008TNF-alpha,Interleukin-6,brainnatriurietic peptide(BNP)20BikeXu et al.[18]60(28)2002TNF-alpha Unknown Unknown ∗%change in6-minute walk distance(Peak VO2not measured).#Study used in this paper.training demonstrated reduced TNF-alpha receptor levels (TNFR1and TNFR2)and a significant(7.5%)increase in peak VO2in patients with ischemic cardiomyopathy, although changes in IL-6and TNF-alpha were not apparent [16].This effect on circulating levels of TNF-alpha receptors is also reported after6weeks of cycle ergometry[17].In this study,there were no alterations in IL-6,C-reactive protein (CRP),or TNF-alpha.In addition,electrical muscle stim-ulation provided no changes in any of the aforementioned rsen et al.[8]reported an11%increase in peak VO2following3months of endurance training;TNF-alpha was significantly reduced,and this decrease was significantly correlated to the increase in peak VO2.Adamopoulos[14] reported a13%increase in functional capacity with a 12-week cycle ergometry training program,which correlated with lower levels of soluble adhesion molecules.The authors later reported a strong and highly significant correlation between improvements in peak VO2(15%)and reduction in TNF-alpha,soluble TNFR-1and-2,and IL-6[12].Plasma TNF-alpha is also documented to decrease after twice daily6-minute walk tests in NYHA II/III heart failure patients[18].A recently published study reported absent von Willebrand factor(vWF)release upon exercise testing in heart failure patients;this normalised following6months of exercise training;other plasma endothelial markers were unaltered [19].Changes in skeletal muscle,but not systemic expression of TNF-alpha,IL-1-beta,and IL-6have been reported in heart failure patients undertaking a regimen of10minutes cycling,4–6times daily for6months[2].This exercise program resulted in large changes in functional capacity (29%),nearly twice the mean expected increment(17%) shown from our review of81heart failure exercise training studies[20].This study suggested the existence of a cytokine cascade where levels may be changed at altered rates in different tissues.As heart failure exercise training studies are often small,we sought by pooling data from four studies to establish whether exercise training programs were able to modulate systemic cytokine levels.A second aim was to establish if differences in ExT regimens are related to the degree of change in cytokines and peak VO2.2.MethodsWe searched PUBMED and MEDLINE for exercise training studies in heart failure patients that had measured one or more of the proinflammatory cytokines.The full list of studies is summarized in Table1.The focus of this work was interleukin-6and TNF-alpha as these cytokines were measured in10exercise training studies,the correspondence authors of which were contacted for their cooperation in collaboration.Authors were requested to provide individual patient data from their study;four centres provided data (Table2).One study was a conference proceedings abstract [21].Sufficient data were not available to analyse changes in other cytokines.Table2:Clinical characteristics and pharmacotherapy of the106 patients.Clinical characteristicsAge(Years)61.8±9.9 Male(%)98(92.5) Body mass(kg)78.7±13.7 Peak VO2(ml·kg−1·min−1)16.9±4.4 Diabetes(%)11(10) Previous myocardial infarction(%)86(81) Atrialfibrillation(%)27(26) NYHA class II/III49/57 LVEF(%)30±6.9 MedicationsBeta-blocker(%)44(42) ACE-inhibitor/antagonist(%)95(90) Digoxin(%)67(63) Nitrates(%)40(38)2.1.Blood Sampling and Analysis.In3studies,plasma or serum samples were obtained by venipuncture(arterial cannula used in Larsen’s study)and stored on ice.In all studies,venipuncture collections were taken between 0900,and1200,at least24hours and not more than 5days after the last exercise session,thus negating the effects of the intervention.Within one hour,samples were centrifuged at4◦C,1500–2000RPM for10minutes,and then separated into aliquots and stored at between−75◦C and −80◦C.Concentrations of IL-6or TNF-alpha were measured by commercially available enzyme-linked immunosorbent assays(ELISAs)(R&D systems Minneapolis,Minnesota) in all4studies.The intra-and interassay coefficients ofvariation were<10%for all assays.In one study,16healthy, male volunteers of approximately the same age(62±5years) served as controls[22]although this data was not included in our analyses.2.2.Metabolic Exercise Testing and Exercise Training.All four collaborating investigators completed baseline and posttraining metabolic exercise tests to establish functional capacity.Larsen and Smart used cycle ergometers with a15W and 10W per min stepped protocol,respectively;LeMaitre and Ferraz used a modified Bruce treadmill protocol.One study used a regime of supervised aerobic exercise training3times per week.Two studies used supervised cycle ergometry as the primary mode of exercise training[21,22], and one study used both home-based and neuromuscular stimulation of the legs[17].2.3.Data Extraction.Mode of training,program duration and exercise intensity were examined.Baseline and post-training cytokine levels,peak VO2,left ventricular ejection fraction(LVEF),clinical,demographic,and pharmacological characteristics of patients are shown in Table2.Table3:Exercise program parameters and change in primary outcome measures in the4studies.Ferraz Larsen LeMaitre Smart Weeks2412616 Minutes/Wk1359015090 Freq.sessions/Wk3353 Intensity(%max)67807070 Total hours545415482.4.Statistical Analysis.Paired student t-tests were used to analyse baseline and postintervention changes in cytokines and peak VO2.ANOV A(2×4)was used to analyse differences between the four datasets.Pearson correlation coefficients were established for change in cytokines and peak VO2.Univariate and multivariate regression analysis with change in TNF-alpha as the dependent variable were used to determine factors leading to cytokine change.Data are expressed as mean+/−standard deviation unless otherwise stated.Significance was accepted at the5%level(P<.05).3.Results3.1.Baseline Measures.The four collaborating authors pro-vided data on106patients(98male,age62±10yrs,body weight79±14Kg).Patients were moderately impaired(peak VO216.9±4.4mls/kg/min),with moderate LV systolic dys-function(EF30±6.9%).Seventy eight%(83)had an ischaemic cardiomyopathy(Table2).Adherence data relating to training regimes were87.2±1.9%[21]and85±12%[28] and were unavailable for the other2studies.3.2.Training Regimes.Regimes varied between3and5 exercise sessions per week,at an intensity of58–80%of peak VO2.Program durations were between6and24weeks, 90–150minutes per week,and total program hours varied between15and54hours(Table3).3.3.Pooled Posttraining Changes.After training,peak VO2 increased by1.4±3.4mL/kg/min or9%(P<.001)from 16.9±4.4to18.4±4.5,serum TNF-alpha decreased from a baseline value of13±15.2pg/mL by1.9±8.6pg/mL(P= .02),and IL-6increased slightly from a baseline value of 7.8±11.4pg/mL by0.5±5.4pg/mL(P=.32).Cytokinechanges for each study can be seen in Figure1.Body weight was unchanged following exercise training.None of the clinical,demographic,or pharmacologic variables were correlated with changes in circulating IL-6or TNF-alpha following training.The correlations between change in posttraining peak VO2and changes in TNF-alpha(r=0.023, P=.82)and IL-6(r=−0.12,P=.21)were not significant. Change in TNF-alpha was correlated with exercise session duration and anerobic threshold(both r=0.21,P= .31),univariate but not multivariate analysis identified that previous myocardial infarction,longer exercise session duration,and higher body mass index predicted change in TNF-alpha(r2=0.18,P=.001).302520151050−5−10−15−20−25IL-6TNF-αPeak VO 2Figure 1:Change in cytokines and peak VO 2across the four studies.3.4.Optimal Exercise Program Components for Peak VO 2and Cytokine Changes.A total exercise program duration of 54hours appeared to be superior than 15or 18hours in e ffecting change in peak VO 2(P <.001);however,no di fference was seen for change in cytokine levels.The longest program duration resulted in a greater increment in peak VO 2compared to 12weeks (P =.003)and 6weeks (P =.001),while peak VO 2or 6-minute walk distance was unchanged in the ExT programs of 6and 12weeks duration.4.DiscussionPooled data from four studies demonstrated that alterations in levels of the cytokines IL-6and TNF-alpha are not nec-essarily uniform.Increments in peak VO 2following exercise training are widely accepted;however,they may be unrelated to changes in cytokine levels.Moreover,changes in particular cytokines appear to be independent of one another.One can-not be sure about the variable e ffects of the di fferent program parameters and exercise adherence rates;nevertheless,the mean change in functional capacity from the four studies was 8%,suggesting that cumulatively the four exercise programs provided stimulus for a possible favourable change in cytokine expression.Interpretation of this pooled data is limited by the fact that several other centres did not supply data.Table 2suggests that study participants showed heterogeneity for age,peak,VO 2and beta-blocker use.4.1.Expectations of Favourable Changes in Cytokine Expres-sion.Moderate endurance activity in frail,elderly,but otherwise healthy persons has previously been reported to influence circulating cytokine levels [29].As our patients had mild to moderate heart failure,it is not surprising to observe that levels of systemic TNF-alpha were decreased after training,thereby initiating anti-inflammatory e ffects.The finding that IL-6was unchanged after training is more puzzling.However,one study has suggested that IL-6produced by exercising muscle is thought to exert an anti-inflammatory e ffect [30].These data suggest that production and removal of TNF-alpha and IL-6may be,at least partially,from independent mechanisms and may have opposing e ffects (inflammatory versus anti-inflammatory).Recent clinical trials have not shown benefit from treatments that target TNF-alpha.A clinical trial of etanercept (a TNF-alpha antagonist)therapy has cast doubt on the role of cytokines in the pathogenesis of heart failure [31].There are then implications for health professionals or researchers in the process of designing an exercise program for heart failure patients.Primary end points of CHF exercise programs should perhaps not include lowering cytokine levels as they may represent surrogate markers of e fficacy;this may be particularly true in patients with milder degrees of CHF.In this population,program design may be better focussed on the parameters such as program frequency (sessions/week),duration (number of weeks),and intensity that may have a greater e ffect on peak VO 2changes.Peak VO 2improvement from exercise training may be linked to attenuated levels of oxidative stress which in turn may attenuate cytokine expression.Previous work in healthy older adults [32]and heart failure patients [33]has shown intermittent exercise programs to be at least more e ffective in improving peak VO 2than a continuous regime that would produce greater cumulative oxidative stress.In our work,peak VO 2was not significantly changed in patients who exercised despite utilizing a reasonable volume of exercise to elicit functional capacity changes.In heart failure,the e ffect of inflammation,which may be due partly to inactivity,may manifest in the terminal disease phase.The study by Adamopoulos et al.[14]may provide the best evidence to date linking change in peak VO 2and cytokines in heart failure patients.The small cytokine change shown in our studies may be due to the fact that our patients exhibited mild to moderate heart failure symptoms.The par-ticipants in the study of Adamopoulos et al.[14]exhibited moderate to severe symptoms.In addition,our participants had higher left ventricular ejection fractions (30%versus 24%)than those of Adamopoulos et al.[14].Exercise train-ing has been shown to significantly reduce the local muscle expression of TNF-alpha,IL-1-beta,IL-6,and iNOS in the skeletal muscle of CHF patients [8].In turn,physical exercise has been shown to improve both basal endothelial nitric oxide (NO)formation and agonist-mediated endothelium-dependent vasodilation of the skeletal muscle vasculature in patients with CHF.The correction of endothelium dysfunction is associated with a significant increase in exercise capacity [34].These local anti-inflammatory and systemic e ffects of exercise may attenuate the catabolic wasting process associated with CHF progression [3].In addition to an overall beneficial e ffect on exercise capacity,combined endurance/resistance exercise training has an anti-inflammatory e ffect in patients with heart disease [16].These skeletal muscle and anti-inflammatory changes may explain why alterations in TNF-alpha levels are most likely to be observed in patients with moderate or severe heart failure.4.2.Conclusions.Exercise training reduces levels of TNF-alpha but not IL-6in CHF.However,across a heterogenic patient group,change in peak VO2was not correlated with alterations in cytokine levels.While greater exercise volume (number of hours)was superior in improving peak VO2,no particular characteristic of ExT regimes appeared superior in effecting change in serum cytokines. 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1.在突触间隙处ACh作用消失的主要方式是
A.被MAO灭活
B.被胆碱酯酶破坏
C.被神经末梢重新摄取
D.进入血管被带走
E.被COMT灭活
2.去甲肾上腺素作用消失的主要原因是
A.被酶破坏
B.被氧化
C.水解
D.摄取1
E.摄取2
3.α受体不存在于下列哪一组织?
A.皮肤粘膜血管平滑肌
B.骨骼肌纤维
C.膀胱括约肌
D.瞳孔扩大肌
E.胃肠括约肌
4.下列哪种表现不属于ß受体兴奋的效应。
A.支气管舒张
B.血管扩张
C.心脏兴奋
D.瞳孔扩大
E.肾素分泌
5.胆碱能神经不包括：
A 交感、副交感神经节前纤维
B 大部分交感神经节后纤维
C 副交感神经节后纤维
D 运动神经
E 支配汗腺分泌的神经
6.不属于β受体效应的是：
A 膀胱逼尿肌收缩
B 支气管扩张
C 心率加快
D 骨骼肌血管扩张
E 脂肪分解
7.β1受体主要分布于
A.肝脏
B.支气管平滑肌
C.血管
D.心脏
E.突触前膜
8.某受体激动后，引起支气管平滑肌松弛，此受体为：
A．受体 B. ß1受体 C. ß2受体 D.M受体 E.N1受体
1．B 2。
D 3。
B 4。
D 5。
B 6。
A 7.D .8.C
1.治疗青光眼宜首选
A.新斯的明
B.毒扁豆碱
C.加兰他敏
D.毛果芸香碱
E.以上均可
2.治疗重症肌无力药是
A.山莨若碱
B.琥珀胆碱
C.新斯的明
D.筒箭毒碱
E.毛果芸香碱
3.属于有机磷酸酯类中毒N2样症状的是
A.瞳孔缩小
B.大汗淋漓
C. 腹痛和腹泻
D.肌肉震颤
E.流涎
4.新斯的明的禁忌症为
A.手术后腹气胀、尿潴留
B.青光眼
C.机械性肠梗阻
D.重症机无力
E.阵发性室上性心动过速
5.以下何药不属于胆碱酯酶抑制药
A.加兰他敏
B.新斯的明
C.毒扁豆碱
D.吡斯的明
E.阿托品
6.解救有机磷中毒应用阿托品过量，宜用何药解救
A.新斯的明
B.毒扁豆碱
C.吡斯的明
D.毛果芸香碱
E.加兰他敏
7.切除支配虹膜的神经（即去神经眼）后再滴人入毛果芸香碱，则应：
A扩瞳 B.缩瞳 C.先扩瞳后缩瞳 D.先缩瞳后扩瞳 E.无影响
1.D
2.C
3.D
4.C
5.E
6.D
7.B
1.阿托品对眼的作用为
A．扩瞳、视近物清楚B．扩瞳、调节痉挛C.扩瞳、降低眼内压
D．扩瞳、调节麻痹E. 缩瞳、调节麻痹
2.阿托品治疗何种休克是可不受极量限制
A.出血性休克
B.感染性休克
C.心源性休克
D.神经性休克
E.过敏性休克
3.用药后引起口干、便秘、散瞳作用的药物是
A.普萘洛尔
B.酚妥拉明
C.阿托品
D.新斯的明
E.肾上腺素
4.胆绞痛时常利用
A.阿托品+哌替啶
B.阿托品+去痛片
C.阿托品+阿司匹林
D.阿托品+扑热息痛
E.以上均可
5.胃肠绞痛可选用
A.乙酰胆碱
B.新斯的明
C.毒扁豆碱
D.阿托品
E.阿司匹林
6..阿托品对有机磷酸酯类中毒症状无效的是：
A流涎 B.瞳孔缩小 C.大小便失禁 D.肌震颤 E.腹痛
7.山莨菪碱主要用于治疗
A 虹膜炎
B 胃肠绞痛和感染性休克
C 心动过速
D 青光眼E尿潴留
8.有关阿托品的各项叙述，错误的是.
A．阿托品可用于各种内脏绞痛B．可用于治疗前列腺肥大
C．对中毒性痢疾有较好的疗效D．可用于全麻前给药以制止腺体分泌
E．能解救有机磷酸酯类中毒
9.关于阿托品作用描述不正确的是
A.口干
B.多汗
C.中枢兴奋
D.心率加快
E.升高眼压
10.以下何药为骨骼肌松弛药
A.新斯的明
B.山莨菪碱
C.琥珀胆碱
D.阿托品
E.丙胺太林
11.解救筒箭毒碱中毒宜选用
A.阿托品
B.氯化钙
C.新斯的明
D.毛果芸香碱
E.丙胺太林
1.D
2.B
3.C
4.A
5.D
6.D
7.B
8.B
9.B 10.C 11.C
1.可兴奋a受体的药物是
A.酚妥拉明
B.酚苄明
C.间羟胺
D.普柰洛尔
E.异丙肾上腺素
2.肾上腺素不宜用于
A.支气管哮喘
B.过敏性休克
C.心跳骤停
D.甲亢
E.鼻出血
3.青霉素引起的过敏性休克宜首选
A.去甲肾上腺素
B.异丙肾上腺素
C.多巴胺
D.肾上腺素
E.阿托品
4.肾上腺素与局麻药合用的局麻目的是：
A.扩张气管，保持呼吸道通畅
B.预防过敏性休克的发生
C.预防手术出血
D.使局麻时间延长，减少吸收中毒
E.使局部血管扩张，使局麻药吸收加快
5.麻黄碱可用于何种哮喘
A.支气管哮喘急性发作
B.慢性哮喘
C.哮喘持续状态
D.心源性哮喘
E.以上均可
6.防治硬膜外和蛛网膜下腔麻醉时引起低血压的药是
A.东莨菪碱
B.后马托品
C.麻黄碱
D.新斯的明
E.DA
7.可增强心肌收缩力，又可扩张肾血管的药物是
A.肾上腺素
B.新福林
C.间羟胺
D. 多巴胺
E.麻黄碱
8.去甲肾上腺素正确的给药方法是
A.皮下注射
B.肌肉注射
C.静脉注射
D.静脉点滴
E.皮内注射
9.休克伴肾功能不良者应禁用
A.酚妥拉明
B.普柰洛尔
C.多巴胺
D.异丙肾上腺素
E.去甲肾上腺素
10.应用后脉压明显增大的药物是
A.NA
B.间羟胺
C.麻黄碱
D.肾上腺素
E.异丙肾上腺素
11.心动过缓传导阻滞宜选用
A.酚妥拉明
B.新斯的明
C.阿托品
D.普萘洛尔
E.苯肾上腺素
12.过量最易引起心律失常，心室颤动的药物是
A.肾上腺素
B.异丙肾上腺素
C.多巴胺
D.间羟胺
E.麻黄碱
1.C
2.D
3.D
4.D
5.B
6.C
7.D
8.D
9.E 10.E 11.C 12.A
1.肾上腺嗜鉻细胞瘤的鉴别诊断及防治的药是
A.东莨菪碱
B.噻吗洛尔
C.酚妥拉明
D.新斯的明
E.普奈洛尔
2.血栓闭塞性脉管炎宜选用
A.新斯的明
B.普萘洛尔
C.肾上腺素
D.酚妥拉明
E.间羟胺
3.以下何药为ß受体阻断剂
A.酚妥拉明
B.普萘洛尔
C.酚苄明
D.妥拉苏林
E.阿托品
4.β受体阻断药可治疗
A.支气管哮喘
B.心功能不全
C.甲状腺功能亢进
D.窦性心动过缓
E.房室传导阻滞
5. a受体阻断药的主要不良反应是
A.血糖过低
B.支气管哮喘
C.直立性低血压
D.心力衰竭
6. 肾上腺素的升压作用可被酚妥拉明
A.减弱
B.加强
C.不变
D.翻转
7.兼具抗心律失常，抗高血压，抗心绞痛的药物是
A.阿托品
B.普萘洛尔
C.异丙肾上腺素
D.硝酸甘油
E.可乐定
8.支气管哮喘患者禁用
A.肾上腺素
B.阿托品
C.异丙肾上腺
D.麻黄碱
E.普萘洛尔
9.长期使用β受体阻断剂突然停药可产生
A.心动过缓
B.血压过低
C.支气管哮喘
D.反跳现象
1.C
2.D
3.B
4.C
5.C
6.D
7.B
8.E
9.D。