2011年10月自考《生理心理学》必背知识10
生理心理学笔记总结归纳
精心整理第一章绪论1.生理心理学：生理心理学是研究心理现象的生理机制，即研究外界事物作用于脑而产生心理现象的物质过程的科学。
生理心理学正是以脑为中心，研究心理的生理机制或行为的生理机制。
2.研究对象和任务：生理心理学的研究对象是心理活动的生理机制，因此，研究并3.4.生理心理学研究方法和技术：●脑立体定位技术●脑损伤法●原理：大脑皮层机能定位说、大脑皮层机能等势说●具体方法：不可逆损伤:横断损伤吸出损伤电解损伤●可逆损伤:扩布性阻抑冰冻方法神经化学损伤●刺激法（电刺激法，化学刺激法）原理：任何心理和生理活动都是由神经系统的兴奋所引起，电刺激和化学刺激可以代替外部刺激。
●电记录法：原理：神经系统的兴奋是以生物电的形式表现出来的。
●生物化学分析法原理：机体活动受化学物质的影响（递质、受体），并且能●●耗竭能够提高皮层的脑电活动。
上行胆碱能系统的作用机制：一种可能性是胆碱能投射通过提高新意刺激的作用，帮助了刺激在皮层水平的加工，另一可能是通过提高信号/噪声比的机制而起作用。
4）上行5—HT系统的功能：5-HT的操作影响到与行为抑制有关的过程。
总结：蓝斑皮层NE系统有维持紧张或唤醒的情境下辨别能力的保护功能，因而参与了选择性注意的加工；中脑边缘DA系统和中脑纹状体DA系统有助于不同形式的行为激活，从而在认知或运动的传出中扮演重要角色；皮层胆碱能系统促进刺激在皮层水平的加工，在注意和记忆信息加工中处于基础地位；5-HT能系统有助于行为抑制即降低无关信息引起的活动，他与上述三个系统的功能是对立的。
这些上行网状模式，前额叶损伤导致了行动的选择性和组织性受到了破坏。
背外侧前额叶和扣带回是参与对许多不同新意刺激或微弱提示活动的注意的脑区。
注意的生理学过程：注意的转移机制：优势兴奋中枢的转移——优势兴奋中心从其他区域转移到这种强烈刺激的皮层代表点。
注意产生的中枢过程是兴奋和抑制的相互诱导大脑皮层上兴奋和抑制的相互诱导服从于优势原则——当有集体把某种事物作为自己心理活动的对象时，该事物在大脑皮层上引起一个强烈的优势兴奋中心，这个优势兴奋中心对皮层其他区域较弱的兴奋起抑制作用。
生理心理学
1.生理心理学是通过实验的方法研究外界事物作用于脑而产生心理现象的生理过程，主要揭示人类自身心理现象和行为的生理机制的科学。
心理学+信息科学+神经科学2.生理心理学研究技术和方法：脑立体定位技术、脑损伤法、刺激法、电记录法、生物化学分析法、分子遗传学法、脑成像技术。
3.电刺激法：用无伤害性的电流刺激脑的特定部位，观察心理行为的变化以确定该脑部位的功能；或者在使用电流刺激脑的某部位时记录其他脑部位的诱发电位等，以推测两个或多个脑区之间是否存在直接或间接关系。
4.化学刺激法：在脑的局部区域注射神经递质的激动剂等，观察它们对心理行为的影响。
警觉网络--影响注意系统从而改善对目标的动作速度脑内网状上行激活系统（去甲肾上腺素、多巴胺、胆碱、5-羟色胺）5.注意的神经网络定向网络--调整注意焦点到目标区域，并限制对指向区域的信息的输入。
顶叶、中脑的上丘和丘脑执行网络--注意的目标选择并执行。
额叶的部分区域包括扣带回6.注意从其产生的方式上来说是一种定向反射；注意产生的中枢过程是兴奋和抑制的相互诱导。
敏感化：神经系统中一些特殊细胞对任何刺激都有反应，随着刺激强度增大，更多的细胞参与反应，若某较弱刺激持续作用，相应的神经元放电也7.神经活动过程的双重模型会增加。
习惯化：某刺激重复出现时，参与相应反应的神经细胞就会疲劳；随刺激的每次重复，细胞的反应逐渐减弱。
8.感受器的适宜刺激：某能量形式的刺激作用于感受器，只需要极小强度就能引起相应的感觉。
这种能量刺激形式或种类就是该感受器的适宜刺激。
9.换能作用：感受器把作用于他们的各种有效刺激转换为相应的传入神经纤维上的动作电位或峰电位。
10.动作电位：是指可兴奋细胞受到刺激时在静息电位的基础上产生的可扩布的电位变化过程。
11.感受器的适应现象：刺激作用于感受器时，刺激仍在持续作用，但神经纤维的传入冲动频率已开始下降。
12.三级细胞：光感受细胞（视杆+视锥）；双极细胞；神经节细胞13.外侧膝状体：给光中心和撤光中心通道；XYW通道；左右信息通道；方位敏感性信息通道；空间频率通道；运动方向信息通道；颜色信息通道14.视皮层功能柱：有相同功能特性的皮层细胞，按规则的空间结构排列起来构成柱状。
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。
生理心理学考点整理
生理心理学复习第一章、绪论1.学科性质：政：传统观点认为生理心理学是心理学与生理学之间的边缘科学，近年来认为是心理学、神经科学和信息科学之间的边缘科学。
2.生理心理学与各个学科之间的融合：（1）与生理学、神经生理学：都是以动物为实验对象；都是以生理活动的控制为自变量，以心理和行为反响为因变量；（2）与普通心理学：都涉及到心理活动的生理机制问题。
（3）与神经心理学：都要了解心理活动的解剖学和生理学根底。
（4）与认知生理心理学：认知生理心理学是在生理心理学的根底上开展起来的，重视对高等灵长类动物的复杂认知活动的研究。
3.相关概念：〔1〕生理心理学与心理生理学：之间的差异越来越小，几乎可以等同。
心理生理学更加注重生理变化。
〔2〕精神病学与神经病学：精神病是一些心理活动障碍或疾病的总称；神经病指神经系统的器质性病变。
都与脑或神经系统障碍的问题有关，可以丰富、补充生理心理学的知识。
4.生理心理学研究的根本观点：一切心理过程都是脑细胞的有组织的整体活动；不无视整个神经系统的组织等级〔或水平〕关系。
5.传统生理心理学的研究途径〔研究途径的融合〕：（1）临床病理的研究：Phineas.Gage〔铁棍、额叶损伤--性情大变〕；前额白质切除术〔治疗精神病〕；（2）动物实验的研究：对动物的脑或整体施加干预；控制动物的行为〔PPT1-29〕6.生理心理学的研究方法〔传统的干预与测量技术，现代认知成像技术〕〔PPT1-30～42〕：〔1〕传统的干预与测量技术有脑实体定位技术、神经解剖技术、脑损伤技术、电刺激法、生物化学技术、电记录技术、脑成像技术〔传统的三大脑造影技〕、行为测量技术；〔2〕现代认知成像技术：计算机断层扫描构像技术〔CT〕、核磁共振扫描技术〔MRI〕、功能性核磁共振扫描技术〔fMRI〕、正电子发射断层构像技术〔PET〕。
7.脑损伤技术：通过破坏脑皮层或其他构造〔尤其高等动物脑深部构造〕来研究其机能。
〔PPT1-32〕（1）横断损伤：在中脑水平上〔上丘与下丘之间〕横断脑，横断以下局部称孤立大脑动物。
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。
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. AcknowledgmentThis work is supported in part by an MBF Research Grant Award2003and a scholarship from the National Heart Foundation of Australia.References[1]J.Niebauer,“Inflammatory mediators in heart failure,”Inter-national Journal of Cardiology,vol.72,no.3,pp.209–213, 2000.[2]S.Gielen,V.Adams,S.M¨o bius-Winkler et al.,“Anti-inflammatory effects of exercise training in the skeletal muscle of patients with chronic heart failure,”Journal of the American College of Cardiology,vol.42,no.5,pp.861–868,2003. [3]S.D.Anker and S.Von Haehling,“Inflammatory mediators inchronic heart failure:an overview,”Heart,vol.90,no.4,pp.464–470,2004.[4]J.Or´us,E.Roig,F.Perez-Villa et al.,“Prognostic value of serumcytokines in patients with congestive heart failure,”Journal of Heart and Lung Transplantation,vol.19,no.5,pp.419–425, 2000.[5]M.Rauchhaus,W.Doehner,D.P.Francis et al.,“Plasmacytokine parameters and mortality in patients with chronic heart failure,”Circulation,vol.102,no.25,pp.3060–3067, 2000.[6]A.Deswal,N.J.Petersen,A.M.Feldman,J.B.Y oung,B.G.White,and D.L.Mann,“Cytokines and cytokine receptors in advanced heart failure:an analysis of the cytokine database from the Vesnarinone Trial(VEST),”Circulation,vol.103,no.16,pp.2055–2059,2001.[7]S. D.Anker,W.Steinborn,and S.Strassburg,“Cardiaccachexia,”Annals of Medicine,vol.36,no.7,pp.518–529, 2004.[8]rsen,S.Lindal,P.Aukrust,I.Toft,T.Aarsland,and K.Dickstein,“Effect of exercise training on skeletal musclefibre characteristics in men with chronic heart failure.Correlation between skeletal muscle alterations,cytokines and exercise capacity,”International Journal of Cardiology,vol.83,no.1,pp.25–32,2002.[9]D.Tousoulis,M.Charakida,and C.Stefanadis,“Inflammationand endothelial dysfunction as therapeutic targets in patients with heart failure,”International Journal of Cardiology,vol.100,no.3,pp.347–353,2005.[10]S.Ichihara,Y.Yamada,G.Ichihara et al.,“Attenuation ofoxidative stress and cardiac dysfunction by bisoprolol in an animal model of dilated cardiomyopathy,”Biochemical and Biophysical Research Communications,vol.350,no.1,pp.105–113,2006.[11]O.Parodi,R.De Maria,and E.Roubina,“Redox state,oxida-tive stress and endothelial dysfunction in heart failure:the puzzle of nitrate-thiol interaction,”Journal of Cardiovascular Medicine,vol.8,no.10,pp.765–774,2007.[12]S.Adamopoulos,J.Parissis,D.Karatzas et al.,“Physical train-ing modulates proinflammatory cytokines and the soluble Fas/soluble Fas ligand system in patients with chronic heart failure,”Journal of the American College of Cardiology,vol.39, no.4,pp.653–663,2002.[13]S.Adamopoulos,J.T.Parissis,and D.T.Kremastinos,“Newaspects for the role of physical training in the management of patients with chronic heart failure,”International Journal of Cardiology,vol.90,no.1,pp.1–14,2003.[14]S.Adamopoulos,J.Parissis,C.Kroupis et al.,“Physical train-ing reduces peripheral markers of inflammation in patients with chronic heart failure,”European Heart Journal,vol.22, no.9,pp.791–797,2001.[15]ani,vie,and M.R.Mehra,“Reduction inC-reactive protein through cardiac rehabilitation and exercise training,”Journal of the American College of Cardiology,vol.43, no.6,pp.1056–1061,2004.[16]V.M.Conraads,P.Beckers,J.Bosmans et al.,“Combinedendurance/resistance training reduces plasma TNF-αreceptor levels in patients with chronic heart failure and coronary artery disease,”European Heart Journal,vol.23,no.23,pp.1854–1860,2002.[17]J.P.LeMaitre,S.Harris,K.A.A.Fox,and M.Denvir,“Changein circulating cytokines after2forms of exercise training in chronic stable heart failure,”American Heart Journal,vol.147, no.1,pp.100–105,2004.[18]D.Xu,B.Wang,Y.Hou,H.Hui,S.Meng,and Y.Liu,“Theeffects of exercise training on plasma tumor necrosis factor-alpha,blood leucocyte and its components in congestive heart failure patients,”Zhonghua Nei Ke Za Zhi,vol.41,no.4,pp.237–240,2002.[19]L.W.E.Sabelis,P.J.Senden,R.Fijnheer et al.,“Endothelialmarkers in chronic heart failure:training normalizes exercise-induced vWF release,”European Journal of Clinical Investiga-tion,vol.34,no.9,pp.583–589,2004.[20]N.Smart and T.H.Marwick,“Exercise training for patientswith heart failure:a systematic review of factors that improve mortality and morbidity,”American Journal of Medicine,vol.116,no.10,pp.693–706,2004.[21]A.Ferraz,E.A.Boochi,R.S.Meneghelo,I.I.Umeda,andN.Salvarane,“High sensitive C-reactive protein is reduced by exercise training in chronic heart failure patients:a prospective,randomized,controlled study,”Circulation,vol.110,pp.793–794,2004.[22]rsen,P.Aukrust,T.Aarsland,and K.Dickstein,“Effectof aerobic exercise training on plasma levels of tumor necrosis factor alpha in patients with heart failure,”American Journal of Cardiology,vol.88,no.7,pp.805–808,2001.[23]S.Adamopoulos,A.J.Coats,F.Brunotte et al.,“Physicaltraining improves skeletal muscle metabolism in patients with chronic heart failure,”Journal of the American College of Cardiology,vol.21,no.5,pp.1101–1106,1993.[24]A.I.Karavidas,K.G.Raisakis,J.T.Parissis et al.,“Functionalelectrical stimulation improves endothelial function and reduces peripheral immune responses in patients with chronic heart failure,”European Journal of Cardiovascular Prevention and Rehabilitation,vol.13,no.4,pp.592–597,2006.[25]rsen,K.B.Helle,M.Christensen,J.T.Kvaloy,T.Aars-land,and K.Dickstein,“Effect of exercise training on chro-mogranin A and relationship to N-ANP and inflammatory cytokines in patients with chronic heart failure,”International Journal of Cardiology,vol.127,no.1,pp.117–120,2008.[26]outaris,A.Dritsas,M.D.Brown et al.,“Immuneresponse to inspiratory muscle training in patients with chronic heart failure,”European Journal of Cardiovascular Pre-vention and Rehabilitation,vol.14,no.5,pp.679–685,2007.[27]J.Niebauer,A.L.Clark,k.M.Webb-Peploe,and A.J.Coats,“Exercise training in chronic heart failure:effects on pro-inflammatory markers,”European Journal of Heart Failure, vol.7,no.2,pp.189–193,2005.[28]N.Smart,“Effects of exercise training on functional capacity,quality of life,cytokine and brain natriuretic peptide levels in hart failure patients,”Journal of Medical and Biological Sciences,vol.2,no.1,2008.[29]J.S.Greiwe,B.Cheng,D.C.Rubin,K.E.Yarasheski,and C.F.Semenkovich,“Resistance exercise decreases skeletal muscletumor necrosis factorαin frail elderly humans,”FASEB Journal,vol.15,no.2,pp.475–482,2001.[30]A.M.W.Petersen and B.K.Pedersen,“The anti-inflammatoryeffect of exercise,”Journal of Applied Physiology,vol.98,no.4, pp.1154–1162,2005.[31]D.L.Mann,J.J.V.McMurray,M.Packer et al.,“Targetedanticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL),”Circulation,vol.109,no.13,pp.1594–1602, 2004.[32]N.Morris,G.Gass,M.Thompson,G.Bennett,D.Basic,andH.Morton,“Rate and amplitude of adaptation to intermittentand continuous exercise in older men,”Medicine and Science in Sports and Exercise,vol.34,no.3,pp.471–477,2002. 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生理心理学必备考点
生理心理学必备考点生理心理学期末复习1. “全或无”定律每个神经元都有一个刺激阈值，对阈值以下的刺激不发生反应，对阈值以上的刺激，不论其强弱均给出同样幅值的神经脉冲发放。
2. 统觉性失认症患者对一个复杂事物只能认知其个别属性,但不能同时认知事物的全部属性,故又称同时性视觉失认症。
这种失认症可能是V2区皮层以及与支配眼动的皮层结构间联系受损,如与中脑的四叠体上丘或顶盖前区眼动中枢的联系遭到破坏,不能通过眼动机制连续获得外界复杂物体的多种信息3. 感受野在神经系统中，每一个神经元在它的感受器都有其代表区（范围），只要这个代表区受到刺激，这个神经元就产生反应，这个代表区就被称为神经元的感受野。
4. 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。
5. 朝向反射由新异性强刺激引起机体的一种反射活动，表现为机体现行活动的突然中止，头面部甚至整个机体转向新异刺激发出的方向，通过眼耳的感知过程探究新异刺激的性质及其对机体的意义。
6. 多模式感知细胞颞下回的一些神级元，不仅对复杂视觉刺激物单位发放率增加和发生最大的反应，而且对多种其他感觉刺激均可引起其单位发放率的变化。
因此，这类神级元称为多模式感知细胞。
7. ADHD儿童注意缺陷多动障碍8.失认证是感觉到的物象与记忆的材料失去联络而变得不认识。
9.辐辏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；相反，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。
10. 中枢神经系统中枢神经系统分为脊髓和脑，脑又分为大脑小脑间脑脑干，脑干又包括延脑桥脑中脑。
11. 级量反应其电位的幅值随阈上刺激强度增大而变高，反应频率并不发生变化。
简答题1.简述感觉系统的基本功能①区别不同形式的能量②反应刺激的不同强度和质量③反应的信度④反应的速度⑤抑制无关信息2. 知觉的恒常性是指什么？当客观事物本身不变，但它给予我们的感觉刺激，由于某些别的条件的变化而在一定限度内有变化时，我们的知觉不变。
生理心理学复习资料
生理心理学主要内容导论（学科本质、历史发展、研究方法）人体的神经系统各种心理现象的的生理心理学基础●感觉的生理心理学基础●知觉的生理心理学基础●注意的生理心理学基础●记忆的生理心理学基础●言语、思维的生理心理学基础●本能与动机的生理心理学基础●情绪与情感的生理心理学基础●人格的生理心理学基础第一章导论学科本质、研究意义、历史发展、研究方法生理心理学的学科本质一、定义：生理心理学是研究心理现象的生理机制，即研究外界事物作用于脑而产生心理现象的物质过程的科学。
二、研究对象：心理现象的生理机制，尤其是脑机制。
三、研究任务：研究并揭示心理现象产生过程中有机体的生理活动过程，特别是中枢神经系统和大脑的活动方式。
四、学科特点：基础性；理论性；交叉性的边缘学科。
——生理心理学与生理学、神经解剖学、神经生理学、生物化学、药物学、神经病学、神经心理学、内分泌学以及行为遗传学等都有密切的联系。
五、需具备的知识：1. 心理活动的基本概念心理活动是脑对外界世界的反映过程。
外部刺激→【心理活动】→反应[认识过程一一感知、记忆、思维、想象等心理过程[情感过程一一对事物的态度体验过程[意志过程一一意志行动的心理过程心理状态一一注意、灵感、激情、心境、信心、犹豫等。
个性心理[个性倾向性一一需要、动机、兴趣、信念、理想、价值观等[个性心理特征一一能力、气质、性格2. 精神疾病与精神病学的基础知识精神病是一些心理活动发生障碍的各种疾病的总称。
精神障碍是一类具有诊断意义的精神方面的问题，特征为认知、情绪、行为等方面的改变，可伴有痛苦体验和/或功能损害。
阿尔茨海默病（认知、记忆损害、人格改变）抑郁症（病态抑郁体验）儿童注意缺陷障碍（多动）。
精神病学（精神医学）是研究精神疾病病因、发病机制、临床表现、疾病发展规律以及治疗和预防的一门学科。
研究对象：由重性精神障碍向轻性精神障碍转变服务模式：封闭式管理转向开放式或半开放式管理新的药物出现、重视康复、预防复发精神障碍患者的预后已大为改观。
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原文地址：初中化学《化学式、化学方程式和反应现象归纳大全作者：永久的磐石一、化学式书写二、化学方程式、反应现象、应用1. 2Mg+O2点燃或Δ2MgO 剧烈燃烧.耀眼白光.生成白色固体.放热.产生大量白烟白色信号弹2. 2Hg+O2点燃或Δ2HgO 银白液体、生成红色固体拉瓦锡实验3. 4Al+3O2点燃或Δ2Al2O3银白金属变为白色固体4. 3Fe+2O2点燃Fe3O4剧烈燃烧、火星四射、生成黑色固体、放出大量热5. C+O2点燃CO2剧烈燃烧、白光、放热、使石灰水变浑浊6. S+O2点燃SO2剧烈燃烧、放热、刺激味气体、空气中淡蓝色火焰.氧气中蓝紫色火焰7. 2H2+O2点燃2H2O 淡蓝火焰、放热、生成使无水CuSO4变蓝的液体（水）高能燃料8. 4P+5O2点燃2P2O5剧烈燃烧、大量白烟、放热、生成白色固体证明空气中氧气含量9. CH4+2O2点燃2H2O+CO2蓝色火焰、放热、生成使石灰水变浑浊气体和使无水CuSO4变蓝的液体（水）甲烷和天然气的燃烧10. 2KClO3 MnO2Δ 2KCl +3O2↑ 生成使带火星的木条复燃的气体实验室制备氧气11. 2KMnO4ΔK2MnO4+MnO2+O2↑ 紫色变为黑色、生成使带火星木条复燃的气体实验室制备氧气12. 2HgOΔ2Hg+O2↑ 红色变为银白、生成使带火星木条复燃的气体拉瓦锡实验13. 2H2O通电 2H2↑+O2↑ 水通电分解为氢气和氧气电解水14. Cu2(OH)2CO3Δ2CuO+H2O+CO2↑ 绿色变黑色、试管壁有液体、使石灰水变浑浊气体铜绿加热15. NH4HCO3ΔNH3↑+ H2O +CO2↑ 白色固体消失、管壁有液体、使石灰水变浑浊气体碳酸氢铵长期暴露空气中会消失16. Zn+H2SO4=ZnSO4+H2↑ 有大量气泡产生、锌粒逐渐溶解实验室制备氢气17. Fe+H2SO4=FeSO4+H2↑ 有大量气泡产生、金属颗粒逐渐溶解18. Mg+H2SO4=MgSO4+H2↑ 有大量气泡产生、金属颗粒逐渐溶解19. 2Al+3H2SO4=Al2(SO4)3+3H2↑ 有大量气泡产生、金属颗粒逐渐溶解20. Fe2O3+3H2Δ 2Fe+3H2O 红色逐渐变为银白色、试管壁有液体冶炼金属、利用氢气的还原性21. 2Na+Cl2Δ或点燃2NaCl 剧烈燃烧、黄色火焰离子化合物的形成、22. H2+Cl2点燃或光照2HCl 点燃苍白色火焰、瓶口白雾共价化合物的形成、制备盐酸23. CuSO4+2NaOH=Cu(OH)2↓+Na2SO4蓝色沉淀生成、上部为澄清溶液质量守恒定律实验24. 2C +O2点燃2CO 煤炉中常见反应、空气污染物之一、煤气中毒原因25. 2CO+O2点燃2CO2蓝色火焰煤气燃烧26. C + CuO 高温2Cu+ CO2↑ 黑色逐渐变为红色、产生使澄清石灰水变浑浊的气体冶炼金属27. 2Fe2O3+3C 高温4Fe+ 3CO2↑ 冶炼金属 Fe3O4+2C高温3Fe + 2CO2↑ 冶炼金属28. C + CO2高温2CO29. CO2 + H2O = H2CO3碳酸使石蕊变红证明碳酸的酸性30. H2CO3ΔCO2↑+ H2O 石蕊红色褪去31. Ca(OH)2+CO2= CaCO3↓+ H2O 澄清石灰水变浑浊应用CO2检验和石灰浆粉刷墙壁32. CaCO3+H2O+CO2= Ca(HCO3)2白色沉淀逐渐溶解溶洞的形成，石头的风化33. Ca(HCO3)2Δ CaCO3↓+H2O+CO2↑ 白色沉淀、产生使澄清石灰水变浑浊的气体水垢形成.钟乳石的形成34. 2NaHCO3ΔNa2CO3+H2O+CO2↑ 产生使澄清石灰水变浑浊的气体小苏打蒸馒头35. CaCO3高温 CaO+ CO2↑ 工业制备二氧化碳和生石灰36. CaCO3+2HCl=CaCl2+ H2O+CO2↑ 固体逐渐溶解、有使澄清石灰水变浑浊的气体实验室制备二氧化碳、除水垢37. Na2CO3+H2SO4=Na2SO4+H2O+CO2↑ 固体逐渐溶解、有使澄清石灰水变浑浊的气体泡沫灭火器原理38. Na2CO3+2HCl=2NaCl+ H2O+CO2↑固体逐渐溶解、有使澄清石灰水变浑浊的气体泡沫灭火器原理39. CuO +CO Δ Cu + CO2黑色逐渐变红色，产生使澄清石灰水变浑浊的气体冶炼金属40. Fe2O3+3CO高温 2Fe+3CO2冶炼金属原理41. C2H5OH+3O2点燃2CO2+3H2O 蓝色火焰、产生使石灰水变浑浊的气体、放热酒精的燃烧42. Fe+CuSO4=Cu+FeSO4银白色金属表面覆盖一层红色物质湿法炼铜、镀铜43. Mg+FeSO4= Fe+ MgSO4溶液由浅绿色变为无色44. Cu+2AgNO3=2Ag+ Cu(NO3)2红色金属表面覆盖一层银白色物质镀银45. Zn+CuSO4= Cu+ZnSO4青白色金属表面覆盖一层红色物质镀铜46. Fe2O3+6HCl=2FeCl3+3H2O 铁锈溶解、溶液呈黄色铁器除锈47. Al2O3+6HCl=2AlCl3+3H2O 白色固体溶解48. CuO+2HCl=CuCl2+H2O 黑色固体溶解、溶液呈蓝色49. MgO+2HCl=MgCl2+ H2O 白色固体溶解 CaO+2HCl=CaCl2+ H2O 白色固体溶解50. NaOH+HCl=NaCl+ H2O 白色固体溶解51. Cu(OH)2+2HCl=CuCl2+2H2O 蓝色固体溶解52. Mg(OH)2+2HCl=MgCl2+2H2O 白色固体溶解53. Al(OH)3+3HCl=AlCl3+3H2O 白色固体溶解胃舒平治疗胃酸过多54. Fe(OH)3+3HCl=FeCl3+3H2O 红褐色沉淀溶解、溶液呈黄色55. Ca(OH)2+2HCl=CaCl2+2H2O56. HCl+AgNO3= AgCl↓+HNO3生成白色沉淀、不溶解于稀硝酸检验Cl—的原理57. Fe2O3+3H2SO4= Fe2(SO4)3+3H2O 铁锈溶解、溶液呈黄色铁器除锈58. Al2O3+3H2SO4= Al2(SO4)3+3H2O 白色固体溶解59. CuO+H2SO4=CuSO4+H2O 黑色固体溶解、溶液呈蓝色60. 2NaOH+H2SO4=Na2SO4+2H2O61. Cu(OH)2+H2SO4=CuSO4+2H2O 蓝色固体溶解62. 2Al(OH)3+3H2SO4=Al2(SO4)3+3H2O 白色固体溶解63. 2Fe(OH)3+3H2SO4=Fe2(SO4)3+3H2O 红褐色沉淀溶解、溶液呈黄色64. Ba(OH)2+ H2SO4=BaSO4↓+2H2O 生成白色沉淀、不溶解于稀硝酸检验SO42—的原理65. BaCl2+ H2SO4=BaSO4↓+2HCl 生成白色沉淀、不溶解于稀硝酸检验SO42—的原理66. Ba(NO3)2+H2SO4=BaSO4↓+2HNO3生成白色沉淀、不溶解于稀硝酸检验SO42—的原理67. CuO+2HNO3=Cu(NO3)2+H2O 黑色固体溶解、溶液呈蓝色68. NaOH+HNO3=NaNO3+ H2O69. Cu(OH)2+2HNO3=Cu(NO3)2+2H2O 蓝色固体溶解70. Fe(OH)3+3HNO3=Fe(NO3)3+3H2O 红褐色沉淀溶解、溶液呈黄色71. 2NaOH+CO2=Na2CO3+ H2O 吸收CO、O2、H2中的CO2、72. 2NaOH+SO2=Na2SO3+ H2O 2NaOH+SO3=Na2SO4+ H2O 处理硫酸工厂的尾气（SO2）73. FeCl3+3NaOH=Fe(OH)3↓+3NaCl 溶液黄色褪去、有红褐色沉淀生成74. AlCl3+3NaOH=Al(OH)3↓+3NaCl 有白色沉淀生成75. MgCl2+2NaOH = Mg(OH)2↓+2NaCl76. CuCl2+2NaOH = Cu(OH)2↓+2NaCl 溶液蓝色褪去、有蓝色沉淀生成77. CaO+ H2O = Ca(OH)2白色块状固体变为粉末、生石灰制备石灰浆78. Ca(OH)2+Na2CO3=CaCO3↓+2NaOH 有白色沉淀生成工业制烧碱、实验室制少量烧碱79. Ba(OH)2+Na2CO3=BaCO3↓+2NaOH 有白色沉淀生成80. Ca(OH)2+K2CO3=CaCO3↓ +2KOH 有白色沉淀生成81. CuSO4+5H2O= CuSO4·H2O 白色粉末变为蓝色检验物质中是否含有水82. CuSO4·H2OΔ CuSO4+5H2O 蓝色晶体变为白色粉末83. AgNO3+NaCl = AgCl↓+NaNO3白色不溶解于稀硝酸的沉淀（其他氯化物类似反应）应用于检验溶液中的氯离子84. BaCl2 + Na2SO4= BaSO4↓+2NaCl 白色不溶解于稀硝酸的沉淀（其他硫酸盐类似反应）应用于检验硫酸根离子85. CaCl2+Na2CO3= CaCO3↓+2NaCl 有白色沉淀生成86. MgCl2+Ba(OH)2=BaCl2+Mg(OH)2↓ 有白色沉淀生成87. CaCO3+2HCl=CaCl2+H2O+CO2↑88. MgCO3+2HCl= MgCl2+H2O+ CO2↑89. NH4NO3+NaOH=NaNO3+NH3↑+H2O 生成使湿润石蕊试纸变蓝色的气体应用于检验溶液中的铵根离子90. NH4Cl+ KOH= KCl+NH3↑+H2O 生成使湿润石蕊试纸变蓝色的气体。