Respiration is one of the most basic motor activities crucial for survival of the individual. It is under total control of the central nervous system, which adjusts respiratory depth and frequency depending on the circumstances the individual finds itself. For this reason this volume not only reviews the basic control systems of respiration, located in the caudal brainstem, but also the higher brain regions, that change depth and frequency of respiration. Scientific knowledge of these systems is crucial for understanding the problems in the many patients suffering from respiratory failure. - This well-established international series examines major areas of basic and clinical research within neuroscience, as well as emerging subfields.
Front Cover 1
Breathing, Emotion and Evolution 4
Copyright 5
Contributors 6
Preface 12
Contents 14
Chapter 1: Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympat 24
1. Introduction 25
2. Respiratory Modulation of Sympathetic Activity 25
3. Respiratory Baroreflex 28
4. Respiratory-sympathetic Chemoreflex 31
5. Chronic Intermittent Hypoxia 34
6. Unified Theoretical Framework for Respiratory-Sympathetic Coupling: Limitations and Perspectives 38
Acknowledgments 41
References 41
Chapter 2: Coupling of respiratory and sympathetic activities in rats submitted to chronic intermittent hypoxia 48
1. Sympathetic Nervous System and Its Interaction with the Respiratory Network 48
2. Central Mechanisms Underlying respiratory-sympathetic Coupling 51
3. Relevance of Respiratory-Sympathetic Coupling Dysfunctions to the Development of Systemic Hypertension 54
4. Perspectives 57
Acknowledgments 57
References 58
Chapter 3: Function and modulation of premotor brainstem parasympathetic cardiac neurons that control heart rate by hypoxia-, 62
1. Introduction 63
2. Autonomic Control of Cardiac Function 63
3. Responses to Hypoxia 64
4. Cardiovascular Regulation During Sleep 67
5. Cardiovascular Changes with sleep-related Diseases such as OSA 72
6. Conclusions 73
Acknowledgments 73
References 73
Chapter 4: Discharge properties of upper airway motor units during wakefulness and sleep 82
1. Introduction and Background 83
2. Upper Airway Muscle Recording and Analysis Techniques 84
3. Upper Airway Motor Unit Discharge Patterns 85
4. Manipulations of sleep-wake State and Respiratory Drive 87
5. Overview 94
References 96
Chapter 5: Effects of calcium (Ca2+) extrusion mechanisms on electrophysiological properties in a hypoglossal motoneuron: Ins 100
1. Introduction 101
2. Methods 103
3. Results 106
3.1. Ca2+ Extrusion Mechanisms 106
3.2. Addition of BK Channels-Type I Firing 107
3.3. Addition of Ca2+ Buffering-Type D Firing 108
3.4. Combining BK Channels and Ca2+ Buffering 111
3.5. Ca2+ Diffusion 111
4. Discussion 114
4.1. Ca2+ Extrusion Mechanisms 115
4.2. Stable Modification to Firing Frequency 116
4.3. Type I and D Firing Behaviors 116
4.4. Context-Dependent Properties 116
4.5. Putative Mechanistic Explanations of Behavior 117
4.6. Long-Term Linear Decay of Frequency 117
4.7. Conclusion 117
Acknowledgment 118
References 118
Chapter 6: Using a computational model to analyze the effects of firing frequency on synchrony of a network of gap junction-c 122
1. Introduction 123
2. Methods and Simulation Details 124
2.1. Simulations with Different Levels of Gap Junction Coupling Strength 126
3. Results 127
3.1. Influence of Changes in SK Conductance and Input Current on Firing Frequency 127
3.2. Influence of Firing Frequency on Network Synchrony 129
3.3. Influence of Coupling Strength Extremes on Synchrony 131
4. Discussion 131
References 133
Chapter 7: The physiological significance of postinspiration in respiratory control 136
1. Introduction 137
2. Postinspiration During Eupnea 138
2.1. A General Definition of Postinspiration in Mammals 138
2.2. Laryngeal Adductor Muscle Activation in Postinspiration Brakes Expiratory Airflow 139
2.3. Postinspiratory Activity in the Crural Diaphragm 139
2.4. State Dependency and Variable Expression of Eupneic Postinspiratory Laryngeal Adduction 141
3. Postinspiratory Activity During Breath-Holding and Expulsive Reflexes that Protect the Respiratory Tract 141
4. Postinspiratory Activity During Nonventilatory Behavior 142
4.1. Vocal Fold Tensioning is Essential for Vocalization 142
4.2. Swallowing is Associated with the Postinspiratory Phase 142
4.3. Postinspiration During Defecation, Retching, and Vomiting 143
5. Central Origins of Postinspiratory Motor Activity 143
5.1. Reflections on the Role of Postinspiratory Neurons in Respiratory Rhythm and Pattern Formation 144
6. Clinical Implications of Disturbances to Postinspiratory Control 145
7. Concluding Remarks and Outlook 146
References 147
Chapter 8: Expiration: Breathing's other face 154
1. How Air Breathing Evolved Is Still Debated 155
2. The Evolution of the Aspiration Pump Began with an Expiratory Pump 155
3. In the Ancestral Breathing Cycle, Inspiration Follows Expiration, Which Is in Turn Followed by Glottal Closure 156
4. The end-inspiratory Pause Is a Major Controlled Variable in the Cycle 157
5. The Phases of the Respiratory Cycle in Mammals Appear to Be Homologous to Those in Reptiles 159
6. The Postinspiratory Pause Is a Major Controlled Variable in the Cycle 160
7. The Occurrence of Active Expiration in Mammals 161
8. Control of Expiration 164
9. Presence of an Expiratory Rhythm Generator 164
10. Phylogeny of the Rhythm Generators 165
11. Summary 165
Acknowledgment 166
References 166
Chapter 9: The effects of head-up and head-down tilt on central respiratory chemoreflex loop gain tested by hyperoxic rebrea. 172
1. Introduction 173
1.1. Respiratory Chemoreceptors 173
1.2. Central Respiratory Chemoreceptors 174
1.3. Testing and Modeling the Central Chemoreflex 174
1.3.1. Hyperoxic Steady-State Methods 175
1.3.2. Hyperoxic Rebreathing Methods 175
1.4. Central Respiratory Chemoreflex Loop Gain 176
1.5. Controller Gain 177
1.6. Mixing Gain 178
1.7. Plant Gain 178
1.8. Tilt and Pulmonary Mechanics 178
1.9. Aim and Hypothesis 179
2. Methods 179
2.1. Subject Recruitment and Inclusion Criteria 179
2.2. Subject Instrumentation and Data Collection 180
2.3. Experimental Protocol 180
2.4. Data Analysis and Statistics 180
2.4.1. Baseline Data 180
2.4.2. Central Respiratory Chemoreflex in Response to Hyperoxic Rebreathing 180
2.4.3. Statistics 182
3. Results 182
3.1. Baseline Measurements 183
3.2. Respiratory Variables During Tilt and Hyperoxic Rebreathing 184
4. Discussion 184
4.1. Baseline Measures 185
4.2. Body Position and Central Chemoreflex Loop Gain 185
4.3. Critique of Methods 186
4.3.1. Hyperoxia and Prior Hyperventilation Duration 187
4.3.2. Analysis 188
4.4. Isolation of Plant Gain 188
4.5. Loop Gain Terminology 188
5. Conclusion 190
Acknowledgments 190
References 190
Chapter 10: The challenges of respiratory motor system recovery following cervical spinal cord injury 196
1. Cervical Spinal Cord Injury and the Deficit in Respiratory Motor Function 198
2. Organization of the Respiratory Motor Circuitry and the Crossed Phrenic Phenomenon 199
3. Modeling Respiratory Motor Function Following Cervical Spinal Cord Injury 201
3.1. Cervical Spinal Cord Injury 201
3.2. Acute Models of Cervical SCI and the Effect upon the Respiratory Motor System 202
3.3. Contusion and Chronic Models of Cervical SCI and the Affect upon the Respiratory Motor System 203
3.4. Endogenous Respiratory Motor System Recovery Following Subacute/Chronic Cervical Spinal Cord Injury 205
3.5. The Limitations of Spinal Cord Injury Models 206
4. Intrinsic Factors Controlling Respiratory Motor Recovery Following Cervical SCI 206
4.1. Adenosine A1 and cAMP 206
4.2. Gq Protein Signaling Cascades: Intermittent Hypoxia, 5-HT2, and Phrenic LTF 207
4.3. Gs Protein Signaling Cascade: Adenosine and 5-HT7 211
4.4. Optogenetics 212
5. Extrinsic Factors Controlling Respiratory Motor Recovery Following Cervical SCI 212
5.1. Inflammation 212
5.2. Grafting Tissue 214
5.3. Reduction of the Glial Scar 215
6. Future Directions: Integration of Treatment Strategies and Outcome Measures 217
6.1. Integration of Treatment Strategies 217
6.2. Assessment of Treatment Strategies Currently Overlooked in the Respiratory Motor System Model 219
6.3. Assessment of Multiple Outcome Measures 220
7. Concluding Remarks 220
Acknowledgments 221
References 221
Chapter 11: Intermittent hypoxia-induced respiratory long-term facilitation is dominated by enhanced burst frequency, not am. 244
1. Introduction 245
2. Methods 246
2.1. Animals 246
2.2. Experimental Protocol 246
2.3. Data Acquisition and Analysis 246
3. Results 247
3.1. Characteristics of EMGdia Activity Under BL Conditions and During Exposure to CO2 and a Single Bout of Acute Hypoxia 247
3.2. Response to AIH Trials 248
3.3. Response Following AIH Trials 249
4. Discussion 253
References 256
Chapter 12: Chronic nitric oxide synthase inhibition does not impair upper airway muscle adaptation to chronic intermittent h 260
1. Introduction 261
2. Methods 262
2.1. Chronic Intermittent Hypoxia 262
2.2. Experimental Procedure 263
2.3. Protocol 263
2.4. MHC Fiber Typing 264
2.5. Image Capture and Analysis 264
2.6. Data Analysis 265
3. Results 265
3.1. Body Mass and Hematocrit 265
3.2. Peak Force 265
3.3. Force-Frequency Relationship 265
3.4. Fatigue Index 266
3.5. MHC Fiber Type 266
4. Discussion 267
Acknowledgment 271
References 271
Chapter 13: The generation of pharyngeal phase of swallow and its coordination with breathing: Interaction between the swallo 276
1. Introduction 277
1.1. Definition of Swallow 277
1.2. Experimental Provocation of Swallow 278
1.3. The Swallow CPG 278
1.3.1. Dorsal Swallowing Group 279
1.3.2. Ventral Swallowing Group 280
2. Swallow and Breathing Coordination: ``Safe Swallows´´ 281
2.1. Swallow Initiation in Specific Phases of the Respiratory Cycle 281
2.2. Arrest of Respiratory Airflow During Swallow: ``Swallow-Apnea´´ 282
2.3. Expiration and Phase Resetting Following Swallow 282
3. Interaction Between Swallow and Respiratory CPGs Enabling Swallowing and Breathing Coordination 283
3.1. Gating of Swallow Initiation in Specific Phases of the Respiratory Cycle 285
3.2. Laryngeal Adduction During Swallow 287
3.3. Minimized Breathing Movements During Swallow: ``Swallow-Breath´´ 287
3.4. Respiratory Phase Resetting Following Swallows 289
4. Summary and Perspectives 290
References 292
Chapter 14: Control of coughing by medullary raphé 300
1. Introduction 300
2. Raphé Neurons and Respiratory Control 302
3. Raphé Neurons Control of Coughing and Other Reflex Behaviors 303
3.1. Resumé 303
3.2. Methodology 305
3.3. Reflex Responses Strength Control 306
3.4. Motor Pattern of Reflex Response 309
4. Concluding Remarks 311
Acknowledgment 312
References 312
Chapter 15: The respiratory-vocal system of songbirds: Anatomy, physiology, and neural control 320
1. Introduction 321
2. Peripheral Mechanics of Breathing in (Song)birds 322
2.1. Lungs 322
2.2. Air Sacs and Respiratory Muscles 324
2.3. Syrinx 327
2.4. Upper Vocal Tract 330
2.5. Chemoreceptors 331
3. Central Organization of Respiratory-Related Neurons 331
3.1. Respiratory Muscle Motoneurons 331
3.2. Organization of Respiratory-Related Neurons in the Brainstem 332
3.3. Respiratory-Vocal Circuitry 334
3.4. Physiological Properties of Hindbrain Respiratory Neurons in Songbirds 335
4. Linking the ``song System´´ to the Vocal-respiratory Hindbrain 338
4.1. Functional Organization of the Song Motor Pathway 338
4.2. A Sparse Neural Code for Song 340
4.3. HVC and Its Control of Respiratory Timing During Song 342
4.4. The Song System Provides Direct Drive to the Respiratory System 343
5. Song Production and the ``respiratory-thalamo-cortical´´ Pathway 344
5.1. The ``Respiratory-Thalamic´´ Pathway is Necessary for Song 344
5.2. A Role for the Respiratory System in Hemispheric Coordination 346
5.3. Neural Properties of the Respiratory-Thalamic Pathway 346
5.4. Integrating the Respiratory System with Song Control 347
6. Concluding Remarks 350
Acknowledgments 350
References 350
Chapter 16: The lamprey blueprint of the mammalian nervous system 360
1. The Motor Infrastructure 361
1.1. The Brainstem-Spinal Cord Control of Locomotion 361
1.2. Respiratory Control 361
1.3. The Control of Eye, Orienting, and Evasive Motor Behavior in the Optic Tectum/Superior Colliculus 363
1.4. General Comments on the Motor Infrastructure 363
2. The Forebrain Control of the Brainstem-Spinal Cord Motor Programs 363
2.1. The Control of Dopamine Neurons from the Lateral Habenulae 367
2.2. Pallium and the Layered Neocortex 368
3. Conclusion 369
Acknowledgments 369
References 369
Chapter 17: The midbrain periaqueductal gray changes the eupneic respiratory rhythm into a breathing pattern necessary for s. 374
1. Introduction 375
2. Functional Segregation Within the PAG 376
3. The PAG Connectome 377
4. PAG integrates Respiratory Responses 380
5. PAG-induced Respiratory Patterning 382
5.1. PAGdm Generates Slow and Deep Breathing 383
5.2. PAGdl Generates Tachypnea 384
5.3. PAGl Generates Inspiratory Apneusis 384
5.4. PAGvl Generates Breath Hold 384
5.5. PAGvl Generates Irregular Breathing and Apnea 386
6. Vocalization: A Modified Form of Breathing 387
7. PAG Control of the Crural and Costal Diaphragm 389
8. PAG Control of Intra-abdominal Pressure 389
9. PAG Control of Medullary Respiratory Neurons 391
9.1. PAG Modulates the Activity of Medullary Late-I and Post-I Neurons 391
9.2. PAG Modulates the Pre-I Neurons in the Pre-Bötzinger Complex Phasically and Tonically, As Well As Silences Them When Re. 393
10. Hypothalamic Mediation of Dorsal PAG-induced Respiratory Effect 394
11. Pharmacology of PAG-Induced Respiratory Modulation 395
12. PAG, Serotonin, and Level-Setting Systems 395
13. Chemosensory, Upper Airway, and Pulmonary Afferent Information to the PAG 397
14. Amygdala-PAG Interactions 398
15. Breathing and the PAG: Therapeutic Targets for the Treatment of Emotional and Psychiatric Disorders 399
16. Conclusion 399
Acknowledgment 401
References 401
Index 408
Other volumes in Progress in Brain Research 420
Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympathetic nervous system
Yaroslav I. Molkov*,1; Daniel B. Zoccal†; David M. Baekey‡; Ana P.L. Abdala§; Benedito H. Machado¶; Thomas E. Dick||; Julian F.R. Paton§; Ilya A. Rybak# * Department of Mathematical Sciences, Indiana University—Purdue University Indianapolis, IN, USA
† Department of Physiology and Pathology, Dentistry School of Araraquara, São Paulo State University, Araraquara, São Paulo, Brazil
‡ Department of Physiological Sciences, University of Florida, Gainesville, FL, USA
§ School of Physiology and Pharmacology, Bristol Heart Institute, University of Bristol, Bristol, UK
¶ Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil
|| Departments of Medicine and Neurosciences, Case Western Reserve University, Cleveland, OH, USA
# Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA, USA
1 Corresponding author: Tel.: + 1-317-274-6934; Fax: + 1-317-274-3460 email address: ymolkov@iupui.edu
Abstract
Respiratory modulation seen in the sympathetic nerve activity (SNA) implies that the respiratory and sympathetic networks interact. During hypertension elicited by chronic intermittent hypoxia (CIH), the SNA displays an enhanced respiratory modulation reflecting strengthened interactions between the networks. In this chapter, we review a series of experimental and modeling studies that help elucidate possible mechanisms of sympatho-respiratory coupling. We conclude that this coupling significantly contributes to both the sympathetic baroreflex and the augmented sympathetic activity after exposure to CIH. This conclusion is based on the following findings. (1) Baroreceptor activation results in perturbation of the respiratory pattern via transient activation of postinspiratory neurons in the Bötzinger complex (BötC). The same BötC neurons are involved in the respiratory modulation of SNA, and hence provide an additional pathway for the sympathetic baroreflex. (2) Under hypercapnia, phasic activation of abdominal motor nerves (AbN) is accompanied by synchronous discharges in SNA due to the common source of this rhythmic activity in the retrotrapezoid nucleus (RTN). CIH conditioning increases the CO2 sensitivity of central chemoreceptors in the RTN which results in the emergence of AbN and SNA discharges under normocapnic conditions similar to those observed during hypercapnia in naïve animals. Thus, respiratory–sympathetic interactions play an important role in defining sympathetic output and significantly contribute to the sympathetic activity and hypertension under certain physiological or pathophysiological conditions, and the theoretical framework presented may be instrumental in understanding of malfunctioning control of sympathetic activity in a variety of disease states.
Keywords
respiratory–sympathetic interactions
baroreflex
chronic intermittent hypoxia
hypertension
modeling
1 Introduction
The respiratory rhythm and sympathetic activity are generated centrally within the brainstem. Neuronal circuits that generate and modulate respiratory and sympathetic activities appear to interact and this interaction depends on various sensory afferents (Gilbey, 2007). Here, we review possible respiratory–sympathetic interactions proposed in our recent experimental and modeling studies. These hypothetical interactions are used to explain the mechanisms of the respiratory modulation seen in sympathetic output (Section 2); the changes in the respiratory patterns due to baroreceptor stimulation (Section 3); the changes in the patterns of respiratory-modulated sympathetic activity (Section 4); and the plasticity seen within brainstem respiratory–sympathetic networks in an animal model of sleep apnea (Section 5). Finally, we discuss the limitations and perspectives of the proposed theoretical framework.
2 Respiratory Modulation of Sympathetic Activity
The respiratory rhythm and coordinated motor pattern is provided by a respiratory central pattern generator (CPG) located in the lower brainstem (Bianchi et al., 1995; Cohen, 1979; Lumsden, 1923). The pre-Bötzinger complex (pre-BötC), located within the medullary ventral respiratory column (VRC) is considered a major source of rhythmic inspiratory activity (Koshiya and Smith, 1999; Paton, 1996; Rekling and Feldman, 1998; Smith et al., 1991). The pre-BötC, interacting with the adjacent Bötzinger complex (BötC) containing mostly expiratory neurons (Ezure, 1990; Ezure et al., 2003; Jiang and Lipski, 1990; Tian et al., 1999) represents a core of the respiratory CPG (Bianchi et al., 1995; Richter, 1996; Richter and Spyer, 2001; Rybak et al., 2004, 2007, 2008; Smith et al., 2007, 2009, 2012; Tian et al., 1999). This core circuitry generates primary respiratory oscillations defined by the intrinsic biophysical properties of respiratory neurons involved, the architecture of network interactions between respiratory neural populations within and between the pre-BötC and BötC, and inputs from other brainstem compartments, including the pons, retrotrapezoid nucleus (RTN), raphé, and nucleus tractus solitarii (NTS) (Smith et al., 2012).
The sympathetic nerve activity (SNA) was shown to display respiratory modulation that persisted after vagotomy and decerebration (Adrian et al., 1932; Barman and Gebber, 1980; Habler et al., 1994; Haselton and Guyenet, 1989; Richter and Spyer, 1990; Simms et al., 2009) supporting the idea of a coupling between brainstem respiratory and sympathetic networks. This coupling may represent an important mechanism for coordination of minute ventilation and vasoconstriction/dilation aimed at increasing the efficiency of oxygen uptake/perfusion at rest, and at boosting vasomotion and assisting with perfusion of tissues for maintaining homeostasis during metabolic challenges (Zoccal et al., 2009b). Recent modeling studies also suggest improved efficiency of cardiac function provided by respiratory–sympathetic interactions (Ben-Tal, 2012; Ben-Tal et al., 2012). Therefore, the respiratory modulation may represent a considerable factor contributing to the dynamic control of SNA.
Under baseline conditions (normoxia/normocapnia) SNA usually exhibits positive modulation during inspiration (Fig. 1, upper traces) (Baekey et al., 2008; Malpas, 1998, 2010; Simms et al., 2010; Zoccal et al., 2008, 2009a,b). It has been suggested that this modulation results from specific interactions between respiratory and sympathetic neurons at the level of ventrolateral medulla, where many of the neurons involved in the generation of respiratory and sympathetic activities are located (Habler et al., 1994; Haselton and Guyenet, 1989; Koshiya and Guyenet, 1996; McAllen, 1987; Richter and Spyer, 1990; Zhong et al., 1997). Specifically in this region, the inspiratory and expiratory neurons of the VRC interact with the presympathetic neurons of the rostral ventrolateral medulla (RVLM) as well as with GABAergic interneurons of caudal ventrolateral medulla (CVLM) inhibiting RVLM neurons (Haselton and Guyenet, 1989; Mandel and Schreihofer, 2006; Richter and Spyer, 1990; Sun et al., 1997). It appears that the pons may play a critical role in these interactions. Ponto-medullary transections in situ were shown to significantly reduce or even eliminate the respiratory modulation of SNA (Fig. 1, “after transection”, see also Baekey et al., 2008). This suggests that pontine projections to medullary respiratory and sympathetic neurons are crucial for the respiratory–sympathetic coupling. Accordingly, pontine neurons may have a direct effect on the activity of presympathetic RVLM neurons or they may act indirectly through respiratory neurons in the VRC (Fig. 2A, blue dashed arrows).
| Erscheint lt. Verlag | 4.9.2014 |
|---|---|
| Sprache | englisch |
| Themenwelt | Medizin / Pharmazie ► Medizinische Fachgebiete ► Neurologie |
| Studium ► 1. Studienabschnitt (Vorklinik) ► Physiologie | |
| Naturwissenschaften ► Biologie ► Humanbiologie | |
| Naturwissenschaften ► Biologie ► Zoologie | |
| ISBN-10 | 0-444-63495-9 / 0444634959 |
| ISBN-13 | 978-0-444-63495-5 / 9780444634955 |
| Haben Sie eine Frage zum Produkt? |
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