Studies on Cardiovascular Disorders (eBook)

Heinrich Sauer, Ajay M. Shah, Francisco R. M. Laurindo (Herausgeber)

eBook Download: PDF

2010 | 2010
XVIII, 590 Seiten
Humana Press (Verlag)
978-1-60761-600-9 (ISBN)

Infos

This collection of articles on oxidative stress in clinical practice surveys essential current research in what is a rapidly evolving field. As well as giving the reader a mechanistic overview of how oxidative stress affects cardiovascular disease, it analyzes the potential of a number of therapeutic options that target these pathways. Understanding the complexity of the cellular redox system could lead to the development of better targeted interventions that facilitate patient recovery. Even as large-scale clinical trials of so-called 'simple' antioxidant approaches such as vitamins C and E show that significant benefits for cardiovascular patients remain elusive, Studies on Cardiovascular Disorders demonstrates that such approaches are too simplistic. Beginning with a summary of redox signaling models that could induce the progression of redox-associated cardiovascular disorders, the volume moves on to examine redox-mediated protein modification under physiological and pathophysiological conditions. It provides an outline of the signaling pathways in cardiovascular development during embryogenesis, and what impact these might have in the differentiation process of resident cardiac and blastocyst derived stem cells. Further chapters detail our current knowledge of the influence the sensory nervous system exerts on the cardiovascular system, and the paradoxical role of mitochondria-derived ROS in cardiac protection. In all, almost 30 contributions cover issues as diverse as the antioxidant properties of statins in the heart and the oxidative risk factors for cardiovascular disease in women. A range of medical practitioners will find the contents of Studies on Cardiovascular Disorders provides illuminating insight into the Janus-faced role of ROS in the cardiovascular system.

Inhalt

Preface 5
Contents 9
Contributors 12
1 The Evolving Concept of Oxidative Stress 17
1.1 A Brief Historical Note and Some Definitions 18
1.2 Molecular Damage by Free Radicals and Oxidant Species 19
1.3 The Redox Signaling Concept 21
1.4 Reactivity of Thiols: A Chemical Route for Redox-Dependent Messages 23
1.4.1 Thiol Oxidation Pathways 23
1.4.2 Mechanism for Thiol-Mediated Signal Transduction 27
1.5 The Evolving Characteristic of Redox Signaling Models: Critical Analysis 29
1.6 Compartmentalization: One of Natures Solutions for Redox Signaling Specificity and Robustness 33
1.7 Redox Modularity: A Systems BiologyBased Version of Compartmentalization 34
1.8 Oxidative Stress as Collateral Supra-Modular Signaling: A Proposal 36
1.9 Intermediate States of Redox Signaling vs. Oxidative Stress 37
1.10 Reduction-Dependent Signaling and Reductive Stress 38
1.11 Integration of Oxidative Stress at the Cellular Level: Convergence with Other Types of Stress 39
1.12 Assessment of Disrupted Signaling Due to Oxidative Stress: Problems and Perspectives 40
1.12.1 Approaches for Reactive Species Detection and Oxidative Stress Measurement 41
1.12.2 Approaches for Redox State Measurement 44
1.12.3 How to Choose a Particular Method for Detection of Reactive Species or Oxidative Stress 45
1.13 Redefining Antioxidants and Antioxidant Therapy in a Redox Signaling Scenario 46
1.14 Concluding Remarks 46
References 47
2 Mechanisms of Redox Signaling in Cardiovascular Disease 58
2.1 Overview of Cardiovascular Disease 58
2.2 Oxidative StressA Recurrent Hallmark of Cardiovascular Pathologies 59
2.3 Nondeleterious Roles for Oxidants 60
2.4 Cellular Oxidants 61
2.5 Protein Oxidation Involved in Redox Signaling 62
2.6 Techniques for Monitoring Thiol Redox State 65
2.7 Proteins in the Cardiovascular System That Are Thiol Redox Modulated 66
2.8 Conclusions 67
References 70
3 Reactive Oxygen and Nitrogen Species in Cardiovascular Differentiation of Stem Cells 76
3.1 Introduction 77
3.2 Oxygen and ROS Generation During Embryogenesis 77
3.3 Oxidative Stress During Myocardial InfarctionA Potential Stimulus for Stem Cell Activation 78
3.4 Stem Cells Within the Heart and Potential Redox-Regulated Signaling Pathway Involved in Stem Cell Proliferation and Specification 79
3.5 Impact of Redox-Regulated Pro-angiogenic Signals During Cardiac Infarction 82
3.6 Redox-Regulated Pathways Involved in Mobilization of Stem Cells from the Bone Marrow 83
3.7 NO and ROS in EPC Mobilization and Function 85
3.8 ROS and NO Generation in Bone MarrowDerived Stem Cells 88
3.9 ROS and NO in Cardiovascular Differentiation of Embryonic Stem Cells 89
3.10 Summary and Conclusions 92
References 92
4 Reactive Oxygen Species (ROS) and the Sensory Neurovascular Component 101
4.1 Introduction 101
4.2 The Sensory Neurogenic Component and Vascular Innervation 102
4.2.1 Nerve Activating Mechanisms and Cardiovascular Consequences of Neuropeptide Action 102
4.3 ROS and Localization Within Sensory Nerves 103
4.4 Vascular Effects of ROS 104
4.5 Neuropeptides and Interactions with Vascular-Derived ROS 106
4.6 CGRP 106
4.6.1 CGRP and Protection Against Oxidative Stress as a Consequence of Vasodilator Networks 107
4.6.2 CGRP and Protection via Vasodilator-Independent Mechanisms Against ROS-Mediated Vascular Injury 107
4.6.3 Substance P 108
4.6.4 Influence of Vascular-Derived ROS on Substance P--Induced Vasodilatation 108
4.6.5 Influence of Substance P on Inflammatory ROS Production 109
4.7 TRP Receptor and Localization on Sensory Nerves 109
4.7.1 TRPV1 Receptors and Links with ROS 111
4.7.2 H2O2 as a TRPA1 Receptor Agonist 112
4.7.3 Products of Oxidative Stress as TRPA1 Receptor Agonists 114
4.8 Conclusions and Therapeutic Implications 115
References 115
5 Mitochondrial Reactive Oxygen Species in Myocardial Pre- and Postconditioning 122
5.1 Mitochondrial ROS Generation in the Heart 122
5.2 Regulation of Mitochondrial ROS Generation by Mild Uncoupling Pathways 123
5.3 Mitochondrial Permeability Transition: A Cell DeathInducing Consequence of Mitochondrial Oxidative Stress 125
5.4 Preconditioning and Mitochondrial Redox Signaling 126
5.5 Postconditioning and Mitochondrial Redox Signaling 129
5.6 Concluding Remarks 130
References 130
6 Coenzyme Q9/Q10 and the Healthy Heart 137
6.1 Introduction 137
6.2 A Quick Look Back 138
6.3 Natural Occurrence and Distribution 140
6.4 The Biochemical Background 141
6.5 Physiological Effects 141
6.6 Pharmacokinetics 142
6.7 Cardioprotective Effects 143
6.7.1 Heart Failure 144
6.7.2 Atherosclerosis 145
6.7.3 Hypertension 145
6.7.4 Cardiac and Vascular Surgery 145
6.7.5 Pharmacological Preconditioning Effects 146
6.8 Conclusion 147
References 147
7 Oxidative and Proteolytic Stress in Homocysteine-Associated Cardiovascular Diseases 151
7.1 Introduction 151
7.2 HCY Mechanism of Oxidative and Nitrosative Stress 154
7.3 HHCY, Oxidative Stress, and Myocyte Dysfunction 155
7.4 H2S Hypothesis of Cardioprotection in HHCY 156
7.5 Proliferation and Maintenance of Resident Cardiac Stem Cell, MMP/TIMP Levels, and FoxO Transcription Factor 157
References 159
8 Functional Studies of NADPH Oxidases in Human Vasculature 161
8.1 Introduction 162
8.2 Functional Studies of Oxidative Stress in Human Vasculature 162
8.2.1 Ex Vivo Studies 162
8.2.2 In Vivo Studies 164
8.3 Role of Reactive Oxygen Species in the Regulation of Endothelial Function in Human Vasculature 164
8.4 Vessel Wall Layers Contributing to Total Vascular Superoxide 166
8.5 New Functional Hypothesis of Oxidative Stress 167
8.6 NADPH Oxidases as Main Sources of Reactive Oxygen Species in Human Vasculature 168
8.6.1 Regulation of NADPH Oxidases in Human Vasculature 171
8.6.2 Central Role of NADPH Oxidases in Regulating Oxidative Stress 172
8.7 Risk Factors for Atherosclerosis and Vascular NADPH Oxidases 172
8.8 NADPH Oxidases in Bypass Graft Conduit Vessel Disease and Dysfunction 173
8.9 Functional Studies of Genetic Regulation of NADPH Oxidases 174
8.10 Conclusions 174
References 175
9 Relationship of the CYBA Gene Polymorphismswith Oxidative Stress and Cardiovascular Risk 180
9.1 Introduction 181
9.2 The NADPH Oxidase System 181
9.3 p22 phox Genetic Variants and Cardiovascular Disease 182
9.3.1 C242T Polymorphism 183
9.3.2 A640G Polymorphism 187
9.3.3 -930 A/G Polymorphism 187
9.3.4 -675 A/T Polymorphism 189
9.3.5 Other CYBA Polymorphisms 189
9.4 Genetic and Environmental Interactions 190
9.5 Summary and Conclusions 192
References 193
10 Redox-Related Genetic Markers of CardiovascularDiseases 198
10.1 Introduction 198
10.2 Phenotypic Quality 199
10.3 Strategies to Unravel the Genetics of Redox-Related Diseases 201
10.3.1 Candidate Gene Approach 201
10.3.1.1 NADPH Oxidase 201
10.3.1.2 Superoxide Dismutase 203
10.3.1.3 Other Redox-Related Candidate Genes 204
10.3.2 Rodent Models and Translational Approaches 205
10.3.3 Genome-Wide Association Studies 207
10.3.4 Mitochondria 208
10.4 Interactions Between Genes and Environment 209
10.4.1 Antioxidant Therapy 209
10.4.2 Smoking 210
10.4.3 Medication and Pharmacogenetics 210
10.5 Regulation of Transcription 211
10.6 Summary and Conclusions 211
References 212
11 NADPH Oxidases and Blood-Brain Barrier Dysfunctionin Stroke 221
11.1 Introduction 221
11.2 The Clinical Setting of Stroke 222
11.3 Reactive Oxygen Species in Ischemic Brain Injury 223
11.4 NADPH Oxidases in the Central Nervous System 223
11.5 The Role of NADPH Oxidases in Ischemic Stroke 225
11.5.1 NADPH Oxidases in Ischemia/Reperfusion Outside of the Brain 225
11.5.2 Cerebral NADPH Oxidases and Ischemic Brain Injury 226
11.6 The Blood-Brain Barrier 227
11.6.1 Structural Components of the Blood-Brain Barrier 227
11.6.2 In Vivo Regulation of the Blood-Brain Barrier 228
11.6.3 Blood-Brain Barrier Dysfunction in Stroke 229
11.6.4 Mechanisms of Blood-Brain Barrier Opening 230
11.7 The Role of NADPH Oxidases in Blood-Brain Barrier Dysfunction 231
11.8 Summary and Conclusion 234
References 234
12 Smoking-Induced Oxidative Stress in the Pathogenesisof Cardiovascular Diseases 241
12.1 Introduction 242
12.2 Smoking as a Source for Oxidative Stress in the Cardiovascular System 242
12.2.1 Generation of Oxidants and Radicals by Combustion of Cigarette Constituents 242
12.2.2 Secondary Generation of Oxidants and Radicals by Cigarette Smoke in the Cardiovascular System 243
12.2.2.1 Secondary Oxidative Stress in the Vessel Wall by Smoking-Caused Inflammation 243
12.2.2.2 Oxidative Stress by Smoking-Caused Reduction of Physiological Antioxidants 244
12.2.2.3 Smoking-Mediated Modulation of Gene Expression as a Source for Cardiovascular Oxidative Stress 245
12.2.2.4 Cigarette Smoke--Contained Metals, a Source for Chronic Oxidative Stress in the Vessel Wall 246
12.3 Smoking-Caused Oxidative Stress as a Pathophysiological Factor in Cardiovascular Disease Initiation and Progression 246
12.3.1 The Role of Smoking-Caused Oxidative Stress in CVD Initiation 246
12.3.1.1 Impact of Smoking on Endothelial Function 246
12.3.1.2 Smoking and the Autoimmune Hypothesis of Atherosclerosis 247
12.3.1.3 Smoking and Lipid Oxidation 247
12.3.2 The Role of Smoking-Caused Oxidative Stress in CVD Progression 248
12.3.2.1 Smoking-Mediated Oxidative Stress and Inflammation in CVD Progression 248
12.3.2.2 Smoking-Induced Vascular Aging as a CVD-Promoting Factor 249
12.3.2.3 Smoking, Oxidative Stress, and Thrombogenesis 249
12.3.3 Oxidative Stress--Independent Mechanisms in CVD Initiation and Progression 249
12.3.3.1 Nonoxidative Smoke Chemicals and CVD Initiation 249
12.3.3.2 Smoking, Collagen Synthesis, and Plaque Stability 250
12.4 Summary and Conclusions 251
References 251
13 Oxidative Stress in Vascular Aging 254
13.1 Introduction 254
13.2 Oxidative Stress in Vascular Aging: Role of NAD(P)H Oxidases 255
13.3 Role of Mitochondrial Oxidative Stress in Arterial Aging 256
13.4 Low-Grade Vascular Inflammation During Aging: Role of Oxidative Stress 259
13.5 Caloric Restriction Attenuates Vascular Oxidative Stress in Aging 260
13.6 Attenuation of Age-Related Vascular Oxidative Stress by the Caloric Restriction Mimetic Resveratrol 262
13.7 Conclusions 263
References 263
14 Oxidative Stress and Cardiovascular Diseasein Diabetes Mellitus 271
14.1 Introduction 271
14.2 Enzymatic Sources of Reactive Oxygen Species in Diabetes 272
14.2.1 DAG-PKC Activation 272
14.2.2 NADPH Oxidase 274
14.2.3 Cellular Respiration 274
14.2.4 Oxidative Stress and Advanced Glycation End Products 274
14.2.5 Oxidative Stress and the Polyol Pathway 276
14.3 Role of Reactive Oxygen Species in the Cardiovascular Consequences of Diabetes 277
14.3.1 Endothelial Dysfunction 278
14.3.2 Diabetes and Hypertension 280
14.3.3 Diabetes and Atherosclerosis 281
14.3.4 Diabetes and Thrombosis 282
14.3.5 Diabetic Cardiomyopathy 282
14.3.6 Arrhythmia 283
14.4 Summary 284
References 284
15 Reactive Oxygen Species, Oxidative Stress, and Hypertension 288
15.1 Introduction 289
15.2 Biology of ROS 290
15.3 Production and Metabolism of ROS in the Cardiovascular System 291
15.3.1 Xanthine Oxidase 291
15.3.2 Uncoupled Nitric Oxide Synthase 292
15.3.3 Mitochondrial Respiratory Enzymes 293
15.3.4 ROS-Generating Nox Family NAD(P)H Oxidases 294
15.3.4.1 Distribution of Noxes in the Vascular Wall 296
15.3.4.2 Regulation of Noxes 296
15.4 Protecting Against Oxidative Stress: Antioxidant Defenses 297
15.5 ROS and Vascular (Patho)Biology in Hypertension 298
15.6 Oxidative Stress in Experimental Hypertension 299
15.7 Oxidative Stress and Clinical Hypertension 301
15.8 Antioxidant Therapy and Human Hypertension 303
15.9 Other Possible Strategies to Reduce Oxidative Stress 304
15.10 Conclusions 305
References 306
16 Peripartum Cardiomyopathy: Role of STAT-3 and Reactive Oxygen Species 323
16.1 Introduction 324
16.2 Oxidative Stress and Antioxidative Defense During Pregnancy and Postpartum 325
16.2.1 Oxidative Stress Factors 325
16.2.2 Antioxidant Capacity 325
16.2.3 Summary 326
16.3 Peripartum Cardiomyopathy (PPCM) 327
16.4 Potential Risk Factors for PPCM 327
16.4.1 Infectious Agents 327
16.4.2 Autoimmune Responses 328
16.4.3 Preeclampsia 328
16.4.3.1 Oxidative Modification of Lipids 329
16.4.3.2 Activation of the Immune System by Oxidative Stress Mechanisms 329
16.4.3.3 Asymmetric Dimethylarginine (ADMA) 330
16.5 Mechanistic Insights into the Pathophysiology of Peripartum Cardiomyopathy 331
16.5.1 The Estrogen-PI3-Akt Connection 331
16.5.2 STAT3, the Guardian of Postpartum Hearts 331
16.5.3 STAT3 and Antioxidant Pathways in the Postpartum Heart: An Important Role for MnSOD 332
16.5.4 Oxidative Stress and High Prolactin Levels: A Detrimental Combination 333
16.5.5 Impact of the 16-kDa Prolactin on the Cardiovascular System 334
16.6 How Relevant is the STAT3Oxidative StressProlactin Hypothesis for Human PPCM 335
16.6.1 Gene Polymorphisms and Dysregulation of STAT3 Signaling Pathways in Human PPCM 335
16.6.2 Evidence for the Oxidative Stress--Prolactin Hypothesis in Human PPCM 336
16.6.2.1 Oxidative Stress and Inflammation 336
16.6.2.2 Cathepsin D, Prolactin Cleavage, and Bromocriptine 336
16.6.2.3 16-kDa Prolactin in Prepartum Cardiovascular Disease 337
16.6.2.4 Summary 337
16.6.3 Prolactin, Bromocriptine, and the Risk for Thrombosis 337
16.7 Summary and Conclusions 338
References 339
17 Oxidative Stress and Inflammation after CoronaryAngiography 344
17.1 Introduction 344
17.2 Oxidative Stress During Percutaneous Coronary Intervention 345
17.3 Antioxidant Approaches in Clinical Practice 345
17.3.1 Myeloperoxidase (MPO) as a Biomarker of Oxidative Stress in Cardiovascular Disease 346
17.3.2 Role of PMNLs 349
17.4 Summary 350
References 351
18 Oxidative Stress in Cardiac Transplantation 354
18.1 Introduction 354
18.2 Oxidative Stress in Human Cardiac Transplantation 355
18.3 Rationale for Antioxidant/Vitamin Intervention 357
18.4 Donor Heart Preservation, Ischemia-Reperfusion Injury, and Oxidative Stress 358
18.5 Specific Role of Superoxide 359
18.5.1 Superoxide in Cardiac Transplantation 359
18.5.2 Superoxide in Cardiac Rejection 359
18.5.3 Direct Measures of Superoxide in Cardiac Grafts 360
18.6 NADPH Oxidase in Cardiac Transplantation 363
18.7 Apoptosis and Oxidative Stress in Cardiac Transplantation 363
18.7.1 Role of Ischemia-Reperfusion--Induced Apoptosis 363
18.7.2 Role of Intrinsic vs. Extrinsic Pathways of Ischemia-Reperfusion--Induced Apoptosis 364
18.7.3 Relationship of Oxidative Stress and Apoptosis in Cardiac Rejection 364
18.8 Reactive Oxygen Species and Immune Suppression 365
18.8.1 Cyclosporine-Induced Production of Superoxide 365
18.8.2 Cyclosporine-Induced Oxidative Stress 366
18.8.3 Reactive Oxygen and Other Immunosuppressant Agents 366
18.8.4 Immunosuppression, Cytomegalovirus, and Oxidative Stress 367
18.9 The Triad of the Renin-Angiotensin System, Tgf-, and Oxidative Stress in Transplantation 368
18.9.1 Effect of Angiotensin II on the Heart 368
18.9.2 TGF-, Oxidative Stress, and Cardiac Transplantation 368
References 370
19 Oxidative Stress and Atrial Fibrillation 377
19.1 Introduction 377
19.2 The Electrical Basis of AF 380
19.3 The Central Role of Myocardial Fibrosis, Inflammation, and Oxidative Stress in AF 381
19.4 Biomarkers and Cellular Mechanisms of Oxidative Stress in AF 382
19.5 Oxidative Stress and Thromboembolism in AF 385
19.6 Therapeutic Implications of Increased ROS in AF 386
19.7 Conclusion 387
References 387
20 Oxidative Stress and the Antioxidative Capacityin Myocardial Infarction 392
20.1 Introduction 392
20.2 Cardiac Oxidative Stress and Antioxidant Capacity 393
20.2.1 Reactive Oxygen Species Production 393
20.2.2 Occurrence of Cardiac Oxidative Stress Following Myocardial Infarction 394
20.3 Oxidative Stress and Cardiac Remodeling and Dysfunction 394
20.3.1 Cardiomyocyte Apoptosis in the Infarcted Heart 394
20.3.2 Oxidative Stress and Cardiac Inflammatory Response in the Infarcted Heart 398
20.3.3 Oxidative Stress and Cardiac Fibrosis Following Infarction 399
20.3.4 Oxidative Stress and Cardiac Hypertrophy Following Infarction 400
20.3.5 Oxidative Stress and Heart Failure 401
20.4 Summary 402
References 402
21 Oxidative Stress and Redox Signalling in CardiacRemodelling 407
21.1 Introduction 408
21.2 ROS, Oxidative Stress, and Redox Signalling 408
21.3 Cardiac Sources of ROS 409
21.4 ROS and Cardiac Hypertrophy 411
21.5 Extracellular Matrix Modification and Interstitial Fibrosis 413
21.6 ROS and Apoptosis 415
21.7 ROS, Contractile Dysfunction, and Energetics 416
21.8 Therapeutic Intervention 417
21.9 Conclusions 418
References 419
22 Oxidative Stress and Cardiovascular Fibrosis 427
22.1 Introduction 427
22.2 Congestive Heart Failure: Epidemiology and Risk Factors 428
22.3 Oxidative Stress in the Initiation/Progression of Vascular Disease 430
22.4 Oxidative Stress Pathways in Cardiovascular Disease 431
22.5 Biomarkers of Oxidative Stress Pathways 434
22.6 NOX Enzymes and Cardiovascular Fibrosis 436
22.7 Therapeutic Implications for Cardiovascular Fibrosis 437
References 438
23 Oxidative Risk Factors for Cardiovascular Disease in Women 444
23.1 Introduction 445
23.2 Role of Lipid Peroxidation in the Epidemiology of CVD in Women 445
23.3 Summary 449
References 450
24 Protective Effects of Food on Cardiovascular Diseases 455
24.1 Oxidative Stress 455
24.2 L-arginine 457
24.3 Lycopene 457
24.4 Phenols and Polyphenols 459
24.5 Dietary Fiber 462
24.6 Fatty Acids 463
24.7 Phytosterols 464
24.8 Ethanol and Nonethanolic Components of Wine 464
References 465
25 Novel Synthetic Antioxidants and Nitrated Lipids: From Physiology to Therapeutic Implications 472
25.1 Introduction 472
25.2 Natural Antioxidants and Prevention of Cardiovascular Disease 473
25.2.1 Introduction to Vitamin E 473
25.2.2 Randomized and Placebo-Controlled Studies for Primary and Secondary Prevention of Atherosclerosis 477
25.3 Synthetic Antioxidants Represent an Exciting Novel Strategy to Prevent Cardiovascular Disease 480
25.4 Nitrolipids 489
25.5 Conclusions 490
References 490
26 Thioredoxin in the Cardiovascular SystemTowards a Thioredoxin-Based Antioxidative Therapy 498
26.1 Introduction 498
26.2 Actions of TRX 499
26.2.1 Antioxidant Properties 499
26.2.2 Signaling 500
26.2.3 Transcription 501
26.2.4 Survival 502
26.3 Regulation of TRX Activity 503
26.3.1 Oxidation 503
26.3.2 Nitrosylation 503
26.3.3 Glutathionylation 504
26.3.4 Nitration 505
26.4 Perturbation of TRX in Vascular Disease 505
26.4.1 Plasma Levels 505
26.4.2 Expression 506
26.5 Expression and Actions of a TRX Inhibitor 506
26.5.1 TRX-Interacting Protein 506
26.6 Genetic Manipultion of TRX Expression 507
26.6.1 Transgenic Mice 507
26.7 Therapeutic Use of TRX 508
26.8 Summary and Conclusions 509
References 510
27 The Protective Effect of Melatonin on the Heart 516
27.1 Melatonin and the Heart 516
27.2 Melatonin and Ischaemia/Reperfusion Injury 518
27.3 Role of the Melatonin Receptors in Cardioprotection 519
27.4 Antiadrenergic Actions of Melatonin 521
27.5 Melatonin and Mitochondria 522
27.6 Melatonin and Intracellular Ca 2 Handling 524
27.7 Reversal of Harmful Effects of Clinically Used Drugs 525
27.8 Melatonin as Cardioprotective Agent in Humans 526
References 527
28 Exercise-Induced Cardioprotection: Overview with an Emphasis on the Role of Antioxidants 534
28.1 Introduction 534
28.2 Principles of Myocardial IR Injury 535
28.3 Oxidative Stress in Myocardial IR Injury 536
28.3.1 Calcium Regulation, Proteolysis, Membrane Integrity, and Inflammation 537
28.4 Exercise-Induced Protection Against Myocardial IR Injury: Overview of Putative Mechanisms 539
28.4.1 Coronary Circulation 539
28.4.2 Myocardial Heat Shock Proteins 539
28.4.3 Regulation of Calcium 542
28.4.4 ATP-Sensitive Potassium Channels and Protein Kinase C 542
28.5 Role of Antioxidants in Exercise-Induced Cardioprotection 543
28.5.1 An Introduction to Intrinsic Defenses 543
28.5.2 Exercise, Enzymatic Antioxidants, and Cardioprotection 544
28.5.3 Exercise and Nonenzymatic Compounds That Scavenge ROS 547
28.6 Oxidative Stress Prevention in the Exercised Heart: A Unique Form of Cardioprotection 548
28.7 Conclusions and Summary 549
References 550
29 Antioxidative Properties of Statins in the Heart 556
29.1 Introduction 556
29.2 Properties of HMG-CoA Reductase Inhibitors (Statins) 557
29.2.1 Mechanism Mediating Cholesterol-Dependent Effects of Statins 557
29.2.2 Mechanism Mediating Cholesterol-Independent Effects of Statins 558
29.3 Pathophysiology of Oxidative Stress 558
29.4 Antioxidative Effects of Statins in the Myocardium 559
29.4.1 Effects of Statins on Ventricular Myocardium and Cardiac Function 559
29.4.2 Effects of Statins on Atrial Myocardium and Atrial Fibrillation 560
29.5 Potential Effects of Statin Withdrawal 561
29.6 Summary and Conclusions 562
References 562
Index 566

Produkt-Details

• Erscheint lt. Verlag: 11.9.2010
• Reihe/Serie: Oxidative Stress in Applied Basic Research and Clinical Practice
• Reihe/Serie: Oxidative Stress in Applied Basic Research and Clinical Practice
• Zusatzinfo: XVIII, 590 p.
• Verlagsort: Totowa
• Sprache: englisch
• Themenwelt: Medizinische Fachgebiete ► Innere Medizin ► Kardiologie / Angiologie
• Themenwelt: Studium ► 1. Studienabschnitt (Vorklinik) ► Biochemie / Molekularbiologie
• Themenwelt: Naturwissenschaften ► Biologie ► Mikrobiologie / Immunologie
• Themenwelt: Naturwissenschaften ► Biologie ► Zellbiologie
• Themenwelt: Technik
• Schlagworte: Angiography • Atrial Fibrillation • Cardiovascular • Cardiovascular System • Enzyme • Gene • heart • Influence • Oxidative stress • Physiology • Protein • Stem Cells • stroke • Transplantation • vascular disease
• ISBN-10: 1-60761-600-9 / 1607616009
• ISBN-13: 978-1-60761-600-9 / 9781607616009