The aetiology of deep venous thrombosis: a critical, historical and epistemological survey
Gespeichert in:
| Hauptverfasser: | , |
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| Format: | Buch |
| Sprache: | English |
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Berlin [u.a.]
Springer
2008
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| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XXI, 318 S. Ill. 235 mm x 155 mm |
| ISBN: | 9781402066498 9781402066504 |
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| 245 | 1 | 0 | |a The aetiology of deep venous thrombosis |b a critical, historical and epistemological survey |c Paul S. Agutter ; P. Colm Malone |
| 264 | 1 | |a Berlin [u.a.] |b Springer |c 2008 | |
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Datensatz im Suchindex
| _version_ | 1804137631767855104 |
|---|---|
| adam_text | Contents
Preface v
Acknowledgments vii
Synopsis ix
Chapter 1 Introduction to the Study of Deep Venous Thrombosis 1
1.1 Incidence 1
1.2 Pathology 3
1.3 Aetiology: The Consensus Model 4
1.4 The Dominance of the Consensus Model 7
1.5 Virchow s Triad 8
1.6 An Alternative Viewpoint 9
Chapter 2 The Coagulation Cascade and the Consensus
Model of DVT 11
2.1 The Cascade Model of Blood Coagulation 11
2.2 The Origin of the Consensus Model of DVT 13
2.3 The Coagulation Cascade Today 16
2.3.1 Platelet Activation and Congregation: Local
Vasoconstriction 17
2.3.2 The Contact ( Intrinsic ) System 19
2.3.3 The Tissue Factor ( Extrinsic ) System 20
2.3.4 Fibrinogenesis 20
2.3.5 Fibrinolysis 23
2.3.6 Controlling Coagulation 25
2.4 Disorders of Coagulation 27
XV
xvi Contents
Chapter 3 Hypercoagulability 31
3.1 Introduction 31
3.2 The General Use of the Term Hypercoagulability 32
3.3 Early Evidence for Hypercoagulability Conditions 32
3.4 Testing the Hypercoagulability Hypothesis 33
3.5 Inherited Thrombophilias 34
3.6 Acquired Thrombophilias 36
3.7 Thrombophilia and DVT 37
3.8 Testing for Thrombophilias 38
3.9 Implications for Prophylaxis and Therapy 39
3.10 Reflection 40
Chapter 4 Historical Roots 41
4.1 Two Approaches to Biomedical Research 41
4.2 Semantic Issues 42
4.3 The Ancient World 44
4.4 Binary Oppositions in 17th-18th-Century Medicine.... 45
4.5 Harvey and the Physiological Approach 48
4.6 The 18th Century: Solidism, Humoralism
and the Work of Boerhaave 49
4.7 Hunter and Hewson 51
4.8 Late 18th- and Early 19th-century Studies
of Blood Chemistry 54
4.9 The 18th-Century Pioneers of Haemostatics
and Haemodynamics 54
Chapter 5 Coagulation and its Disorders: A History
of Haematological Research 57
5.1 Introduction 57
5.2 Phase 1: 1835-1893 58
5.2.1 Haemophilia and the Study of Coagulation 59
5.2.2 Buchanan 59
5.2.3 Buchanan s Influence: The Impact
of Mechanistic Materialism 60
5.2.4 The Classical Hypothesis
of Blood Coagulation 63
5.3 Phase 2: 1893-1947 64
5.3.1 Prothrombin and its Conversion
to Thrombin 64
5.3.2 Heparin, Vitamin K and the Dominance
of In Vitro Studies 65
5.4 Philosophical and Semantic Considerations 66
5.5 Reflective Anamnesis 67
Contents xvij
Chapter 6 Virchow and the Pathophysiological Tradition
in the 19th Century 71
6.1 Introduction 71
6.2 Cruveilhier 72
6.2.1 Previous Insights into Thromboembolism 73
6.2.2 Cruveilhier s Contribution 74
6.3 Other Formative Influences on Virchow 75
6.4 Resolving the Conflict: Virchow s Synthesis 77
6.5 Virchow on the Structure of a Thrombus 79
6.6 Virchow on Oxygen and Thromboembolism 81
6.7 Virchow versus Cruveilhier 81
6.8 The Possible Source of Virchow s Triad 83
6.9 Reflective Anamnesis 84
Chapter 7 The Pathophysiological Tradition after Virchow 87
7.1 Problems of Nomenclature: Phlebitis and
Inflammation 87
7.1.1 Pus 89
7.2 Leukocytes, Phagocytosis and Thrombosis 91
7.3 Platelets 93
7.4 The Persistence of the Phlebitis Concept 95
7.5 Continuation of the Pathophysiological
Perspective: Welch and Aschoff 96
7.6 The Role of Leukocytes Reconsidered 99
Chapter 8 Interrupted Circulation: The Stasis Hypothesis
and the Significance of Venous Valves 103
8.1 Introduction 103
8.2 The Maturation of the Circulation Hypothesis 104
8.3 Connections with the Revolution in Mechanics 106
8.4 The Discovery of Venous Valves 107
8.5 The Significance of Venous Valves 109
8.5.1 The Venous Valves and DVT 110
8.6 The Persistence and Misleading Character
of the Stasis Concept 111
8.6.1 Inherent Difficulties in the Stasis Dogma 111
8.6.2 The Survival of the Stasis Dogma
in the 19th Century 112
8.6.3 Stasis and the Consensus
Model of DVT Aetiology 113
8.6.4 Sevitt on the Aetiology of DVT 114
8.6.5 The Consensus Model
and the VVP as Sites of Thrombogenesis 115
xviii Contents
8.7 Is the Current (Mis)Use of Blood Stasis
Equivalent to Virchow s Interrupted Circulation ? 116
8.7.1 Pulsatile Blood Movement in Veins 116
8.7.2 Compression of Veins
in the Soles of the Feet 117
8.7.3 Effects of Standing, Sitting and Lying
on the Dynamics of Lower Limb Veins 118
8.8 Towards the Valve Cusp Hypoxia Hypothesis:
I - Altered Blood Movement 119
Chapter 9 Underperfusion of Valve Pockets and the Initiation
of DVT 121
9.1 Introduction 121
9.2 Thrombi Originate in the Venous Valve Pockets 122
9.3 The Morphology and Pathology of Venous Valves 125
9.3.1 Venous Valve Morphology 127
9.3.2 Valve Pathology: The Formation
of Nascent Thrombi within VVP 129
9.3.3 Can the Venous Return Circulation
and Valve Function be Correlated? 132
9.4 The Valve Cycle and the Effects of Non-Pulsatile
Flow 133
9.5 Relevance of Venous Blood Rheology 134
9.5.1 Relevance of the Vasa Venarum 135
9.5.2 Flow Patterns within VVP 137
9.5.3 Implications for the Formation
of Pro-Thrombotic Nidi 137
9.6 Implications for Compression Prophylaxis 138
9.7 Towards the Valve Cusp Hypoxia Hypothesis:
II-VVP Hypoxaemia 139
9.7.1 Hypoxic Injury to the VVP Cusp
Endothelium Is Potentially Thrombogenic:
a Proposal 139
9.7.2 VVP Hypoxaemia and Hypoxic
Injury to the Parietalis Endothelium 143
9.7.3 Testing the Predictions 145
9.8 The Lesson of History 145
Chapter 10 The Role of Endothelial Hypoxia in DVT 147
10.1 Oxygen, the Venous Endothelium and Thrombosis 147
10.2 Hypoxaemia, the Vascular Endothelium
and Thrombosis 148
10.2.1 Association of DVT with
Endothelial Hypoxia 149
10.2.2 Endothelial Hypoxia and Thrombus
Formation in VVP 151
Contents xix
10.2.3 The Significance of Ostial Valves 152
10.2.4 Interpreting Micrographs of Venous
Thrombi: The Tendency
of Thrombi to Embolise 154
10.3 Carbon Monoxide Poisoning and Anaemia 162
10.4 Endothelial Hypoxia and Leukocyte Margination 164
10.5 Aschoff on the Coagulation of Cadaver Blood 165
10.6 Hypoxaemia and Traveller s Thrombosis 166
10.7 Overview: Articulating the Valve Cusp
Hypoxia Hypothesis 168
Chapter 11 The Valve Cusp Hypoxia Hypothesis 169
11.1 Introduction 169
11.1.1 Criteria for an Aetiological Hypothesis 170
11.2 The General Aetiological Sequence: The Trinity 171
11.2.1 Interrupted Flow and Underperfusion
ofVVP 172
11.2.2 The Specific Involvement
of the Valve Cusp Parietalis Endothelium 173
11.2.3 Blood Cell Congregation
and Blood Coagulation 174
11.2.4 Pathological Consequences 177
11.3 Experimental Support for the VCHH 178
11.3.1 Polarographic Demonstration of VVP
Hypoxaemia during Non-Pulsatile Flow 178
11.3.2 Experimental Venous Thrombi
Induced by a Non-Invasive Technique 178
11.4 Clinical Implications 183
11.4.1 The Risks of Sleeping for Long Periods
in the Sitting Position 183
11.4.2 Simpson s Cases 185
11.4.3 Anaesthesia 187
11.4.4 Crucifixion 188
11.4.5 Varicose Veins 188
11.5 Risk Factors for DVT Reconsidered in the Light
of the VCHH 189
11.6 Prophylaxis 190
11.6.1 Our Theory-Based Estimate of 1.5-3 h 191
11.6.2 Lister s Experience 191
11.6.3 Normal Tourniquet Practice 191
11.6.4 Published Traveller s Thrombosis Data 192
11.6.5 Intermittent Positive Pressure
Compression (IPPC) of Feet or Legs 192
11.6.6 The Animal Experiments of Hamer
and Malone (1984) 194
11.7 Reflection 194
xx Contents
Chapter 12 Molecular Changes in the Hypoxic Endothelium 195
12.1 Endothelial Cell Physiology 195
12.2 The VCHH and the Molecular Responses of EC
to Hypoxia 197
12.3 Phenotypic Changes in EC under Hypoxic
Conditions 197
12.3.1 Phenotypic Changes Consequent on Egr-1
Induction 199
12.3.2 Elk-1 andSRF 200
12.3.3 Other Regulators of Egr-1 Expression 202
12.4 Erg-1, Hypoxia and DVT 204
12.5 Thrombin and the PARs 204
12.6 Interactions Between Platelets and the Hypoxic
Endothelium 206
12.6.1 Platelet Congregation
and Implications for DVT 206
12.6.2 Leukocyte-Platelet Complexes
in the Circulation and their Association
with the Hypoxic Endothelium 207
12.7 Endothelial Hypoxia and the Congregation of
Leukocytes 208
12.7.1 Monocytes and Macrophages 209
12.7.2 Neutrophils 210
12.7.3 Effects of Leukocytes
on Injured Endothelium 211
12.8 The Endothelium and Coagulation 212
12.9 The Endothelium and Vasomotor Tone 216
12.10 A Further Comment on Risk Factors 218
12.11 The Unification of Approaches 218
Chapter 13 Cadaver Clots or Agonal Thrombi? 221
13.1 Can Blood Coagulate in a Cadaver? 221
13.2 An Early 20th-century Debate 222
13.3 Aschoff on Post-Mortem Clots 224
13.4 The Debate Reconsidered in the Light of the VCHH . 226
13.4.1 Death from Acute Respiratory Failure 226
13.4.2 Death from Circulatory Failure 227
13.4.3 Summary: The Condition
of the Blood Post-Mortem Depends
on the Mode of Death 228
13.5 Consequences of Positing that All Thrombi Are
Agonal 228
13.5.1 Possible Post-Mortem Changes 229
Contents xx;
13.5.2 Summing up the Argument:
Judicial Implications 229
13.6 Therapeutic and Prophylactic Implications 230
Appendix: Science, Medicine and Philosophy 233
A.I The Two Approaches to Medical Biology 233
A.2 The Philosophical Background to the Schism
of the 1840s 234
A.2.1 The Aftermath of the Scientific Revolution 235
A.2.2 The Empiricist Tradition 235
A.2.3 Hume: The Achilles Heel of Empiricism 236
A.2.4 Kant 237
A.2.5 Naturphilosophie and its Influence on Philosophy
and Science 238
A.2.6 Schopenhauer 239
A.2.7 Significance for 19th-century Physiology
and Pathology 239
A.2.8 The Opening of the Schism 240
A.2.9 The Origin and Development of Mechanistic
Materialism 241
A.3 Mechanism Versus Vitalism: The Distinctiveness
of Vital-Materialism 243
A.3.1 The Mechanism-Vitalism Debate
and its Implications 243
A.3.2 Alternatives to Mechanism
are Often Misrepresented 245
A.3.3 Extreme Mechanism: The 19th-century German
Materialists 245
A.4 The Modern Dominance of the Mechanistic Approach 247
A.4.1 The Metaphysical Dichotomy
in Early 20th-century Biology
and Medicine 247
A.4.2 Some Contributing Factors
to the Hegemony of Mechanism 248
A.4.3 Molecular Motion Versus Bulk
Transport: The Newtonianism of Biochemistry... 249
A.5 Rapprochement between the Mechanistic and
Vital-Materialist Approaches 251
References 255
Author Index 295
Subject Index 30s
|
| adam_txt |
Contents
Preface v
Acknowledgments vii
Synopsis ix
Chapter 1 Introduction to the Study of Deep Venous Thrombosis 1
1.1 Incidence 1
1.2 Pathology 3
1.3 Aetiology: The Consensus Model 4
1.4 The Dominance of the Consensus Model 7
1.5 'Virchow's Triad' 8
1.6 An Alternative Viewpoint 9
Chapter 2 The Coagulation Cascade and the Consensus
Model of DVT 11
2.1 The Cascade Model of Blood Coagulation 11
2.2 The Origin of the Consensus Model of DVT 13
2.3 The Coagulation Cascade Today 16
2.3.1 Platelet Activation and Congregation: Local
Vasoconstriction 17
2.3.2 The Contact ('Intrinsic') System 19
2.3.3 The Tissue Factor ('Extrinsic') System 20
2.3.4 Fibrinogenesis 20
2.3.5 Fibrinolysis 23
2.3.6 Controlling Coagulation 25
2.4 Disorders of Coagulation 27
XV
xvi Contents
Chapter 3 Hypercoagulability 31
3.1 Introduction 31
3.2 The 'General' Use of the Term 'Hypercoagulability' 32
3.3 Early Evidence for 'Hypercoagulability' Conditions 32
3.4 Testing the 'Hypercoagulability' Hypothesis 33
3.5 Inherited Thrombophilias 34
3.6 Acquired Thrombophilias 36
3.7 Thrombophilia and DVT 37
3.8 Testing for Thrombophilias 38
3.9 Implications for Prophylaxis and Therapy 39
3.10 Reflection 40
Chapter 4 Historical Roots 41
4.1 Two Approaches to Biomedical Research 41
4.2 Semantic Issues 42
4.3 The Ancient World 44
4.4 'Binary Oppositions' in 17th-18th-Century Medicine. 45
4.5 Harvey and the 'Physiological' Approach 48
4.6 The 18th Century: Solidism, Humoralism
and the Work of Boerhaave 49
4.7 Hunter and Hewson 51
4.8 Late 18th- and Early 19th-century Studies
of Blood Chemistry 54
4.9 The 18th-Century Pioneers of Haemostatics
and Haemodynamics 54
Chapter 5 Coagulation and its Disorders: A History
of Haematological Research 57
5.1 Introduction 57
5.2 Phase 1: 1835-1893 58
5.2.1 Haemophilia and the Study of Coagulation 59
5.2.2 Buchanan 59
5.2.3 Buchanan's Influence: The Impact
of Mechanistic Materialism 60
5.2.4 The 'Classical Hypothesis'
of Blood Coagulation 63
5.3 Phase 2: 1893-1947 64
5.3.1 Prothrombin and its Conversion
to Thrombin 64
5.3.2 Heparin, Vitamin K and the Dominance
of In Vitro Studies 65
5.4 Philosophical and Semantic Considerations 66
5.5 Reflective Anamnesis 67
Contents xvij
Chapter 6 Virchow and the Pathophysiological Tradition
in the 19th Century 71
6.1 Introduction 71
6.2 Cruveilhier 72
6.2.1 Previous Insights into Thromboembolism 73
6.2.2 Cruveilhier's Contribution 74
6.3 Other Formative Influences on Virchow 75
6.4 Resolving the Conflict: Virchow's Synthesis 77
6.5 Virchow on the Structure of a Thrombus 79
6.6 Virchow on Oxygen and Thromboembolism 81
6.7 Virchow versus Cruveilhier 81
6.8 The Possible Source of 'Virchow's Triad' 83
6.9 Reflective Anamnesis 84
Chapter 7 The Pathophysiological Tradition after Virchow 87
7.1 Problems of Nomenclature: 'Phlebitis' and
'Inflammation' 87
7.1.1 'Pus' 89
7.2 Leukocytes, Phagocytosis and Thrombosis 91
7.3 Platelets 93
7.4 The Persistence of the 'Phlebitis' Concept 95
7.5 Continuation of the Pathophysiological
Perspective: Welch and Aschoff 96
7.6 The Role of Leukocytes Reconsidered 99
Chapter 8 Interrupted Circulation: The 'Stasis' Hypothesis
and the Significance of Venous Valves 103
8.1 Introduction 103
8.2 The Maturation of the Circulation Hypothesis 104
8.3 Connections with the Revolution in Mechanics 106
8.4 The Discovery of Venous Valves 107
8.5 The Significance of Venous Valves 109
8.5.1 The Venous Valves and DVT 110
8.6 The Persistence and Misleading Character
of the 'Stasis' Concept 111
8.6.1 Inherent Difficulties in the 'Stasis' Dogma 111
8.6.2 The Survival of the 'Stasis' Dogma
in the 19th Century 112
8.6.3 'Stasis' and the Consensus
Model of DVT Aetiology 113
8.6.4 Sevitt on the Aetiology of DVT 114
8.6.5 The Consensus Model
and the VVP as Sites of Thrombogenesis 115
xviii Contents
8.7 Is the Current (Mis)Use of 'Blood Stasis'
Equivalent to Virchow's 'Interrupted Circulation'? 116
8.7.1 Pulsatile Blood Movement in Veins 116
8.7.2 Compression of Veins
in the Soles of the Feet 117
8.7.3 Effects of Standing, Sitting and Lying
on the Dynamics of Lower Limb Veins 118
8.8 Towards the Valve Cusp Hypoxia Hypothesis:
I - Altered Blood Movement 119
Chapter 9 Underperfusion of Valve Pockets and the Initiation
of DVT 121
9.1 Introduction 121
9.2 Thrombi Originate in the Venous Valve Pockets 122
9.3 The Morphology and Pathology of Venous Valves 125
9.3.1 Venous Valve Morphology 127
9.3.2 Valve Pathology: The Formation
of Nascent Thrombi within VVP 129
9.3.3 Can the Venous Return Circulation
and Valve Function be Correlated? 132
9.4 The Valve Cycle and the Effects of Non-Pulsatile
Flow 133
9.5 Relevance of Venous Blood Rheology 134
9.5.1 Relevance of the Vasa Venarum 135
9.5.2 Flow Patterns within VVP 137
9.5.3 Implications for the Formation
of Pro-Thrombotic Nidi 137
9.6 Implications for Compression Prophylaxis 138
9.7 Towards the Valve Cusp Hypoxia Hypothesis:
II-VVP Hypoxaemia 139
9.7.1 Hypoxic Injury to the VVP Cusp
Endothelium Is Potentially Thrombogenic:
a Proposal 139
9.7.2 VVP Hypoxaemia and Hypoxic
Injury to the Parietalis Endothelium 143
9.7.3 Testing the Predictions 145
9.8 The Lesson of History 145
Chapter 10 The Role of Endothelial Hypoxia in DVT 147
10.1 Oxygen, the Venous Endothelium and Thrombosis 147
10.2 Hypoxaemia, the Vascular Endothelium
and Thrombosis 148
10.2.1 Association of DVT with
Endothelial Hypoxia 149
10.2.2 Endothelial Hypoxia and Thrombus
Formation in VVP 151
Contents xix
10.2.3 The Significance of Ostial Valves 152
10.2.4 Interpreting Micrographs of Venous
Thrombi: The Tendency
of Thrombi to Embolise 154
10.3 Carbon Monoxide Poisoning and Anaemia 162
10.4 Endothelial Hypoxia and Leukocyte Margination 164
10.5 Aschoff on the Coagulation of Cadaver Blood 165
10.6 Hypoxaemia and 'Traveller's Thrombosis' 166
10.7 Overview: Articulating the Valve Cusp
Hypoxia Hypothesis 168
Chapter 11 The Valve Cusp Hypoxia Hypothesis 169
11.1 Introduction 169
11.1.1 Criteria for an Aetiological Hypothesis 170
11.2 The General Aetiological Sequence: The 'Trinity' 171
11.2.1 'Interrupted Flow' and Underperfusion
ofVVP 172
11.2.2 The Specific Involvement
of the Valve Cusp Parietalis Endothelium 173
11.2.3 Blood Cell Congregation
and Blood Coagulation 174
11.2.4 Pathological Consequences 177
11.3 Experimental Support for the VCHH 178
11.3.1 Polarographic Demonstration of VVP
Hypoxaemia during Non-Pulsatile Flow 178
11.3.2 Experimental Venous Thrombi
Induced by a Non-Invasive Technique 178
11.4 Clinical Implications 183
11.4.1 The Risks of Sleeping for Long Periods
in the Sitting Position 183
11.4.2 Simpson's Cases 185
11.4.3 Anaesthesia 187
11.4.4 Crucifixion 188
11.4.5 Varicose Veins 188
11.5 'Risk Factors' for DVT Reconsidered in the Light
of the VCHH 189
11.6 Prophylaxis 190
11.6.1 Our Theory-Based Estimate of 1.5-3 h 191
11.6.2 Lister's Experience 191
11.6.3 Normal Tourniquet Practice 191
11.6.4 Published Traveller's Thrombosis Data 192
11.6.5 Intermittent Positive Pressure
Compression (IPPC) of Feet or Legs 192
11.6.6 The Animal Experiments of Hamer
and Malone (1984) 194
11.7 Reflection 194
xx Contents
Chapter 12 Molecular Changes in the Hypoxic Endothelium 195
12.1 Endothelial Cell Physiology 195
12.2 The VCHH and the Molecular Responses of EC
to Hypoxia 197
12.3 Phenotypic Changes in EC under Hypoxic
Conditions 197
12.3.1 Phenotypic Changes Consequent on Egr-1
Induction 199
12.3.2 Elk-1 andSRF 200
12.3.3 Other Regulators of Egr-1 Expression 202
12.4 Erg-1, Hypoxia and DVT 204
12.5 Thrombin and the PARs 204
12.6 Interactions Between Platelets and the Hypoxic
Endothelium 206
12.6.1 Platelet Congregation
and Implications for DVT 206
12.6.2 Leukocyte-Platelet Complexes
in the Circulation and their Association
with the Hypoxic Endothelium 207
12.7 Endothelial Hypoxia and the Congregation of
Leukocytes 208
12.7.1 Monocytes and Macrophages 209
12.7.2 Neutrophils 210
12.7.3 Effects of Leukocytes
on Injured Endothelium 211
12.8 The Endothelium and Coagulation 212
12.9 The Endothelium and Vasomotor Tone 216
12.10 A Further Comment on'Risk Factors' 218
12.11 The Unification of Approaches 218
Chapter 13 Cadaver Clots or Agonal Thrombi? 221
13.1 Can Blood Coagulate in a Cadaver? 221
13.2 An Early 20th-century Debate 222
13.3 Aschoff on 'Post-Mortem Clots' 224
13.4 The Debate Reconsidered in the Light of the VCHH . 226
13.4.1 Death from Acute Respiratory Failure 226
13.4.2 Death from Circulatory Failure 227
13.4.3 Summary: The Condition
of the Blood Post-Mortem Depends
on the Mode of Death 228
13.5 Consequences of Positing that All Thrombi Are
Agonal 228
13.5.1 Possible Post-Mortem Changes 229
Contents xx;
13.5.2 Summing up the Argument:
Judicial Implications 229
13.6 Therapeutic and Prophylactic Implications 230
Appendix: Science, Medicine and Philosophy 233
A.I The Two Approaches to Medical Biology 233
A.2 The Philosophical Background to the Schism
of the 1840s 234
A.2.1 The Aftermath of the Scientific Revolution 235
A.2.2 The Empiricist Tradition 235
A.2.3 Hume: The Achilles'Heel of Empiricism 236
A.2.4 Kant 237
A.2.5 Naturphilosophie and its Influence on Philosophy
and Science 238
A.2.6 Schopenhauer 239
A.2.7 Significance for 19th-century Physiology
and Pathology 239
A.2.8 The Opening of the Schism 240
A.2.9 The Origin and Development of Mechanistic
Materialism 241
A.3 Mechanism Versus Vitalism: The Distinctiveness
of Vital-Materialism 243
A.3.1 The Mechanism-Vitalism Debate
and its Implications 243
A.3.2 Alternatives to Mechanism
are Often Misrepresented 245
A.3.3 'Extreme' Mechanism: The 19th-century German
Materialists 245
A.4 The Modern Dominance of the Mechanistic Approach 247
A.4.1 The Metaphysical Dichotomy
in Early 20th-century Biology
and Medicine 247
A.4.2 Some Contributing Factors
to the Hegemony of Mechanism 248
A.4.3 Molecular Motion Versus Bulk
Transport: The 'Newtonianism' of Biochemistry. 249
A.5 Rapprochement between the Mechanistic and
Vital-Materialist Approaches 251
References 255
Author Index 295
Subject Index 30s |
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| discipline | Medizin |
| discipline_str_mv | Medizin |
| era | Geschichte 1800-2007 gnd |
| era_facet | Geschichte 1800-2007 |
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| index_date | 2024-07-02T20:47:13Z |
| indexdate | 2024-07-09T21:15:22Z |
| institution | BVB |
| isbn | 9781402066498 9781402066504 |
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| spelling | Agutter, Paul S. Verfasser aut The aetiology of deep venous thrombosis a critical, historical and epistemological survey Paul S. Agutter ; P. Colm Malone Berlin [u.a.] Springer 2008 XXI, 318 S. Ill. 235 mm x 155 mm txt rdacontent n rdamedia nc rdacarrier Geschichte 1800-2007 gnd rswk-swf Theoriendynamik (DE-588)4117201-2 gnd rswk-swf Venenthrombose (DE-588)4187482-1 gnd rswk-swf Ätiologie (DE-588)4000646-3 gnd rswk-swf Venenthrombose (DE-588)4187482-1 s Ätiologie (DE-588)4000646-3 s Theoriendynamik (DE-588)4117201-2 s Geschichte 1800-2007 z b DE-604 Malone, P. Colm Verfasser aut HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=016486905&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Agutter, Paul S. Malone, P. Colm The aetiology of deep venous thrombosis a critical, historical and epistemological survey Theoriendynamik (DE-588)4117201-2 gnd Venenthrombose (DE-588)4187482-1 gnd Ätiologie (DE-588)4000646-3 gnd |
| subject_GND | (DE-588)4117201-2 (DE-588)4187482-1 (DE-588)4000646-3 |
| title | The aetiology of deep venous thrombosis a critical, historical and epistemological survey |
| title_auth | The aetiology of deep venous thrombosis a critical, historical and epistemological survey |
| title_exact_search | The aetiology of deep venous thrombosis a critical, historical and epistemological survey |
| title_exact_search_txtP | The aetiology of deep venous thrombosis a critical, historical and epistemological survey |
| title_full | The aetiology of deep venous thrombosis a critical, historical and epistemological survey Paul S. Agutter ; P. Colm Malone |
| title_fullStr | The aetiology of deep venous thrombosis a critical, historical and epistemological survey Paul S. Agutter ; P. Colm Malone |
| title_full_unstemmed | The aetiology of deep venous thrombosis a critical, historical and epistemological survey Paul S. Agutter ; P. Colm Malone |
| title_short | The aetiology of deep venous thrombosis |
| title_sort | the aetiology of deep venous thrombosis a critical historical and epistemological survey |
| title_sub | a critical, historical and epistemological survey |
| topic | Theoriendynamik (DE-588)4117201-2 gnd Venenthrombose (DE-588)4187482-1 gnd Ätiologie (DE-588)4000646-3 gnd |
| topic_facet | Theoriendynamik Venenthrombose Ätiologie |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=016486905&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
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