Throughout the centuries, inflammation has been considered as a disease in itself. This misconception arose from the inability to distinguish between inflammatory changes and the insults which induce them. The understanding of the distinction between the genesis of inflammation and the tissue reactions that follow is attributed to JOHN HUNTER, who, at the end of the 18th century, substantially contributed to the analysis of inflammation in objective terms. Today, however, we are still trying to find explanations for Celsus' Signs in terms of structural and functional changes occurring in the inflamed tissue. There are drugs which modulate these signs but, without a detailed knowledge of the basic physiopathological events, it is impossible to understand their mechanism of action. Notwithstanding, the effects of anti­ inflammatory drugs provided new knowledge of the relevance of the signs and symptoms to the sequence of biochemical and morphological changes occurring in inflammation. When we accepted the invitation to edit a Handbook on Inflammation and Anti­ Inflammatory Drugs, we were aware of the magnitude of the task. We knew the impossibility of covering the whole field in detail, especially taking into account the rapid accumulation of experimental knowledge which would, in all likelihood, overtake the process of publication.

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Historical Survey of Definitions and Concepts of Inflammation.- References.- The Inflammatory Reaction.- 1 A Brief History of Inflammation.- A. From the Origins to the 19th Century.- B. Earlier 20th Century.- C. Chemical Mediators: Further Development.- References.- 2 The Sequence of Early Events.- A. Introduction.- B. The Phenomena of the Initial Response to Injury.- I. Changes in Vascular Calibre and Flow.- 1. The Normal Microcirculation.- 2. The Changes Seen After Injury.- II. Increased Vascular Permeability.- 1. Normal Structure of Small Blood Vessels.- 2. Exchanges Across the Wall of Normal Small Vessels.- 3. The Effects of Histamine-Type Permeability Factors-Vascular Labelling.- 4. Increased Permeability in Other Types of Inflammation.- III. Leucocytic Emigration.- 1. Pavementing of Leucocytes.- 2. Leucocytic Emigration.- 3. Chemotaxis.- 4. Mediators of Leucocytic Emigration.- C. Subsequent Course of the Inflammatory Reaction.- I. Resolution.- 1. Inflammatory Exudate.- 2. Polymorphs.- 3. Fibrin.- 4. Dead Tissue Cells.- II. Suppuration.- References.- 3 Mononuclear Phagocytes in Inflammation.- A. Nomenclature of Mononuclear Phagocytes.- B. Approaches to the Characterisation of Mononuclear Phagocytes.- I. Morphology.- II. Cytochemical Characterisation.- III. Functional Characterisation.- IV. Culture Characteristics.- C. The Characteristics of Mononuclear Phagocytes in Relation to Those of Other Cells.- D. Functions of Mononuclear Phagocytes.- E. Origin and Kinetics of Mononuclear Phagocytes During the Normal Steady State.- F. Origin and Kinetics of Mononuclear Phagocytes During an Inflammatory Response.- I. Acute Inflammation.- II. Chronic Inflammation.- G. The Effects of Anti-Inflammatory Drugs.- I. Glucocorticosteroids.- II. Azathioprine.- H. Humoral Control of Monocytopoiesis During Inflammation.- I. The Mononuclear Phagocyte System and Disease.- References.- 4 The Adhesion, Locomotion, and Chemotaxis of Leucocytes.- A. Introduction.- B. Leucocyte Adhesion.- I. General Considerations.- II. Studies of the Adhesion of Leucocytes.- C. Leucocyte Locomotion.- I. Morphological Observations.- II. Contact Inhibition of Movement.- III. Redistribution of Membrane in Moving Cells.- D. Chemotaxis.- I. Chemotaxis and Chemokinesis.- II. Methods for Measuring Leucocyte Chemotaxis.- III. Methods by Which Cells Detect Gradients.- IV. Chemoattractants.- 1. Products of Specific Immune Reactions.- 2. Non-Specific Endogenous Factors.- 3. Exogenous Chemoattractants.- V. Possible Models of Action of Chemoattractants at the Cell Membrane.- VI. Motor Mechanisms in Leucocyte Locomotion and Chemotaxis.- VII. Other Biochemical Mechanisms.- 1. Energy Sources for Locomotion.- 2. Cyclic Nucleotides.- 3. Protein and Nucleic Acid Synthesis.- 4. Effects of Other Agents.- VIII. Migration of Individual Leucocyte Types.- 1. Neutrophils and Mononuclear Phagocytes.- 2. Eosinophils.- 3. Lymphocytes.- IX. Does Chemotaxis Occur in vivo?.- References.- Addendum.- 5 Platelet Aggregation Mechanisms and Their Implications in Haemostasis and Inflammatory Disease.- A. Introduction.- B. Relationship of Morphology to Physiological Function in the Blood Platelet.- I. The Amorphous Coat.- II. The Trilaminar Plasma Membrane.- III. The Surface-Connecting ("Open Channel" or "Cannicular") System.- IV. The Dense-Tubular System.- V. Microtubules.- VI. Microfilaments.- VII. Granules.- VIII. Organelles Concerned With Carbohydrate, Protein and Lipid Metabolism.- C. Mechanisms of Platelet Aggregation.- I. Adhesion and Spreading.- II. The Shape Change.- III. Aggregation.- IV. The Platelet Release Reaction.- V. An Outline of Methods for Studying Platelet Aggregation and Related Processes.- VI. Mechanisms of Platelet Aggregation.- 1. Semantics-First and Second Phase Aggregation.- 2. Mechanisms of Directly Induced Platelet Aggregation.- 3. The Labile Aggregation-Stimulating Substances (LASS) Derived From Arachidonic Aci.- 4. Mechanisms of Aggregation Induced Indirectly (i.e. Mediated Through Pro-Aggregatory Platelet Substances).- 5. "Special Cases" (e.g. Zymosan and Ristocetin.- D. The Role of Platelets in Haemostasis and Haemostatic Defects.- I. Events Occurring in Haemostasis.- II. Haemostatic Defects.- 1. Thrombocytopenia (Decreased Level of Circulating Platelets).- 2. Afibrinogenemia.- 3. Von Willebrand's Disease.- 4. Bernard Soulier (Giant Platelet) Syndrome.- 5. Thrombasthenia.- 6. Storage Pool Disease.- 7. Congenital Aspirin-Like Defects in Aggregation.- 8. Other Platelet Abnormalities.- E. The Role of Platelets in Inflammatory Processes.- I. The Platelet as a Source of Pro-Inflammatory Material.- 1. Mediators of Acute Inflammation Released From Platelets.- 2. Chemotactic Factors From Platelets.- 3. Cationic Proteins and Peptides Which Induce Increased Vascular Permeability.- 4. Pro-Inflammatory and Autolytic Enzymes From Platelets.- II. Evidence for Participation of Platelets in Various Inflammatory Diseases.- 1. Acute Inflammatory Responses Induced in the Rat by Non-Immunological Mechanisms.- 2. Inflammation Produced by Immunological Mechanisms.- F. Concluding Remarks.- I. Haemostasis.- II. Platelet Aggregation Mechanisms.- III. Inflammation.- References.- 6 Regeneration and Repair.- A. The Replacement of Lost Tissue.- I. Tissues Capable of Regeneration.- II. Tissues Incapable of Adequate Regeneration.- B. The Nature of the Stimulus Leading to Formation of Scar Tissue.- C. The Generation of Scar Tissue.- I. Generation of Scar Tissue in the Presence of Fibrin.- II. Generation of Scar Tissue in the Absence of Fibrin.- D. Stages in Scar Tissue Formation.- I. Formation of Capillaries.- II. The Formation of Connective Tissue.- 1. The Cells Involved.- 2. The Non-Fibrous Components of Connective Tissue.- 3. The Fibrous Components of Connective Tissue.- E. The Maturation of Scar Tissue: Contraction.- F. Abnormalities of Scar Tissue.- I. Keloids and Hypertrophic Scars.- II. Dupuytren's Contracture.- III. Scleroderma: Systemic Sclerosis.- IV. Drug-Induced Fibrosis.- G. Healing of Specialised Tissues.- Summary.- References.- 7 Immunological and Para-Immunological Aspects of Inflammation.- A. Introduction.- B. Mechanisms of Reactions in the Skin, Joints, and Body Cavities.- I. Complement-Dependent.- 1. Classical Pathway of Complement Activation.- 2. The Arthus Reaction.- 3. The Alternative Pathway of Complement Activation.- 4. Non-Specific Reactions to Endotoxin and the Local Shwartzman Phenomenon.- II. Cell-Mediated Immunity.- C. Complement-Dependent Inflammation-Classical Pathway.- I. Arthus Reaction.- 1. Experimental.- 2. Clinical.- II. Circulating Immune Co…