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" Histamine and Histamine Antagonists "
Börje Uvnäs
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BL
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734399
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b554230
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Börje Uvnäs
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| Title & Author
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Histamine and Histamine Antagonists\ Börje Uvnäs
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| Publication Statement
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Berlin Springer Berlin, 2013
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| Series Statement
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Handbook of Experimental Pharmacology, 97
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XXVI, 763 Seiten in 1 Teil XXVI, 763 Seiten 101 Figuren, 205 tables, 205 schw.-w. Tabellen 235 x 155 mm
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3642758428
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: 9783642758423
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| Contents
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1 Current Techniques of Histamine Determination.- A. Suggestions to Those Who Have Become Histaminologists at a Time of Overflooding and Biased Information.- References.- B. Bioassays.- I. Introduction.- II. Description.- III. Practicability.- IV. Reliability.- V. Comments.- References.- C. Fluorometric Assays.- I. Introduction.- II. Modifications of the Fluorometric Assay.- III. Strategy for Selecting a Modified Fluorometric Assay for Solving a Specific Analytical Problem.- IV. Combined Method as a Standard Technique for Histamine Assays in Tissues, Body Fluids and Isolated Cells.- 1. Sample-Taking and Preparation.- 2. Homogenization and Centrifugation.- 3. Ion-Exchange Chromatography on Dowex 50W-X8.- 4. Extraction by Solvent Partition.- 5. Condensation Step.- 6. Measurement and Calculation of Histamine Contents.- V. Reliability and Practicability of the Fluorometric Methods.- 1. Detectability (Sensitivity).- 2. Specificity.- 3. Precision.- 4. Accuracy.- 5. Practicability.- VI. Conclusions.- References.- D. Automated Fluorometric Assays.- I. Introduction.- II. Chemistry of the Reactions.- III. Chemical System in Use in the Author's Laboratory.- IV. Carry-Over.- V. Detectability.- VI. Specificity.- VII. With-Run Imprecision.- VIII. Practicability.- IX. Glass Microfibre-Based Histamine Assay.- X. Conclusions.- References.- E. Radioenzymatic Assays in Biological Fluids.- I. Introduction.- II. Assay Procedures.- III. Applications.- IV. Precision, Accuracy and Specificity.- V. Sensitivity.- References.- F. Determination by High-Performance Liquid Chromatography.- I. Techniques.- II. Detection and Derivatization.- III. Performance Characteristics.- 1. Precision.- 2. Accuracy and Specificity.- 3. Detectability.- IV. Coanalysis of Related Compounds.- V. Practicability.- VI. Conclusions.- References.- G. Determination in Biological Samples by Gas Chromatography-Mass Spectrometry.- I. Introduction.- II. Description.- 1. Materials.- 2. Sample Handling.- 3. Extraction Procedure.- 4. Preparation of Standards.- 5. Derivatization.- 6. Gas Chromatography-Mass Spectrometry.- 7. Quantification.- III. Practicability.- IV. Precision, Accuracy and Specificity.- References.- H. Immunologic Methods.- I. Introduction.- II. Description.- III. Practicability.- IV. Precision.- V. Accuracy and Specificity.- VI. Detectability.- VII. Format of the Assessment Report.- References.- J. Measurement of Histamine Metabolites.- I. Introduction.- II. Enhancement of Insights into the Physiological and Pathophysiological Roles of Histamine by Measuring Its Metabolites.- References.- K. Munich Consensus Development Conference on Histamine Determination.- I. Consensus Development Conference: A New Strategy for Solving Problems Not Only in Clinical Medicine But Also in Biomedicine in a Formalized Way.- II. Results: The Consensus Statement.- 1. What Criteria Should be Used to Analyse the Reliability of a Histamine Assay?.- a) Detectability (Sensitivity).- b) Specificity.- c) Precision.- d) Accuracy.- 2. How Reliable at Present are the Principal Assays for Measuring Histamine in Standard Solutions with Authentic Histamine.- 3. How Reliable at Present are the Principal Assays for Measuring Histamine in Human Plasma?.- 4. Is the Usefulness of the Principal Assays for Obtaining Reliable Histamine Values Demonstrated for a Series of Biomedical Conditions and for Some More Complex Situations?.- III. Conclusion.- References.- 2 Heterogeneity of Mast Cells.- A. Introduction: Role and Distribution of Mast Cells.- B. Aspects of Mast Cell Heterogeneity.- I. Histochemical Differences Between Mast Cells.- II. Ultrastructural Differences Between Mast Cells.- III. Differences in Preformed and Newly Synthesized Mast Cell Mediators.- IV. Functional Differences: Variations in Response to Secretory Stimuli and Anti-Allergic Drugs.- C. Origins of Mast Cell Heterogeneity.- D. Summary and Conclusions.- I. Implications of Mast Cell Heterogeneity.- II. Problems of Nomenclature.- III. Conclusions.- References.- 3 Control of the Exocytotic Mechanism in Rat Mast Cells.- A. The Mast Cell and Exocytotic Secretion.- B. Stimulus-Secretion Coupling.- I. Role of Ca2+.- II. Role of ATP.- III. Cell Permeabilisation.- IV. Secretion Induced by Ca2+ from ATP4-Permeabilised Mast Cells.- 1. Secretion Induced by CA2+ from Other Secretory Cells.- 2. Control of Ca2+ Affinity by GTP in Permeabilised Platelets.- V. Calcium Ion Independent Secretion Induced by GTP from Permeabilised Neutrophils.- C. Essential Role for GTP in Exocytosis from Mast Cells.- I. Essential Synergy for Ca2+ and GTP for Secretion from Permeabilised Mast Cells.- 1. Enhancement of Affinity for Ca2+ and Guanine Nucleotide by ATP.- 2. Enhancement of Affinity for GTP by ATP.- 3. Role of ATP in Stimulus-Secretion Coupling.- 4. Role of Protein Kinase C in the Maintenance of Effector Affinity.- 5. Restoration of Responsiveness by ATP to Cells Rendered Refractory Following Permeabilisation.- II. Role of Polyphosphoinositide Metabolites in Exocytosis?.- 1. G-Protein Control of Exocytosis: GE.- 2. Involvement of GE in Other Secretory Cells.- 3. Receptor Control of GE in Mast Cells?.- III. Summary.- D. Kinetics of Exocytosis.- I. Effect of Varying GTP-?-S.- II. Effect of Varying Ca2+.- III. Rate of Arachidonate Production Paralleling Exocytosis.- IV. Inhibition of Onset of Exocytosis by ATP.- 1. A Protein Dephosphorylation Mechanism of Exocytotic Secretion.- V. Summary.- E. Measurement of Membrane Capacitance.- I. Unit Exocytotic Events.- 1. Capacitance Flicker.- 2. Beige Mouse Mast Cells.- F. Conclusion.- References.- 4 Formation of Histamine: Histidine Decarboxylase.- A. Introduction.- B. Distribution.- I. Stomach.- II. Mast Cells.- III. Brain.- IV. Miscellaneous Tissues.- C. Purification.- D. Properties.- E. Inhibitors.- I. In Vitro Studies on HDC Inhibition by FMH.- II. In Vivo Inactivation of HDC and Depletion of Histamine by FMH Administration.- III. Effect of Histamine Depletion by FMH on Physiological Parameters and Possible Use of FMH as a Drug.- F. Changes in HDC Activity with Various Treatments.- G. Antibodies.- References.- 5 Catabolism of Histamine.- A. Introduction.- B. Methylation of Histamine.- I. Ring N-Methylation.- 1. Assay of Histamine N-Methyltransferase.- 2. Properties of Histamine N-Methyltransferase.- 3. Inhibitors of Histamine N-Methyltransferase Activity.- 4. Occurrence and Distribution.- 5. Metabolites.- II. Side-Chain Methylation.- C. Oxidative Deamination of Histamine.- I. Assay of Diamine Oxidase.- II. Occurrence of Diamine Oxidase.- III. Properties of Diamine Oxidase.- IV. Inhibitors.- D. Other Catabolic Pathways of Histamine.- I. Glutamylation of Histamine.- II. Acetylation of Histamine.- References.- 6 Histamine Receptors in Brain.- A. Introduction.- B. Histamine H1 Receptors.- I. Molecular Properties.- II. Distribution in the CNS.- III. Inositol Phospholipid Hydrolysis.- IV. Potentiation of Cyclic AMP Accumulation.- V. Glycogenolysis.- VI. Cyclic GMP Accumulation and Other Biochemical Responses.- VII. Electrophysiological Responses.- C. Histamine H2 Receptors.- I. Molecular Properties.- II. Adenylate Cyclase Activation.- III. Phospholipid Methylation.- IV. Localization.- V. Electrophysiological Responses.- D. Histamine H3 Receptors.- I. Pharmacological Definition and Structure-Activity Relationships.- II. Mediation of Actions.- III. Radiolabelling.- IV. Distribution in the CNS.- E. Conclusions.- References.- 7 Structure and Functions of the Histaminergic Neurone System.- A. Introduction.- B. Location and Distribution of the Histaminergic Neurone System.- I. Neurochemical Studies.- II. Immunohistochemical Studies.- 1. Histaminergic System in Rat Brain.- a) Histidine Decarboxylase as a Marker.- b) Histamine as a Marker.- c) Histaminergic Neurones in the Tuberomammillary Nucleus of Rat Hypothalamus.- d) Organization of Histaminergic Nerve Fibres in Rat Brain.- 2. Central Histaminergic System in Other Species.- III.
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Autoradiographic Studies.- C. Physiological Functions of the Histaminergic Neurone System.- I. General Considerations.- II. ?-Fluoromethylhistidine as a Pharmacological Tool.- III. Possible Physiological Functions Deduced from Neuropharmacological Studies.- 1. Behaviours.- a) Motor Activity.- b) Conditioned Behaviour.- c) Aggression and Depression.- d) Cataleptic Behaviour.- e) Feeding Behaviour.- f) Drinking Behavkmr.- 2. Sleep-Wakefulness.- 3. Antinociception and Analgesia.- 4. Neuroendocrine System.- a) Corticotropin.- b) Somatotropin.- c) Gonadotropin.- d) Prolactin.- e) Thyrotropin.- f) Vasopressin.- 5. Blood Pressure.- 6. Thermoregulation.- D. Conclusion.- References.- 8 Histamine H2 Receptors and Lung Function.- A. Introduction.- B. H2 Receptors and Airway Smooth Muscle.- C. H2 Receptors and Pulmonary Vasculature.- D. H2 Receptors and Mucus Secretion.- E. H2 Receptors and Inflammatory Mediator Release from Lung.- F. H2 Receptors and the Control of Lung Function In Vivo.- G. Concluding Remarks.- References.- 9 Histamine and the Parietal Cell.- A. Introduction.- I. Historical Notes.- II. Experimental Models.- 1. Intact Animals.- 2. Isolated Stomachs.- 3. Isolated Glands.- 4. Isolated Cells.- 5. Subcellular Preparations.- B. Stimulatory Processes at the Parietal Cell.- I. Receptors.- 1. Histamine.- 2. Gastrin.- 3. Acetylcholine.- 4. Adenosine.- 5. Other Receptors.- II. Mode of Action of Secretagogues. Second Messengers.- 1. Histamine.- 2. Gastrin.- 3. Acetylcholine.- III. Histamine as the Final Common Mediator or Just a Cooperative Secretagogue.- 1. The Transmission Hypothesis.- 2. The Permission Hypothesis.- 3. Histamine-Containing Cells.- IV. Mode of Action by Some Gastric Acid Inhibitors.- 1. Adenosine.- 2. Somatostatin.- 3. Prostaglandins.- V. A Different Hypothesis.- C. Effects on the Parietal Cell.- I. The Black Box.- II. The Proton Translocation System. Morphological Transformation.- D. Conclusions.- References.- 10 Do Histamine-Storing Cells in the Gastric Mucosa Mediate the Acid-Stimulating Action of Gastrin?.- A. Introduction.- B. The Histamine as Mediator Hypothesis.- C. The Interaction Hypothesis.- D. Critical Evaluation of Prevailing Models.- E. The Transducer Hypothesis.- F. Gastric Histamine Stores.- I. Enterochromaffin-Like Cells.- II. Mast Cells.- III. Histamine-Containing Neurons.- G. Concluding Remarks.- References.- 11 Histamine in Cardiovascular Function and Dysfunction: Recent Developments.- A. Effects of Histamine on the Heart.- I. Introduction.- II. Sinoatrial Rate.- III. Atrioventricular Conduction.- IV. Automaticity and Triggered Activity.- V. Contractility.- B. Effects of Histamine on Vasculature.- I. Overview: Effects and Mechanisms.- II. Coronary Vessels.- III. Cerebral Vessels.- IV. Pulmonary Vessels.- V. Aorta.- VI. Mesenteric Artery.- VII. Renal Artery.- VIII. Veins.- C. Role of Histamine in Cardiovascular Pathophysiology.- I. Localization and Release.- II. Immediate Hypersensitivity.- III. Myocardial Ischemia.- IV. Atherosclerosis and Diabetes.- D. A Physiological Role for Histamine in the Cardiovascular System?.- References.- 12 Histamine in Anaesthesia and Surgery: Causality Analysis.- A. Introduction.- B. Networks of Experimental and Clinical Evidence Suggesting that Histamine is Significantly Involved in Adverse Reactions During Anaesthesia and Surgery.- I. Hypnotic Agents and the Criteria for Causal Associations.- 1. Koch-Dale Criteria.- 2. Hill Criteria.- II. Clinical Epidemiology of Adverse Reactions.- III. Classification of the Reactions by Mechanisms.- IV. Plasma Substitutes.- V. Narcotics and Muscle Relaxants.- VI. Contrast Media During Operations.- VII. Surgical Manoeuvres and Other Physical and Chemical Measures During Operations.- 1. Diseases with Elevated Plasma Histamine Levels.- 2. Preoperative Measures.- 3. Surgical Procedures.- 4. Postoperative Recovery and Care.- C. Philosophy of Histamine in Anaesthesia and Surgery: H1 + H2 Prophylaxis as a Practical Approach.- References.- 13 Histamine in Duodenal Ulcer, Stress-Induced Lesions, and Upper Gastrointestinal Bleeding: Causality Analysis.- A. Introduction.- B. Methods for Assessing Causal Associations of Histamine as a Mediator of Gastrointestinal Diseases Among Other Candidates.- I. Decision Tree: Meta-Analysis.- II. Koch-Dale and Hill Criteria: Unicausal Analysis.- III. Conditional Probabilities and Causal Networks: Multicausal Analysis.- C. Duodenal Ulcer.- I. Meta-Analysis.- II. Unicausal Analysis.- III. Multicausal Analysis.- D. Stress-Induced Lesions.- I. Meta-Analysis.- 1. Trauma.- 2. Major Surgery.- 3. Cerebral Injury.- 4. Hemorrhagic Shock.- 5. Respiratory Insufficiency.- 6. Fat Embolism.- 7. Renal Insufficiency.- 8. Sepsis and Septic Shock.- 9. Immobilization.- 10. Psychological Stress.- 11. Burns.- 12. Ulcerogenic Drugs.- II. Causality Analysis.- E. Upper Gastrointestinal Bleeding.- I. Meta-Analysis.- II. Causality Analysis.- F. Conclusion.- References.- 14 Histamine and the Blood.- A. Introduction.- B. Amount of Histamine in the Blood.- C. Distribution of Histamine in the Blood.- I. Plasma and Serum.- II. Granular Series of Leucocytes (Basophils, Neutrophils and Eosinophils).- III. Non-Granular Series of Leucocytes (Lymphocytes and Monocytes).- IV. Platelets.- D. Metabolism of Histamine in the Blood.- I. Leucocytes.- II. Changes in Metabolism.- E. Release of Histamine from Blood Cells.- I. Basophils.- II. Eosinophils.- III. Neutrophils.- IV. Lymphocytes.- F. Effects of Histamine on Blood Cells.- I. Neutrophils.- II. Eosinophils.- III. Immunological Reactions.- 1. Histamine as an Immunosuppressive Factor.- 2. Lymphocytes.- G. Histamine-Induced Leucocytosis.- I. Histamine-Related Leucocytosis in Experimental Animals.- II. Effect on Neutrophil Precursors.- III. Histamine and Cell Proliferation.- IV. Effect on Leukaemic Cells.- References.- 15 Histamine in Food.- A. Introduction.- B. Formation and Levels of Histamine in Foods.- I. Formation.- II. Levels.- 1. Fish and Fish Products.- 2. Milk and Cheese.- 3. Wine and Beer.- 4. Other Foods.- III. Measures to Control Histamine Formation.- C. Histamine ("Scombroid") Food Poisoning.- I. Symptoms.- II. Diagnosis and Treatment.- III. Epidemiology.- IV. Role of Histamine.- References.- 16 Role of Histamine in the Actions of Neuropeptides and Local Hormones.- A. Introduction.- B. Mast Cell Heterogeneity.- C. Release of Histamine by the Tachykinins.- I. Substance P.- 1. Studies on Rat Peritoneal Mast Cells.- a) Tachykinin Antagonists.- b) Benzalkonium Chloride.- c) Neuraminidase.- d) Mechanism of Action of Substance P on Mast cells.- 2. In Vivo Studies in Animals.- 3. Studies on Human Mast Cells and Human Skin.- II. Neurokinins.- D. Release of Histamine by Other Neuropeptides.- I. Neurotensin.- II. Somatostatin.- III. Vasoactive Intestinal Polypeptide.- IV. Opioid Peptides.- V. Calcitonin Gene-Related Peptides.- E. Release of Histamine by Local Hormones.- I. Bradykinin and Related Peptides.- II. Prostanoids.- F. Role of Histamine in the Actions of Neuropeptides.- I. Axon Reflexes, Antidromic Vasodilatation and Neurogenic Inflammation.- 1. Nature of the Neurones.- 2. Sensitivity to Capsaicin.- 3. Neuropeptides in Primary Afferent Neurones.- II. Functional Relationship Between Sensory Neurones and Mast Cells.- III. Interactions Between Histamine and Neuropeptides.- G. Conclusion.- References.- 17 Antagonists of H1 Receptors of Histamine: Recent Developments.- A. Introduction.- B. Chemical Types of H1-Antihistaminic Agent.- I. Tertiary Aminoalkyl Ethers.- II. Cyclizines.- III. 1,l-Diaryl-3-Aminopropenes.- IV. Terfenadine.- V. Astemizole.- VI. Tricyclic Derivatives.- VII. Miscellaneous Types.- C. Binding Studies.- D. Steric Aspects.- I. Isomeric Potency and Affinity Ratios.- E. Final Remarks.- References.- 18 Structural Requirements for Histamine H2 Agonists and H2 Antagonists.- A. Introduction.- B. Structural Requirements for H2 Agonism.- I. Introduction.- II. Histamine Analogues.- III.
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Dimaprit Analogues.- IV. Impromidine Analogues.- C. Structural Requirements for H2 Antagonism.- I. Introduction.- II. Cimetidine Analogues.- III. Ranitidine Analogues.- IV. Tiotidine Analogues.- V. Lamtidine Analogues.- VI. Diaryl Analogues.- VII. Miscellaneous.- D. Structural Characteristics of H2 Antagonists in Cytochrome P-450 Inactivation.- I. Introduction.- II. Interaction with Cytochrome P-450.- III. Ligand Interactions of Cimetidine.- IV. Effect of Ranitidine; Structural Requirements in General.- V. Effects of H2 Antagonists on the Oxidase Activity of Cytochrome P-450.- VI. Prevention of Toxicity of Xenobiotics by H2 Antagonists.- VII. Conclusion.- References.
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QP905.B675 2013
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Börje Uvnäs
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