Histamine and Histamine Antagonists (eBook, PDF)

Redaktion: Uvnäs, Börje

• Format: PDF

Produktbeschreibung

This book covers the progress in histamine research during the past two decades. Chapters are devoted to new techniques and new experimental approaches which have brought new knowledge and deeper insights into the biomedical significance of histamine.

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Produktdetails

• Verlag: Springer Berlin Heidelberg
• Seitenzahl: 763
• Erscheinungstermin: 6. Dezember 2012
• Englisch
• ISBN-13: 9783642758409
• Artikelnr.: 53105569

Inhaltsangabe

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 ProteinDephosphorylation 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. 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. ConcludingRemarks.- 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. CerebralInjury.- 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 bythe 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. 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.