By R. J. Gryglewski (auth.), Dr. John R. Vane, Dr. Sergio H. Ferreira (eds.)

ISBN-10: 3642668917

ISBN-13: 9783642668913

ISBN-10: 3642668933

ISBN-13: 9783642668937

Screening and Toxicity of anti inflammatory Drugs.- 19 Screening and evaluate of the efficiency of anti inflammatory medications in vitro.- A. Introduction.- B. interplay With Non-Enzymic Proteins.- I. Binding to Plasma Proteins.- 1. Displacement Reactions.- 2. Disulphide Interchange Reactions.- three. security opposed to Protein Denaturation.- four. Fibrinolytic Activity.- II. interplay With organic Membranes.- 1. results on Erythrocyte Membrane.- 2. results on Lysosomal Membrane.- three. Cytotoxic Properties.- four. results on Leucocyte Migration.- C. interplay With Enzymic Proteins.- I. normal Considerations.- II. interplay With Enzymes inquisitive about Carbohydrate, Protein, and Nucleic Acid Metabolism.- 1. Carbohydrate, Protein, and Amino Acid Metabolism.- 2. Nucleic Acid and Nucleotide Metabolism.- III. Inhibition of Prostaglandin Synthetase.- 1. Prostaglandin Synthetase System.- 2. Assay of Prostaglandin Synthetase Activity.- three. Prostaglandin Synthetase Inhibitors.- four. Inhibition of Platelet Aggregation.- five. results on tender Muscle.- D. Conclusions.- References.- 20 Inhibition of Erythema and native Hyperthermia.- A. Introduction.- B. Ultraviolet (UV) gentle and the Erythematous Response.- C. Instrumentation.- I. mild resources for Induction of Erythema.- II. dimension of Erythema and native Hyperthermia.- 1. Erythema.- 2. pores and skin Temperature.- D. Procedures.- I. Erythema.- 1. UV-Induced.- 2. Thurfyl Nicotinate-Induced.- three. Miscellaneous approaches for generating Erythema.- II. neighborhood Hyperthermia.- 1. neighborhood Hyperthermia in Paws of Rats Injected With Irritants.- 2. neighborhood Hyperthermia in UV-Irradiated Skin.- E. Inhibition of Erythema and native Hyperthermia.- I. UV-Induced Erythema.- 1. Systemic management of Drugs.- 2. Topically or Intradermally.- II. Tetrahydrofurfuryl Nicotinate (THFN) Erythema.- III. different Erythemas.- IV. neighborhood Hyperthermia.- F. Conclusion.- References.- 21 Oedema and elevated Vascular Permeability.- A. normal ideas of Assays.- I. Statistical concerns in Assay Work.- 1. courting of Dose to Effect.- 2. Definition of ED50.- three. self assurance Limits.- four. Coefficent of Variation.- five. The g Value.- 6. The Lambda price, ?.- 7. mistakes of sorts I and II.- B. tools for generating and Measuring Oedema and elevated Vascular Permeability.- I. Oedemas of the Rat’s Paw.- 1. Measurement.- 2. brokers inflicting Paw Oedema; features of Oedemas attributable to a number of Agents.- II. elevated Vascular Permeability.- III. Oedema within the Pleural Space.- C. Conclusion.- References.- 22 temporary Drug keep watch over of Crystal-Induced Inflammation.- A. ancient Aspects.- B. Mechanism of Crystal-Induced Inflammation.- I. Phagocytosis.- II. Membranolysis.- III. Inflammatory Mediators.- IV. Chemotactic Factors.- C. Experimental Models.- I. Animal.- II. Man.- D. remedy of Acute assaults of Gout and Pseudogout.- I. Gout.- II. Pseudogout.- E. Summary.- References.- 23 Experimental types of Arthritis in Animals as Screening checks for medicinal drugs to regard Arthritis in Man.- A. Introduction.- B. merits and downsides of types of Arthritis—Comparison With Acute Models.- C. Adjuvant-Induced Arthritis.- I. First statement. First Use as a reveal for anti inflammatory/ Antirheumatic Drugs.- II. Production.- 1. Adjuvant.- 2. direction of Injection.- three. Species edition and pressure Variation.- four. Time process the Disease.- III. Aetiology.- 1. function of Lymphatic System.- 2. Immunological Mechanisms.- three. Histology.- four. Lysosomal Enzymes.- IV. Assessment.- 1. actual Assessment—Gross Measurements.- 2. Physiological/Functional Parameters.- three. Biochemical Parameters.- four. interval of Dosing of Compounds.- V. impact of Drugs.- 1. Non-Steroid anti inflammatory Drugs.- 2. Steroid anti inflammatory Drugs.- three. Gold, Chloroquine, and Penicillamine.- four. Immunosuppressant Drugs.- five. Antilymphocytic Serum, Antigens.- 6. Non-Specific Inhibition.- 7. The impact of Adjuvant Arthritis on Drugs.- D. Arthritis Produced via Intra-Articular Injection of Antigens and Antibodies.- E. Arthritis Produced by means of Intra-Articular Injection of Lysosome Labilisers.- F. Arthritis caused via Infectious Agents.- E. Conclusions.- References.- 24 Antagonism of Bradykinin Bronchoconstriction by way of anti inflammatory Drugs.- A. Introduction.- B. construction of Kinins and different Mediators of Anaphylaxis within the Lungs.- I. In vitro.- II. In vivo.- III. unlock of Catecholamines in vivo.- C. motion of Bradykinin on Lung Function.- I. Bronchial gentle Muscle in vitro and in vivo.- II. Pulmonary Circulation.- D. unlock of Prostaglandins and Precursors From Lungs by means of Bradykinin.- E. activities of Prostaglandins within the Lungs.- I. Bronchial gentle Muscle.- F. interplay of Bradykinin With Prostaglandins within the Lungs.- I. As a Mediator.- II. As a Potentiator.- III. As a Mediator of Vascular Leakage.- G. Metabolism of Kinins within the Pulmonary Circulation.- H. Inhibition of Bronchoconstriction by means of anti inflammatory Acids.- I. In vivo and in vitro Studies.- II. comparability With different Bronchoconstrictor Agents.- I. attainable activities and Interactions of Kinins and Prostaglandins in Asthma.- J. precis and Conclusions.- References.- 25 Interference of anti inflammatory medicines With Hypotension.- A. Interference of Non-Steroidal anti inflammatory medicines With Hypotensive results of strength Inflammatory Mediators.- I. Kinin Peptides.- II. Prostaglandins.- B. Interference by way of Non-Steroidal anti inflammatory medicinal drugs With the Hypotensive results of brokers That unencumber strength Inflammatory Mediators.- I. Proteolytic Enzymes.- 1. Kininogenases.- 2. Thrombin.- three. different Proteolytic Enzymes.- II. Inhibition of Hypotension because of ingredients That turn on Plasma Kininogenase.- 1. Carrageenin.- 2. different Activators of Plasma Kininogenase.- III. Phospholipase A2.- C. Interference of anti inflammatory medications With Hypotensive Responses to Lipid Derivatives.- I. results of Arachidonic Acid on Arterial Blood Pressure.- 1. Mechanism of motion of Arachidonic Acid on Blood Pressure.- II. results of Fatty Acids except Prostaglandin Precursors.- III. sluggish Reacting Substance C.- 1. Mechanism of motion of gradual Reacting Substance C.- D. Interference of Non-Steroidal anti inflammatory brokers With results of Miscellaneous Agents.- I. Adenosine Nucleotides.- II. Collagen.- III. Anaphylatoxin.- IV. Depressor energetic Substance (DAS).- V. Platelet Clumping Substance.- VI. Barium Sulphate and different Particulate Materials.- E. Interference of Non-Steroidal anti inflammatory brokers With Hypotension in Endotoxin Shock.- I. Dogs.- II. Cats.- III. different Animal Species.- F. Mechanism of motion of Hypotensive brokers prone to Inhibition via Non-Steroid anti inflammatory Drugs.- I. Structure-Activity Correlations.- 1. Thiol and Anti-Oxidant Compounds.- II. Stereospecificity.- III. Mechanism of motion of Hypotensive brokers topic to Inhibition via Non-Steroidal anti inflammatory Drugs.- 1. Bradykinin.- 2. Collagen.- three. Carrageenin.- four. Adenosine Nucleotides.- IV. Conclusions.- 1. Relevance of Hypotensive Responses to irritation and to check of Inflammatory Events.- 2. Multisequential Activation and Acute Hypotensive Responses: customers of Research.- References.- 26 Antagonism of ache and Hyperalgesia.- A. Introduction.- I. Terminology.- II. old advent to Analgesic trying out in Hyperalgesic Animals.- B. Non-Hyperalgesic gentle Analgesic Assays.- I. Stretching Tests.- C. evaluation of gentle Analgesia in Humans.- I. scientific Avaluation of gentle Analgesic Agents.- D. Conclusion.- References.- 27 Inhibition of phone Migration in vivo and Granuloma Formation.- A. common Introduction.- I. Mechanisms of mobile Migration.- II. The series of cellphone Migration.- III. destiny of Emigrated Cells.- 1. Polymorphs.- 2. Mononuclear Cells.- IV. Granuloma Formation and Evolution.- B. types for Leucocyte Emigration in vivo.- I. Generalities.- II. Histological Method.- III. mobile assortment From Cavities.- 1. usual Cavities.- 2. man made Cavities.- IV. mobilephone assortment From Early Granulomata.- V. cellphone Labelling.- C. types for Granuloma Formation in vivo.- I. Cotton-Pellet Granuloma.- II. Granuloma Pouch.- III. Carrageenin Granuloma.- IV. Plastic Ring Granuloma.- V. filter out Paper Granuloma.- D. Inhibition of mobile Migration in vivo.- I. Steroids.- 1. Neutrophils.- 2. Mononuclear Cells.- II. Non-Steroid anti inflammatory Drugs.- III. Immunosuppressive Agents.- IV. Endogenous Substances.- E. Inhibition of Granuloma Formation.- I. Steroid anti inflammatory Drugs.- II. Non-Steroid anti inflammatory Drugs.- III. Immunosuppressive Agents.- IV. Endogenous Substances.- F. Conclusions.- References.- 28 Inhibition of Fever.- A. Introduction.- B. Pathogenesis of Fever.- I. Exogenous and Endogenous Pyrogen.- II. website of motion of Pyrogens.- III. Mechanism of motion of Pyrogens.- 1. swap in Set-Point or Gain?.- 2. function of Prostaglandins.- three. function of Monoamines and Cyclic-AMP.- four. Ionic Mechanisms in Fever.- C. Antipyretics.- I. attainable websites of motion of Antipyretics.- 1. Inactivation of Bacterial Pyrogen (Site I).- 2. Inhibition of Endogenous Pyrogen construction or unlock (Site II).- three. Inhibition of Endogenous Pyrogen task (Site III).- four. entry of Endogenous Pyrogen to the vital frightened procedure (Site IV).- five. Hypothalamic Thermoregulatory Centres (Site V).- 6. Suppression of warmth construction (Site VI).- II. attainable Mechanisms of Antipyretic Action.- 1. Inhibition of Prostaglandin Synthesis/Release.- 2. aggressive Antagonism among Pyrogens and Antipyretics for a Receptor Site.- three. Alteration within the job of Neurones within the Hypothalamus.- III. Antipyresis.- D. Inhibition of Fever via different Means.- I. elevated warmth Loss.- II. Monoamine Blockade and Depletion.- III. Cholinergic Blockade.- E. Conclusion.- References.- 29 overview of the Toxicity of anti inflammatory Drugs.- A. Introduction.- I. old Overview.- B. assessment of Toxicity in Man.- I. Gastrointestinal Tract.- II. important apprehensive System.- III. Dermatological Disorders.- IV. Haematopoietic System.- V. Ocular Disturbances.- VI. Renal part Effects.- VII. Miscellaneous part Effects.- C. equipment Used to guage Toxicity in Animals.- I. Gastrointestinal.- II. Kidney.- III. Haematopoietic System.- IV. Liver.- V. Skin.- VI. Eye.- VII. crucial apprehensive System.- D. Correlation of Experimental versions With medical Toxicity.- I. Non-Steroid anti inflammatory Drugs.- 1. Salicylates.- 2. Indomethacin.- three. Phenylbutazone.- four. Arylalkanoic Acids.- five. Gold.- II. Steroids.- E. Summary.- References.- Pharmacology of the anti inflammatory Agents.- 30 Prostaglandin Synthetase Inhibitors I.- A. Introduction.- B. Inhibiton of Synthetase through Substrate Analogues and Fatty Acid Derivatives.- I. Unsaturated Fatty Acids.- II. Bicyclic Analogues.- C. law of Enzymic components: Co-Factors, Stimulation, and Catabolism.- I. rules of Biosynthesis.- II. Catabolic Enzymes.- D. Inhibition by way of Non-Steroid anti inflammatory Agents.- I. an outline of Structure-Activity Relationship.- 1. Correlation of PG Syntheatase Inhibition With anti inflammatory Action.- 2. normal Structure-Activity Relationship.- II. Salicylates.- III. Indomethacin, Sulindac, and Congeners.- IV. Substituted Aryl Aliphatic Acids.- V. Fenamates.- VI. different Acidic anti inflammatory Agents.- VII. Non-Acidic anti inflammatory Agents.- E. results of Corticosteroids.- F. Inhibition and Stimulation through different Pharmacological Agents.- I. Anti-Arthritic and comparable Compounds.- II. Psychotropic Drugs.- III. Sulphydryl Reagents and Derivatives.- IV. Hormones and Mediators.- V. Inactive Pharmacological Agents.- G. the hunt for brand new Inhibitors.- I. present learn Trend.- II. Biochemical and Physiological Specificity.- III. Pharmacodynamic and Metabolic Control.- IV. Multiple-Action Inhibitors.- V. artificial and Physicochemical Approaches.- H. Pharmacokinetics of Prostaglandin Synthetase Inhibitors.- I. Conclusion.- References.- 31 Mode of motion of anti inflammatory brokers that are Prostaglandin Synthetase Inhibitors.- A. Mediators and Inflammatory Responses.- B. Mechanism of anti inflammatory Action.- I. motion on Step 1: Diminution of the aptitude of Tissue Cells to answer Inflammatory Mediators.- 1. elevated Dilatation and Vascular Permeability.- 2. ache and Hyperalgesia.- three. elevated Fibroblast Proliferation and Secretion.- II. motion on Step 2: Pharmacological Receptor Antagonism.- III. motion on Step three: Inhibition of Extracellular Enzymic actions Which Generate Inflammatory Mediators or reason harm to phone Membranes and/or Tissue Components.- IV. motion on Step four: Inhibition of the discharge of Intracellular Lytic Enzymes or Mediator-Genases or kept Receptor-Mediators.- V. motion on Step five: Inhibition of the Synthesis of Inflammatory Mediators.- 1. Prostaglandin Synthesis and Release.- 2. Prostaglandins and Inflammatory indicators and Symptoms.- three. Correlation among in vitro Inhibition of Prostaglandin Synthesis and anti inflammatory Activity.- four. Inhibition of Prostaglandin Synthesis in vivo and Inflammatory indicators and Symptoms.- VI. motion on Step 6: Inhibition of phone Migration.- VII. motion on Step 7: Inhibition of the new release of the potent Inflammatory Trauma.- C. Side-Effects of anti inflammatory medicines that are Prostaglandin Synthetase Inhibitors.- D. Theories and Theories.- References.- 32 Penicillamine and medicine With a particular motion in Rheumatoid Arthritis.- A. category of Antirheumatic Drugs.- B. Penicillamine.- I. activities in Man.- II. attainable Mode of motion and results in Animal Models.- C. Gold Salts.- D. Chloroquine and different Antimalarials.- E. Levamisole.- F. different Imidazole Derivatives.- G. Immunosuppressives.- H. Alclofenac.- I. Steroids.- J. Summary.- References.- 33 Antagonists of Histamine, 5-Hydroxytryptamine and SRS—A.- A. class of Antihistamines.- B. Histamine H1 Antagonists: Structure-Activity Relationships.- C. Histamine H1 Antagonists: Inhibition of Responses to Histamine serious about Inflammatory and Anaphylactic Reactions.- I. Guinea Pig.- II. Rat.- III. Rabbit.- IV. Mouse.- V. Man.- D. Histamine H2 Antagonists: Chemical Considerations.- E. Inhibition of Cardiovascular Responses to Histamine through H1 and H2 Antagonists.- F. Chemical and Pharmacological sessions of 5-Hydroxytryptamine Antagonists.- I. Chemical Classes.- II. “M” and “D” Receptors.- III. 201C;Musculotropic” and “Neurotropic” Receptors.- G. Antagonists of 5-Hydroxytryptamine: Inhibition of Responses to 5-HT fascinated about Inflammatory and Anaphylactic Reactions.- I. Guinea Pig.- II. Rat.- III. Rabbit.- IV. Mouse.- V. Man.- H. results of Antagonists of Histamine (H1 Receptors) and 5-HT in a variety of different types of Inflammation.- I. Guinea Pig.- 1. Thermal and Ultraviolet Injury.- 2. neighborhood Anaphylaxis.- three. Systemic Anaphylaxis.- four. Compound 48/80 and Polymyxin B.- five. Bradykinin.- II Rat.- 1. Thermal and Ultraviolet Injury.- 2. neighborhood Anaphylaxis.- three. Systemic Anaphylaxis.- four. Compound 48/80, Polymyxin, Dextran, and Egg White.- five. Turpentine Pleurisy.- 6. Carrageenin Oedema.- 7. Croton Oil.- eight. Bradykinin.- III. Rabbit.- 1. Thermal Injury.- 2. Anaphylactic Reactions.- three. irritation linked to Bacterial Infections.- IV. Mouse.- 1. normal Anaphylaxis.- 2. Cutaneous Anaphylaxis.- three. different neighborhood Inflammatory Reactions.- four. Systemic Reactions regarding Inflammation.- V. Man.- 1. Burns.- 2. Compound 48/80 and Polymyxin.- three. hypersensitive reaction States.- four. Rheumatoid Arthritis and 5-HT Antagonists.- VI. Bovine Anaphylaxis.- I. Antagonists of SRS-A.- I. Non-Steroid anti inflammatory Drugs.- II. Polyphloretin Phosphate (PPP).- III. FPL 55712.- IV. Hydratropic Acids.- J. clients for brand spanking new Drugs.- References.- 34 Inhibitors of the discharge of Anaphylatic Mediators.- A. features of Anti-Allergic brokers Discussed.- B. Cromoglycate and comparable Compounds.- I. identity and Screening.- 1. The Passive Cutaneous Anaphylaxis response (PCA) in Rats.- 2. Lung Anaphylaxis in vivo.- three. Passive Peritoneal Anaphylaxis.- four. Human Tissues in vitro.- five. Rat Tissues in vitro.- II. Structure-Activity Relationships.- III. Anti-Allergic Properties.- 1. Tissue and Species Selectivity.- 2. Inhibition of Mast cellphone Reactions Provoked by means of Stimuli except Antigen-Antibody Interactions.- three. Time path Studies.- four. Tachyphylaxis.- IV. reports of the Mechanism of Anti-Allergic Action.- V. different Pharmacological Effects.- VI. Pharmacokinetics.- C. different Inhibitors of Mediator Release.- I. Isosteres of Theophylline.- 1. Structure-Activity Relationships.- 2. Anti-Allergic Properties.- II. Antihistamines and Histamine.- III. Diethylcarbamazine.- 1. Rat Peritoneal Cells in vivo.- 2. Lung Tissue.- three. Human Leucocytes.- four. Passive Cutaneous Anaphylaxis Reactions.- IV. Chlorphenesin.- D. customers for brand spanking new Drugs.- References.- 35 Cytostats With results in continual Inflammation.- A. Introduction.- B. normal Pharmacology of Cytostats powerful in power Inflammation.- I. “Immunosuppressants”.- 1. Alkylating Agents.- 2. Anti-Metabolites.- II. Microtubular Inhibitors.- 1. Colchicine.- C. a few homes of chosen Compounds.- I. Microtubular Inhibitors.- 1. Cytostatic results of Colchicine.- II. Cyclophosphamide.- 1. Metabolism.- 2. homes of a few Metabolites.- three. website of Action.- four. a few Side-Effects.- III. Chlorambucil.- 1. Metabolism.- 2. anti inflammatory Effects.- three. Mode of Action.- IV. Methotrexate.- V. Azathioprine.- D. present Problems.- Appendix. Synovectomy and Destruction of Pannus.- References.- Addendum.- 36 keep watch over of Hyperuricemia.- A. Introduction.- B. Uric Acid Metabolism.- C. Biochemical Pharmacology of Hypouricemic Drugs.- I. medicinal drugs decreasing Uric Acid Synthesis.- 1. Allopurinol and Oxipurinol.- 2. Thiopurinol.- three. different Inhibitors of Uric Acid Synthesis.- II. Uricosuric Agents.- III. Uricolytic Agents.- D. scientific Use of Hypouricemic Drugs.- I. standards for choosing a Hypouricemic Drug.- II. Use of person Hypouricemic Drugs.- III. Toxicity of Hypouricemic Agents.- References.- 37 anti inflammatory Steroids: Mode of motion in Rheumatoid Arthritis and Homograft Reaction.- A. basic Considerations.- B. Scope of the Review.- C. obviously taking place anti inflammatory Steroids.- D. artificial anti inflammatory Steroids.- E. organic actions saw With Physiological quantities of Cortisol-Like Steroids.- I. Metabolic Effects.- 1. Gluconeogenesis.- 2. Protein Metabolism.- three. DNA Synthesis.- four. Molecular foundation for Metabolic Effects.- five. Onset and period of Cortisol Action.- 6. Mechanism of motion of Cortisol.- 7. Glycogenosis.- eight. Lipolysis.- nine. dating to anti inflammatory, Anti-Allergic and Anti-Rheumatic Action.- 10. courting to Clinically bad Effects.- eleven. Implications for the Future.- II. Sodium preserving Activity.- III. keep an eye on of Adrenocorticotrophic Hormone (ACTH) Synthesis and Secretion.- 1. Neuroendocrine Control.- 2. unfavorable suggestions Control.- three. foundation for detrimental suggestions Control.- four. function of Cytoplasmic Steroid Receptors.- five. dating to Clinically fascinating Effects.- 6. courting to Clinically bad Effects.- IV. Cardiovascular Effects.- 1. center and Peripheral Blood Vessels in Adrenalectomised State.- 2. Microcirculation.- three. dating to anti inflammatory, Anti-Allergic, and Anti-Rheumatic Action.- four. courting to Clinically bad Effects.- five. Pharmacological Implications.- F. Mode of motion in Homograft Reaction.- I. Interference With the advance of Circulating Sensitized Lymphocytes.- II. Effectiveness opposed to irritation as a result of in the community Sensitized Lymphocytes.- III. Effectiveness opposed to irritation because of Circulating Sensitized Lymphocytes.- IV. scientific Relevance of Experimental Observations.- V. Relevance to evaluate of more suitable Anti-Rejection and Anti-Rheumatic Drugs.- G. Concluding Remarks.- References.- 38 anti inflammatory brokers of Animal Origin.- A. Introduction.- B. Definition and assessment of anti inflammatory Activity.- C. Mechanisms of Action.- D. person Agents.- I. Alkoxyglyce

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1970), or more precisely with the phospholipid bilayer membranes (McLAUGHLIN, 1973) cannot be excluded. 1. GRYGLEWSKI (GLENN and BOWMAN, 1969) against heat-induced haemolysis. A similar protective action of NSAID has been described for human erythrocytes against hypotonic haemolysis (INGLOT and WOLNA, 1968). , 1975). , 1973). , 1973). , 1975). , 1973) and meclofenamic acid (KALBHEN and LOYEN, 1973) are hardly effective in this respect. , 1970). , 1973). , 1975a). , 1972; KovAcs and GOROG, 1972) and suppress the adhesiveness of leucocytes to plasma-coated glass beads (KOVACS and GOROG, 1972).

The responsiveness of human platelets to the pro-aggregatory effect of collagen is highly variable. , 1973). , 1968). , 1975). g. benzydamine or chloroquine, inhibit the primary-phase aggregation, whereas antiinflammatory corticosteroids are totally ineffective as anti-aggregatory agents (KOVACS and GOROG, 1972). , 1975). , 1971). , 1974a) Recently, ROTH et aI. w. 85000) is irreversibly acetylated by aspirin. Arachidonic acid blocks this active site directed effect of aspirin. , (1975) explains the persistent action of aspirin on platelets (see Section C.

1. , 1970; HASLAM and MCCLENAGHAN, 1974). h) Mode of Action HAMBERG and SAMUELSSON (1974) and SAMUELSSON et aI. 2). , 1975). , 1974; McDONALD and STUART, 1974). , 1975) is biologically similar to RCS (PIPER and VANE, 1969). A labile aggregation-stimulating substance (LASS) of WILLIS and KUHN (1973) and an unidentified factor with aggregatory properties of VARGAFTIG (1973) might be the mixtures of PGG2> PGH 2, and thromboxane A 2. , 1974a). Recently, BUNTING et aI. (1975) and MONCADA et aI. (1976) have identified an enzyme in platelet microsomes which selectively converts PGG 2 and PGH 2 into thromboxane A 2.

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Anti-Inflammatory Drugs by R. J. Gryglewski (auth.), Dr. John R. Vane, Dr. Sergio H. Ferreira (eds.)


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