Recent developments in the pharmacology of inflammatory mediators : proceedings of an international symposium, held in Rotterdam under auspices of the Dutch society for physiology and pharmacology in November 1976
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書誌事項
Recent developments in the pharmacology of inflammatory mediators : proceedings of an international symposium, held in Rotterdam under auspices of the Dutch society for physiology and pharmacology in November 1976
（Agents and actions supplements, AAS 2）
Birkhäuser, 1977
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注記
Literaturangaben
This symposium was held on November 27th, 1976 at the faculty of medicine , Erasmus University Rotterdam.
内容説明・目次
内容説明
In previous studies (1,2) we demonstrated the occurrence of a foetal protein after injury in the rat. This protein, behaving as an acute phase protein, proved to be already known as slow a2 glo- bulin (3), or reproduction associated protein (4). Furthermore it is identical to aM foetoprotein (also known as a2FP or aMFP (5) ). This protein is quite different to the well-known a-foetoprotein (aFP), occurring in man and other species during liver carcinoge- nesis and some other tumours. aMfoetoprotein (aMFP) is a glycoprotein with a mol.w. of 800.000. It is produced in the liver (6,2) and in the normal adult rat the plasma concentrations are rather low, about 0 - 40 ~g/ml. During fetal development the plasma level in the fetus is much higher (about 6000 ~g/ml), diminishing rapidly after birth to adult levels. But after injury (laparotomy, deep incision, partial hepatectomy followed by regeneration, BaS04 or CdS04 intraperitoneally), plasma levels increase fastly, reaching peak values of 1000 - 8000 ~g/ml after 24 - 48 hrs, declining thereafter gradually.
Also very small lesions, as orbital punction, venasection, cannulations, small infections and so on, cause moderate rises of plasma levels up to 80 - 120 ~g/ml. During fetal stage the inflammatory reaction often lacks some of its characteristic features: oedema and infiltration of leucocytes are often rather scanty (7). Also is known that in exudates proteins occur, inhibiting experimen- tal inflammations (8,9).
目次
Opening remarks.- Involvement of mediators in the interaction of platelets and carrageenan.- Platelets and mediators in the carrageenin rat paw oedema.- Comparison of the mediator release from platelets and the development of acute inflammation in rats which lack prostaglandin precursors.- Glucocorticoid effect on the prostaglandin system in adipose tissue.- Effect of glucocorticosteroids on the release of prostaglandin-like substances in anaphylaxis.- Effects of anti-inflammatory drugs on the carrageenin-induced hind paw inflammation of rats deprived of endogenous precursors of prostaglandins.- Metyrapone: A possible tool in investigating the role of endogenous corticosteroids in inflammation.- Prostaglandins and complement changes in some conditions related to inflammation.- Involvement of complement and kinins in some non-immunogenie paw inflammations in rats.- Inflammatory responses of the rabbit eye to prostaglandins.- Some biochemical complexities of inflammatory disease affecting drug action.- Inflammation inhibiting properties of rat alpha-foetoprotein (rat-alpha2-macroglobulin), an acute phase reactant.- Biodistribution of salicylates: A clue to the understanding of some effects and side-effects.
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