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Biomedical subjects

J Damas

Publications and source records attributed to J Damas.

At least 109 records · Page 6Linked to original sources
PubMed1985

Effect of serum proteins from normal and turpentine-treated rats on prostaglandin synthesis by peritoneal cells.

The influence of serum from normal and turpentine-treated rats on prostaglandin synthesis by peritoneal cells has been investigated. Both types of serum had the same inhibitory effect on the formation of myostimulating prostaglandin-like substances and of 14C-PGE2 by rat peritoneal cells in the presence of 82 or 100 mumol of arachidonic acid. On guinea-pig peritoneal cells, the serum from turpentine-treated rats had a smaller inhibitory effect than normal serum on 14C-PGE2 and 14C-HETE formation from 2 mumol of arachidonic acid. Thus the acute inflammatory reaction produced by turpentine did not increase the inhibitory effect of rat serum on prostaglandin synthesis. It is suggested that the anti-inflammatory effect of counter irritation by turpentine does not depend on prostaglandin synthesis inhibition but has to be attributed to some other mechanisms.

Animals↗
PubMed1985

Human kininogens of low and high molecular mass: quantification by radioimmunoassay and determination of reference values.

Kininogens of low and high molecular mass, highly purified from human plasma, were used to raise antisera in rabbits. To obtain immunologically intact tracers, we labeled the kininogens by the lodogen method, followed by double chromatography, first on Sephadex G50 and then on Sephadex G200 for high-molecular-mass kininogen or on G100 for low-molecular-mass kininogen. Both assays are sensitive, accurate, and reproducible. On an equimolar basis, the high-molecular-mass kininogen cross reacted completely in the determination of low-molecular-mass analyte. Moreover, the radioimmunoassay for the former was highly specific. After optimizing the time and temperature of incubation to provide rapid and reliable results, we determined 95% reference intervals from a large sample of healthy subjects (250 men, 200 women): 109-272 and 69-116 mg/L for the low- and high-molecular-mass kininogens, respectively.

Adult↗
PubMed1984

The mechanism of the anti-inflammatory effect of turpentine in the rat.

The influence of counter irritation by turpentine on carrageenan-oedema, leucocyte count, plasma kininogen stores and composition of sponge-induced exudates has been investigated in the rat. Counter irritation reduced the carrageenan-oedema in normal as well as in adrenalectomized rats. It induced leucopenia with lymphopenia but did not modify the plasma kininogen stores. In turpentine-pretreated rats, the exudates induced by sponge implantation 18 h previously had a lower content in leucocytes. Their levels in beta-glucuronidase and beta-galactosidase were slightly reduced, their content in PGE2 was not modified and their level in malonaldehyde was increased. The exudates induced by sponge implantation 4 h previously had a lower content in leucocytes and PGE2 while their level in kinins was not modified. The mechanism of the anti-inflammatory effect of counter irritation by turpentine is discussed. We suggest that the main factor involved is a decrease in leucocyte accumulation into the exudates.

Adrenalectomy↗
PubMed1984

Inflammation in the rat paw due to urate crystals. Involvement of the kinin system.

Monosodium urate and uric acid crystals induced kinin formation in Wistar rat plasma. They were inactive in the Brown Norway rat plasma which did not contain high molecular weight kininogen and had a low level in prekallikrein. Crystal-induced inflammation in the Brown Norway rat paw developed later and reached only 70% of the values observed in Wistar rats. Captopril, a kininase inhibitor, enhanced the oedema induced in the Wistar rat but did not affect the oedema in the Brown Norway rat. The leucocyte accumulation in the peritoneal cavity after uric acid injection was similar in both strains. The kinin system appeared to be involved in the inflammatory process induced in the rat by urate and uric acid crystals, as it is involved in carrageenan oedema.

Animals↗
PubMed1984

[The concept of mediators in acute inflammatory reactions].

The evolution of ideas about inflammation oscillates between two poles: sometimes the cell aspects of inflammation are described, with leucocyte adhesion to the vessel wall followed by migration into the tissues and phagocytosis - at other times it is the turn of the chemical intermediaries accounting for the damage to blood vessels, in which case vasodilatation, permeability and chemotaxis are given particular emphasis. The present tendency is to concentrate on the origin of these intermediaries and their relationship to the different cell populations found in situ. Before defining the relationship between cells and acute inflammatory mediators, an inventory needs to be drawn up of the latter. They can be divided into three main categories, according to the manner of their involvement at the site of inflammation: preformed agents, which are then released; mediators formed as a result of enzyme influences, cell-derived or not, from inactive precursors; the enzymes themselves which attack the structures involved in the lesion. These various mediators are thus traceable to specific mechanisms of formation or release, from cell populations that are now clearly identified. From an understanding of how the inflammatory focus has been colonised by the different leucocyte populations and a knowledge of their enzymatic potential, conclusions can be drawn not only about the mediators concerned but more especially about the pharmacological agents that must be mobilised in order to neutralise their clinically apparent effects.

Acute Disease↗
PubMed1984

[Role of the kallikrein-kininogen-kinin system in the inflammatory reaction and septic shock].

Kinins, which are vasodilatory, permeability-increasing, pain-producing polypeptides, are formed from inactive precursors: kininogens. Their actions make kinins a particularly powerful potential pro-inflammatory factor. However the absence of specific antagonists has so far made it impossible to ascribe them a definite role in inflammation. Two studies of experimental endotoxemia in burns patients, septicemia and septic shock have demonstrated the following facts: activation occurs of specific ( pKK ) and non-specific (plasminogen-plasmin system) kininogenases , K-HMW and K-LMW levels are significantly decreased. Kininogen consumption corresponds to increased BDK production. This would therefore appear to be one of the humoral factors responsible for haemodynamic changes. Though measurement of kininogen levels is still a painstaking process, the development of chromogenic substrates has made pKK and KK measurement simple and fast. Once they have been validated physico-pathologically in a large number of patients, such assays should take their place among the diagnostic weapons of clinical biology at the disposal of clinicians.

Animals↗
PubMed1984

[Prostaglandins and leukotrienes].

Two classes of arachidonic acid derivatives can be formed by two distinct enzyme systems. Cyclo-oxygenases synthesise prostaglandins, prostacyclin and thromboxane A2 which all possess both pro- and anti-inflammatory properties. Lipoxygenases synthesise on the one hand chemotactic factors, the hydroxylated derivatives of arachidonic acid, the most powerful of which is leukotriene B4, and on the other hand the broncho-constricting and permeability-increasing factors, leukotrienes C4, D4 and E4. A variety of pharmacological agents can decrease the formation of these compounds or inhibit their actions.

Animals↗
PubMed1984

The role of the kinin system in various inflammatory models in the rat.

The plasma of a peculiar strain of Brown Norway rats (BN/May Pfd f) is devoid of high molecular weight kininogen and poor in kallikrein. This strain could be used to estimate the involvement of the kinin system in inflammatory processes. In these rats, the oedema induced by kaolin, carrageenans, uric acid and urate crystals exhibited a small development, while the oedemas induced by 48/80, dextran, zymosan, trypsin, nystatin, concanavalin A and heating were not reduced. The exudates withdrawn from Brown Norway rats contained no kinin and a low level of PGE2. The involvement of the kinin system in these inflammatory models is discussed.

Animals↗
PubMed1983

Mast-cell heterogeneity in the rat.

In the rat, O-hydroxy ethyl rutoside derivatives release histamine and serotonin from skin mast-cells, but not from peritoneal mast-cells. These cellular populations do not exhibit identical pharmacological properties.

Animals↗
PubMed1983

Prostaglandin biosynthesis is not affected by the anti-inflammatory effect of turpentine.

In turpentine-pretreated rats, the development of carrageenan induced oedema is reduced, while dextran and PGE2-induced oedemas are not influenced. In these pretreated rats, carrageenan oedema is potentiated by arachidonic acid, the hypotensive effect of arachidonic acid is not decreased and the production of malonaldehyde by platelets is not inhibited. Thus, the reduction of carrageenan oedema in turpentine treated-rats does not appear to depend on an endogenous PG synthesis inhibition, while plasma level of acute phase reactants is greatly increased.

Animals↗
PubMed1983

[The participation of platelets in anaphylactic shock in the rat].

In the IgE-sensitized Brown Norway rats, the intravenous antigen challenge resulted in systemic anaphylactic shock without thrombocytopenia. In the IgG-sensitized Wistar rats, thrombocytopenia occurred during the anaphylactic shock. It is linked with circulating immun-complexes. Treatment of IgG-sensitized Wistar rats by antiplatelet serum, by promethazine (anti-H1), cyproheptadine (anti-5-HT1) or phenidone, a cyclo-oxygenase and lipoxygenase inhibitor, did not protect against the anaphylactic shock. In the rat, platelets did not play a significant rôle in the pathogenesis of the various forms of the anaphylactic shock.

Anaphylaxis↗