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Biomedical subjects

G Remacle-Volon

Publications and source records attributed to G Remacle-Volon.

27 records · Page 2Linked to original sources
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 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 The exudates withdrawn from Brown Norway rats contained no kinin and a low level of PGE2.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

[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↗
PubMed1982

[Interaction of polymorphonuclear leukocytes, bradykinin and carragenin. Transference reaction in the rat].

1. Injected in the paw of the rat, polymorphonuclear leucocytes do not increase the oedematogen action of bradykinin, but increase the action of lambda carrageenan. 2. This potentiation of carrageenan action is not modified when PG biosynthesis in leucocytes is inhibited by indomethacin or aspirin. It does not appear in rats previously treated by indomethacin or aspirin. 3. Our results suggest that rat polymorphonuclear leucocytes increase the inflammatory reaction, when they are stimulated by carrageenan, by the release of a phospholipase A2 activity which induces PG biosynthesis in rat paw tissues.

Animals↗
PubMed1981

[Cardiovascular reactivity to arachidonic acid, prostaglandin E2, prostacyclin and bradykinin in carrageenan treated rats].

In the rat, during carrageenan-induced peritonitis, the hypotensive activity of arachidonic acid, which depends on PG biosynthesis, is increased during the first hours, and thereafter is not modified. The vasodilator action of PGE2 is reduced during the first day while the actions of PGI2 and bradykinin are not modified. The concentrations of plasma albumin and haptoglobin, two inhibitors of PG biosynthesis are reduced during the first hours. Thereafter the concentration of haptoglobin is increased by 100% while the concentration of albumin remains diminished. During this peritonitis, no plasmatic inhibitory influence on PG synthesis is seen. The anti-inflammatory action of carrageenans does not depend on PG synthesis inhibition.

Animals↗
PubMedDate not supplied

Inhibition by WEB 2086, a PAG-acether antagonist of oedema and peritonitis induced by zymosan in rats.

WEB 2086 reduced the increase in vascular permeability induced by platelet-activating factor (PAF-acether) in rat abdominal skin. Injected alone, WEB 2086 did not modify the oedema induced by zymosan in rat paw. However, administered with methysergide and mepyramine, WEB 2086 reduced the development of this oedema during the first two hours. WEB 2086 also reduced the volume of the exudate induced by zymosan in the peritoneal cavity and its content in leucocytes. Methysergide and mepyramine reduced the volume of the peritoneal exudate. BW755C inhibited the peritoneal accumulation of fluid and of leucocytes. Indomethacin was inactive. The inhibitory effect of WEB 2086 suggests that PAF-acether is involved in the inflammatory responses induced by zymosan in rats beside other endogenous factors such as lipoxygenase products and mast cell amines.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMedDate not supplied

[Kinins and oedema induced by different carrageenans (author's transl)].

1. The oedema induced in the paw of the Wistar rat by local injection of three different carrageenans allows us to determine the inflammatory activity of these sulphated polysaccharides. This activity is greatest for the lambda type, it is reduced for the iota compound and is smallest for the kappa carrageenan. 2. Reduction of plasmatic stores of kininogens by ellagic acid or inhibition of kinin formation by hexadimethrine reduce the inflammatory reaction induced by the three carrageenans. Inhibition of kininases by phenanthroline increases the oedema. Thus the kinin system is involved in the development of this type of oedema. 3. In Brown-Norway rats, which lack of plasmatic kallikrein and kininogens, the inflammatory activity of the three carrageenans is very small. By comparing the activity in Wistar rats and in Brown-Norway rats, it is concluded that the kinin system is the most important factor in the development of the inflammatory reaction induced by the three types of carrageenans.

Animals↗