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V Bourdon

Publications and source records attributed to V Bourdon.

At least 37 records · Page 2Linked to original sources
PubMed1990

Proteinase inhibitors, kinins and the inflammatory reaction induced by sponge implantation in rats.

We studied the influence of aprotinin and soya bean trypsin inhibitor (SBTI) on the inflammatory reaction induced by the implantation of dry sponges in normal Wistar rats and in kininogen-deficient Brown Norway rats, during the first day after the implantation. In normal rats, aprotinin reduced the volume and total protein content of the exudates at 3 h but not thereafter. Aprotinin also markedly reduced the immunoreactive kinins and kallikrein in the exudates. Aprotinin did not modify the volume of the exudates of the Brown Norway rats. SBTI reduced the inflammatory reaction in both rat strains but did not significantly modify the formation of immunoreactive kinins. The inflammatory reaction developed more slowly in Brown Norway rats. The kinin system is thus involved during the first hours of the development of this acute inflammatory reaction. The anti-inflammatory effect of SBTI does not depend on the inhibition of kinin formation.

Animals↗
PubMed1990

Kinins and peritoneal exudates induced by carrageenin and zymosan in rats.

1. Kinins were measured by a radioimmunoassay in the inflammatory exudates induced by carrageenin or zymosan in the peritoneal cavity of normal Wistar rats and of kininogen-deficient Brown Norway rats. 2. After administration of carrageenin to normal rats, levels of immunoreactive kinins showed a single peak during the first two hours and then decreased. The presence of kinins preceded and accompanied the exudation of 125I-labelled albumin. Kinins were identified as bradykinin by chromatography. 3. Captopril, an inhibitor of kininase 2, increased the level of kinins and the volume of the exudates after carrageenin treatment. In Brown Norway rats, the volume of the exudates was small and contained little or undetectable amounts of immunoreactive kinins. 4. During zymosan-induced peritonitis, the exudates were devoid of immunoreactive kinins in both species. The volume of the exudates was larger in kininogen-deficient rats than in normal rats. 5. We conclude that in rats, the kinin system is a major factor responsible for the development of the inflammatory reactions induced by carrageenin, but is not involved in the reactions induced by zymosan.

Animals↗
PubMed1990

The significance of high molecular weight kininogen for contact activation of rat blood coagulation, in vitro.

The involvement of the high molecular weight rat kininogen in the activation of the rat contact system by kaolin-cephalin, kaolin, sulfatides and ellagic acid has been investigated, using a rat plasma congenitally devoid of this kininogen. Coagulation times induced by these activators were shorter in normal as well as in deficient rat plasma than in normal human plasma. Coagulation times were prolonged in deficient rat plasma, when the incubation times was three min or less. By kaolin or cephalin-kaolin, this prolongation disappeared when the incubation time reached ten min. The activation of plasma prekallikrein developed slowly in deficient plasma with all the triggers but reached control level after ten min of incubation. By kaolin-cephalin, the activation of Hageman factor was weak and slow in deficient plasma during the ten min of incubation. In rat, high molecular weight kininogen plays thus a role in the activation of the contact system by these triggers. But this role seems to be less important than in human plasma.

Animals↗
PubMed1989

Quantification of rat T-kininogen using immunological methods. Application to inflammatory processes.

Antibodies raised in rabbits against rat T-kininogen (alpha 1-cysteine proteinase inhibitor) were used to develop a radioimmunoassay and a nephelometric quantification for T-kininogen. These assays were specific and analytically reliable. We also described a radioimmunoassay for kinin measurement. These immunological methods have been used to study the behaviour of T-kininogen during inflammatory processes and specify the two properties of this kind of kininogen: its inhibitory capacity towards cysteine proteinases and its activity as precursor of T-kinin. Control plasma level of T-kininogen in male rats was lower than that of female rats. The maximum level was observed in plasma, liver, kidney and uterus of female rats during metestrus. After turpentine injection, T-kininogen level increased not only in plasma but also in liver and kidney. In carrageenan-induced peritoneal exudates, we found a large accumulation of T-kininogen and of immunoreactive kinins, these latter being identified by HPLC as bradykinin.

Animals↗
PubMed1989

Presence of T-kininogen and kinins in sponge-induced exudates in rats.

1. The content of kinins and T-kininogen (the third kininogen) in exudates induced by the subcutaneous implantation of saline-soaked sponges have been measured by radioimmunoassay in normal Wistar rats and in Brown Norway rats from a strain which is deficient in high and low molecular weight kininogens. 2. In both strains, sponge implantation induced a rise of T-kininogen in plasma with subsequent accumulation in the sponge exudate. This accumulation correlated with the extravasation of plasma proteins during the first 6 h. Bioassays showed that the T-kinin moiety was retained in T-kininogen. 3. In Wistar rats, a large release of immunoreactive kinins up to a mean value of 6.4 ng ml-1 was observed during the first 6 h and on the second day after the implantation. In Brown Norway rats, the kinin level in the exudates did not exceed 0.53 ng ml-1. 4. Of the kinins present during the first 6 h in the exudates withdrawn from Wistar rats, 60% were identified by high performance liquid chromatography as bradykinin. 5. The volume of the exudate induced by the implantation of dry sponges was smaller in Brown Norway rats than in Wistar rats. 6. We conclude that the role of T-kininogen in this kind of exudate was mainly the inhibition of thiol proteinases and not the release of T-kinin. In Wistar rats, bradykinin acts as a pro-inflammatory factor during the first hours and may play a role during the healing process.

Animals↗
PubMed1985

Pro-inflammatory flavonoids which are inhibitors of prostaglandin biosynthesis.

Catechin dimers induce a large long-lasting oedema when injected in the paw of the rat. This oedema is not inhibited by methysergide, promethazine, indomethacin, phenidone, bromophenacyl bromide and colchicine. It is not modified in rats made leukopenic by methotrexate. It is slightly delayed in Brown Norway rats which were kallikrein-kininogen deficient. Similarly catechin dimers induce the formation of a large peritoneal exudate in the rat. The exudate contains insignificant levels of leucocytes and 5-hydroxytryptamine. It contains kinins but its PG content is very low. The exudate does not activate (14C)-arachidonic acid into PG. Catechin dimers induce kinin formation in rat plasma "in vitro". They inhibit the formation of PG and HETE-like compounds from (14C)-arachidonic acid by rat peritoneal cells "in vitro". Catechin dimers administered at sub-irritant doses reduced carrageenan-induced oedema. Catechin dimers at low doses have an anti-inflammatory effect which may depend on PG synthesis inhibition. At larger doses, they induce inflammatory responses which occur with almost complete lack of participation of PG.

Animals↗
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↗
PubMed1982

[Platelets, lysosomal enzymes and anaphylactic shock in the rat].

1. Rat serum levels in beta-glucuronidase and beta-galactosidase are higher than plasma levels. Rat platelets release these lysosomial enzymes during blood coagulation in vitro. 2. After anaphylactic shock, in the sensitized rat, there is no increase in beta-galactosidase and beta-glucuronidase plasma levels. The tissues of the sensitized rat do not release these enzymes during the antigen-antibody reaction. The blood platelet level is diminished after anaphylactic shock and the serum levels of the lysosomial enzymes are decreased. 3. In thrombopenic rat, anaphylactic shock is identical as in control animals. Rat platelets do not play a significant role in the anaphylactic shock.

Anaphylaxis↗
PubMed1982

[Inhibition of lysosomal enzyme liberation by indomethacin in vivo].

The volume of the peritoneal exudate induced in the rat by iota carrageenan is reduced by subcutaneous administration of indomethacin while the concentrations of three lysosomial enzymes in the exudate are slightly increased or not modified. Thus, the total enzymatic activities of the exudate are reduced by indomethacin. The leucocyte accumulation remains unchanged in the indomethacin treated rats. During the development of the peritoneal exudate, the circulating plasma displays a high degree of lysosomial enzymes activity which is suppressed by indomethacin at the dose of 4 mg/kg.

Animals↗
PubMed1982

[Catecholamine conjugation during pregnancy].

Conjugated urinary catecholamines are increased during normal human pregnancy. The modification in the proportions of conjugated fractions are particularly significant for norepinephrine. They depend on the foetoplacental unit since delivery is followed by a reduction of the urinary concentrations of these conjugated fractions. Such a modification of catecholamine metabolism must be kept in mind when the level of sympathetic nervous system activity is studied during pregnancy.

Amniotic Fluid↗