PubMed Health⌕ Search

Biomedical subjects

G Remacle-Volon

Publications and source records attributed to G Remacle-Volon.

At least 19 recordsLinked to original sources
PubMed1995

Collagenase-induced oedema in the rat paw and the kinin system.

Collagenase (100 micrograms) induced a large plasma extravasation, during the first 15 min after its injection in rat paw, associated with the rapid development of oedema which subsided after 6 h. The extent of the oedema was similar in normal and kininogen-deficient rats. The swelling induced in normal rats was reduced by HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and by three serine protease inhibitors, soybean trypsin inhibitor (SBTI), Leucaena leucocephala trypsin inhibitor 1 (LLTI-1) and Leucaena leucocephala trypsin inhibitor 2 (LLTI-2). These agents had no effect on the oedema induced in kininogen-deficient rats. The swelling was also reduced by methysergide, indomethacin, ketoprofen and methylprednisolone. It was increased by heparin, but it was not modified by mepyramine, WEB 2086 (3-[4-(2-chlorophenyl)-9-methyl-6H-thieno[3,2-f][1,2,4]-triazolo- [4,3-a][1,4]-diazepine-2-yl]-1-(4-morpholinyl)-1-propanone) and NG-nitro-L-arginine. In vitro, collagenase did not release kinins from rat plasma or from purified T-kininogen. LLTI-1 and LLTI-2 did not inhibit collagenase activity for one of its specific substrates. Kinins are thus involved in the development of collagenase oedema in normal rats. Their generation would be indirect following changes in matrix proteins in extravascular spaces. Nevertheless, kinins are not the decisive mediators of the swelling. Serotonin, possibly released from platelets, and prostanoids participate in the inflammatory process.

Animals↗
PubMed1993

Platelet-activating factor and the vascular effects of zymosan in rats.

Platelet-activating factor (PAF; 2.5 micrograms/kg) injected in the tail vein of anaesthetized rats increased the vascular permeability of the duodenum, paws, skin and muscles, as measured by the extravasation of 125I-labelled albumin. It did not affect the permeability of the lungs or the presence of labelled albumin in the liver and spleen. The effects of PAF were dose dependently inhibited by WEB 2086 (ID50: 1.39 to 2.09 mg/kg) and SM-12502 (ID50: 7.17 to 8.36 mg/kg). Zymosan, an activator of the alternative complement pathway (10 or 16 mg/kg), induced protein extravasation in the lungs, duodenum, paws and skin, and the accumulation of labelled albumin in the liver. The effects of zymosan on the duodenum and liver were dose dependently inhibited by WEB-2086 and SM-12502. Both PAF antagonists increased the effects of zymosan in the paws but they did not affect protein extravasation in the lungs. The hypotensive effect of PAF (0.5 micrograms/kg) was inhibited by WEB 2086 (ID50: 1.21 mg/kg) and SM-12502 (ID50: 13.4 mg/kg). Both PAF antagonists reduced the hypotensive effects of zymosan (4 or 16 mg/kg) with a similar relative inhibitory potency. PAF is the major mediator involved in the hypotensive effect of zymosan but plays only a minor role in the permeability-enhancing effect of zymosan, mostly in the splanchnic area.

Animals↗
PubMed1992

Influence of a long-acting bradykinin antagonist, Hoe 140, on some acute inflammatory reactions in the rat.

We studied the influence of Hoe 140, a bradykinin antagonist, on inflammatory reactions induced in rats. Hoe 140 reduced paw oedema induced by bradykinin alone, bradykinin plus prostaglandin (PG) E1, carrageenan, urate crystals or urate crystals plus captopril. The inhibitory effect of Hoe 140 lasted for at least 4 h. Hoe 140 also reduced plasma exudation in sponges implanted in the back of the rat. However it did not modify paw oedema induced by zymosan or by heating the paw at 55 degrees C for 30 s. Carrageenan oedema developed to a small extent in kininogen-deficient rats while the swelling induced by heating the paw of kininogen-deficient rats was the same as that measured in normal animals. Hoe 140 had no effect on the slight swelling induced by carrageenan in kininogen-deficient rats. We conclude that the kinin system is involved in inflammatory reactions induced by carrageenan, urate crystals, sponge implantation but not by zymosan and scalding.

Alprostadil↗
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↗
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↗
PubMed1987

The thrombopenic effect of ellagic acid in the rat. Another model of platelet stimulation "in vivo".

In the rat, intravenous injection of large doses (30 mg/Kg) of ellagic acid (EA) induced a decrease in the plasma level of fibrinogen and in the blood platelet content and an increase of the activated partial thromboplastin time. The long-lasting thrombocytopenia was inhibited by heparin (4 mg/Kg), defibrase (20 U/Kg), clocoumarol (4 mg/Kg) and CCI 17810 (120 mg/Kg). It was not inhibited by aspirin (90 mg/Kg), indomethacin (8 mg/Kg), ketoprofen (4-10 mg/Kg), epsilon-aminocaproic acid (150 mg/Kg), methysergide (4 mg/Kg), chlorpromazine (10 mg/Kg) and promethazine (4 mg/Kg). On the contrary, the small doses of indomethacin (4 mg/Kg) and of ketoprofen (0.5-2 mg/Kg) increased the thrombopenic effect of EA. EA induced the accumulation of Cr51-labelled platelets into the lungs and the liver, accompanied by a 64% fall in Cr51 blood radioactivity. The platelet stimulating effect of EA would depend on an intravascular coagulation which occurs in the whole cardiovascular system. It is suggested that the pro-aggregating derivatives of arachidonic acid had a minor role in this stimulation. The intravascular coagulation induced by EA was accompanied by a swelling of the lymph nodes and of the spleen. In immune platelet depleted rats, EA induced only the swelling of lymph nodes.

Animals↗
PubMed1987

Mechanism of the congestion of lymph nodes induced by ellagic acid in rats.

Intravenous injection of ellagic acid (EA, 30 mg/Kg), an activator of the Hageman factor, induced congestion of lymph nodes and dilatation of the spleen in rats. The dilatation of the spleen was inhibited by heparin, thrombin, defibrase, clocoumarol, lambda carrageenan, SBTI, PCR 4099 and CCI 17810. The congestion of lymph nodes was inhibited by heparin, thrombin, defibrase, clocoumarol, SBTI, lambda carrageenan, aspirin, indomethacin and ketoprofen, phentolamine and hexamethonium. Thrombin, defibrase, lambda carrageenan did not induce any congestion of the lymphoid tissues. These results suggest the the dilatation of the spleen induced by ellagic acid would result from blood coagulation, platelet stimulation and kinin formation. The congestion of lymph nodes would depend on kinins, blood coagulation and prostaglandin;s. The activation of Hageman factor in acute inflammatory reactions could mediate the early congestion of lymph nodes.

Animals↗
PubMed1987

Studies on the vascular and hematological changes induced by ellagic acid in rats.

We compared the major changes induced by ellagic acid (EA), a Hageman factor activator, in normal rats and in kininogen-deficient Brown Norway rats. In normal rats, large doses of EA induced a congestion of lymph nodes, spleen and liver, a prolongation of activated partial thromboplastin time, the consumption of prekallikrein, high molecular weight kininogen and fibrinogen, as well as the stimulation of platelets with their accumulation in lungs, liver and spleen. A systemic hypotension of long duration was also observed. The fibrinogen consumption, the thrombocytopenia and the lengthening of activated partial thromboplastin time were dose-dependent. In kininogen-deficient rats, EA induced only a minimal congestion of lymphoid tissues, the accumulation of platelets in lungs, a decrease of plasma fibrinogen and a short-lasting hypotension. It is concluded that the vascular changes induced by blood coagulation with ellagic acid resulted mainly from kinin formation.

Animals↗
PubMed1986

Mast cell amines and the oedema induced by zymosan and carrageenans in rats.

Cimetidine and metiamide suppressed the paw swelling induced in rats by low doses of histamine while these H2 antagonists had little effect on the oedema induced by 100 micrograms of histamine and inhibited by mepyramine. When administered 0.5 h before the inflammagens, H2 antagonists reduced the oedema induced by zymosan and iota carrageenan; they had a slight effect on the oedema induced by lambda and kappa carrageenans and no effect on the oedema induced by compound 48/80. When administered 18 h before the inflammagens, cimetidine greatly increased zymosan oedema and slightly increased lambda carrageenan oedema. Mepyramine, methysergide or depletion of the 5-hydroxytryptamine stores in mast cells by pretreatment with reserpine inhibited the oedema induced by compound 48/80 and zymosan but did not affect the oedema induced by lambda and kappa carrageenans. Histamine may play a dual role in inflammatory reactions. Mast cell amines take a part in the development of zymosan oedema though they play a minor role in the oedema induced by the carrageenans.

Amines↗
PubMed1986

Further studies of the mechanism of counter irritation by turpentine.

The influence of counter irritation by turpentine (0.2 ml) on zymosan- and carrageenan-oedemas was investigated in the rat. Zymosan-oedema was inhibited by mepyramine and methysergide and by leucopenia. It was not modified by captopril and developed normally in kininogendeficient Brown Norway rats. Leucocytes and mast cell amines but not kinins are thus involved in zymosan-oedema. The last phase of this reaction was inhibited by counter irritation alone, but the odema was largely depressed by counter irritation in rats pretreated with mepyramine and methysergide. Carrageenan-oedema was increased by kininase inhibitors and inhibited by leucopenia in normal rats. This inflammatory reaction had a small developement and was not increased by kininase inhibitors in kininogen-deficient BN rats. Leucocytes and kinins participate in the developement of this inflammatory reaction in normal rats while kinins are lacking in deficient rats. Counter irritation depressed carrageenan-oedema in deficient Brown Norway rats and suppressed the potentiating effect of kininase inhibitors in normal rats. Carrageenan oedema was nearly abolished in turpentine-treated leucopenic rats. These results suggest that the anti-inflammatory effect of counter irritation by turpentine could depend on a reduction of leucocyte accumulation into zymosan-oedema and on a reduction of both kinin formation and of leucocyte accumulation into carrageenan-oedema. The significance of T-kininogen as acute phase reactant is discussed.

Animals↗
PubMed1986

[Anti-inflammatory effect of ACTH in the rat].

In rats, ACTH reduced the oedemas induced by zymosan and lambda carrageenan. ACTH reduced the volume of the exudate induced by sponge implantation and its content in proteins, beta-galactosidase, beta-glucuronidase and PGE2. The inhibitory effect of ACTH was suppressed by adrenalectomy which increased the carrageenan-oedema. The inhibitory effect of ACTH was also suppressed by 17 alpha-methyltestosterone. Corticosterone reduced carrageenan-oedema. The inhibitory effect of corticosterone was suppressed by cycloheximide and actinomycin D. These results suggest that rat adrenal steroids, among which corticosterone, can modulate the reactivity of the animal towards irritating processes. The anti-inflammatory effect of rat adrenal steroids would depend on the formation of lipocortin-like peptides.

Adrenocorticotropic Hormone↗
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↗