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Biomedical subjects

J Damas

Publications and source records attributed to J Damas.

At least 73 records · Page 4Linked to original sources
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 Of the kinins present during the first 6 h in the exudates withdrawn from Wistar rats, 60% were identified by high performance liquid chromatography as bradykinin. 5.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↗
PubMed1988

[Hepatic protein synthesis of the kallikrein-kininogen-kinin system].

Plasma prekallikrein and kininogens were assayed by specific enzymatic and immunological methods in cirrhotic patients with terminal liver failure and during oestrogenic impregnation. In cirrhotic patients plasma levels of these substances were significantly lowered and they correlated negatively with necrosis enzymes. A highly significant positive correlation was found between coagulation factor values and the levels of prekallikrein and kininogens. During oestrogenic impregnation the levels of the constituents of the kallikrein-kinin system were significantly increased when compared with reference values. These findings indicate that plasma concentrations of prekallikrein and kininogens are dependent upon liver synthesis capacity.

Female↗
PubMed1988

[The so-called "contact" system of plasma: consequences of the activation of the Hageman factor].

The contact system of plasma includes 4 zymogens, Hageman factor, pre-kallikrein, factor XI and plasminogen, and a cofactor, the high molecular weight kininogen (HMWK). The activation of the contact system leads to the production of bradykinin, blood coagulation, fibrinolysis, complement activation and neutrophil stimulation. Consequently these phenomena generate a lot of pro-inflammatory factors which contribute to the local and systemic inflammatory processes.

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↗
PubMed1987

[Exploration of endogenous mechanisms controlling the inflammatory reaction, by the study of counter-irritation: release of prostaglandins, formation of kinins and accumulation of leukocytes].

This review was focused on counter irritation by turpentine in the rat. The involvement of sympathetic system, adrenal steroids, beta-endorphin, axon reflexes, haptoglobin, alpha-2-macroglobulin, complement activation, prostaglandin synthesis, kinin formation and leukocyte accumulation was considered as possible explanation of the anti-inflammatory effect of counter irritation by turpentine. The main mechanism consists of the reduction of leucocyte accumulation.

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↗