Search PubMed⌕ Search

Biomedical subjects

J Damas

Publications and source records attributed to J Damas.

At least 91 records · Page 5Linked to original sources

Plasma prokallikrein and kininogens in burned patients.

Using specific immunological (1) and enzymatic (2) methods, we have measured prokallikrein, total, high, and low molecular weight kininogens in 36 severely burned patients. At admission to the intensive care unit, all constituents were significantly decreased when compared to previously defined reference intervals. The values remained low during the three first days after burn. The changes affecting total and low molecular weight kininogens were significantly correlated (p less than 0.05) with the severity of the burn area. Prokallikrein and kininogens levels were also closely related to the concentrations of C3c and C4 complement factors.

Adult↗

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↗

Acute phase plasma proteins in kininogen-deficient Brown Norway rats.

We examined whether Brown Norway rat plasma (BN/May Pfd f) contains alpha 1-cysteine proteinase inhibitor (alpha 1-CPI), also called major acute phase alpha 1-protein or T-kininogen. T-kininogen is a low molecular weight kininogen from which kinin can be released by trypsin but not by kallikreins. The BN plasma reacted with rabbit anti-alpha 1-CPI gamma globulins. Purified alpha 1-CPI released a kinin-like activity with trypsin and with homogenate of salivary glands, as Brown Norway rat plasma did. High concentration of added rat urine induced a small release (10%) of kinin from alpha 1-CPI. Preincubation of Brown Norway rat plasma with rabbit anti-rat alpha 1-CPI gamma-globulins nearly suppressed the kinin-forming substrate of trypsin in this plasma. These results indicated that plasma of our Brown Norway rats contains only alpha 1-CPI as kinin-forming substrate. This plasma contains low amount of alpha 2-macroglobulin, while its content in orosomucoid and haptoglobin was a little larger than that of Wistar rat plasma.

Acute-Phase Proteins↗

[Stimulation of rat mastocytes and molecular oxygen].

Free peritoneal mast-cells of the rat are stimulated in vitro by molecular oxygen as well as by hydrogen peroxide. Histamine release is also observed in vivo when molecular oxygen or diluted solutions of hydrogen peroxide are injected into the peritoneal cavity of the rat. Inflammatory lesions are produced (vascular congestion, oedema, exudate) which are suppressed by pretreatment with anti-H1 antihistaminics. When hydrogen peroxide solutions are more concentrated, inflammation is also provoked but antihistaminics are no more inhibitory. Mast-cells of the skin and of the lungs are not stimulated neither by molecular oxygen, nor by hydrogen peroxide.

Animals↗

[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↗

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↗

Optimized determination of plasma prokallikrein on a Hitachi 705 analyser.

Manual determination of plasma prokallikrein using a chromogenic substrate is tedious. We describe the optimal conditions of enzymatic quantification by a fully automated method enabling rapid availability of the results and an easier estimation of this interesting compound in clinical chemistry.

Heparin↗

Influence of oral contraceptives and pregnancy on constituents of the kallikrein-kininogen system in plasma.

We measured kininogens of low and high molecular mass along with prokallikrein activity in plasma of women with a normal menstrual cycle. We observed no difference between results for the follicular and luteal phases. We assayed the same constituents in women who were taking oral contraceptives (combined estroprogestative) and found that activity of prokallikrein and concentrations of low- and high-molecular-mass kininogens were significantly increased. Lastly, we studied the components of the kallikrein-kininogen system during pregnancy. We also observed a marked increase in their concentrations in plasma, despite a decrease in total proteins. Specifically, prokallikrein and kininogens increase continuously with gestational age, reaching their maxima around the eighth month of pregnancy. At that time, more than 50% of observed results fall outside the normal reference interval. Our observations are even more striking when prokallikrein and kininogens are expressed in units per gram of total proteins, to account for the hemodilution. After delivery, the concentrations of prokallikrein and low- and high-molecular-mass kininogens decline promptly, returning to normal within three days.

Adult↗