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Biomedical subjects

J E Vincent

Publications and source records attributed to J E Vincent.

At least 55 records · Page 3Linked to original sources
PubMed1982

The effect of ticlopidine on the aggregation of rat blood platelets and on the formation of metabolites from arachidonic acid and 8,11,14-eicosatrienoic acid in rat platelets during aggregation, and in the rat kidney.

The effect of ticlopidine after oral administration was determined on the aggregation of rat blood platelets and on the formation of cyclo-oxygenase, and lipoxygenase metabolites from arachidonic acid (AA) and 8,11,14-eicosatrienoic acid in rat platelets and in the kidney. 1. Platelet aggregation is inhibited by ticlopidine. The effect is dependent on the dose administered and the amount of collagen used to induce the aggregation. 2. After the incubation of platelets with [1-(14)C]AA and aggregation by collagen, the following substances are formed: thromboxane B2 (TxB2), 12L-hydroxy-5,8, 10-heptodecatrienoic acid (HHT), 12L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) small amounts of PGE2 and PGD2 and an unknown metabolite. Ticlopidine administration during 3 days leads to an increase in the amounts of TxB2, PGE2, HHT and the unknown metabolite and a decrease in that of AA dependent on the dose administered. After 30 mg/kg the amount of HETE is decreased. 3. Under the same conditions, TxB1, PGE1, 12L-hydroxy-8,10-heptadecadienoic acid (HHD) and HETE (trienoic) are formed from [1-(14)C]8,11,14-eicosatrienoic acid. After 300 mg/kg ticlopidine the amounts of TxB1, PGE1 and HHD are increased. 4. In the rat kidney, [1-(14)C]AA is transformed into PGF 2 alpha, TxB2, PGE2, PGD2, PGA2, HHT and HETE. After ticlopidine administration, PGF 2 alpha, PGE2, PGD2 and PGA2 are increased, depending on the dose administered. 5. In this tissue, PGF 1 alpha, TxB1, PGD1, PGA1, HHD, HETE (trienoic) and an unknown metabolite are formed from [1-(14)C]eicosatrienoic acid. There is no effect from the administration of ticlopidine on the formation of these substances. 6. These results indicate that ticlopidine increases the synthesis of PGs and related substances in rat platelets and the kidney. This effect is due to an enhanced metabolism of AA.

8,11,14-Eicosatrienoic Acid↗
PubMed1981

Contractile characteristics of the rat stomach strip and the rabbit aorta and mesenteric artery.

A comparison was made of the dose-response curves obtained in the measurement of the prostaglandin E- and thromboxane A2-like activities using a cascade system consisting of a rabbit aorta strip and mesenteric artery and a rat fundus strip. The results indicate that the contractile properties of these tissues are different. In platelets during aggregation, the TxA2-like activity was measured by bioassay; the amount of TxB2 by a radioimmunological method.

Animals↗
PubMed1981

Effect of ergotamine on platelet prostaglandin synthesis--in vitro and in vivo experiments.

We studied the effect of ergotamine on the formation of metabolites of [1 - 14C] arachidonic acid by human blood platelets incubated with ergotamine (10(-5) or 5.10(-5)M) in vitro or after 0.5 mg i.m. administration in vivo. The in vitro experiments confirmed our earlier observation that ergotamine inhibits prostaglandin synthesis. This effect, however, seemed to be restricted to the toxic dose range of the drug as in vivo it occurred only in those subjects who became nauseated or vomited after administration of the drug.

Adolescent↗
PubMed1981

Conversion in vitro of prostaglandin endoperoxide into prostaglandins by arteries from pregnant and non-pregnant human uteri.

The enzymatic and non-enzymatic conversion in vitro of the prostaglandin endoperoxide (PGH2) into prostaglandins and thromboxane by human uterine arterial tissue was investigated. Segments of uterine arteries were obtained from six pregnant and six non-pregnant women. Slices of tissue were incubated with isotopically-labelled PGH2 and the products formed were determined by means of thin-layer chromatography. Only PGF2 alpha and PGI2 were formed by enzymatic conversion. Uterine arterial tissue from pregnant women produced significantly more PGF2 alpha than tissue from non-pregnant women, whereas no significant difference in formation of PGI2 could be demonstrated.

Arteries↗
PubMed1980

Determination of the formation of thromboxane B2 (TxB2), 12L-hydroxy-5,8,10 heptadecatrienoic acid (HHT) and 12L-hydroxy-5,8,10,14 eicosatrienoic acid (HETE) from arachidonic acid and of the TxB2 :HHT, TxB2 :HETE and (TxB2 +HHT) :HETE ratio in human platelets. Possible use in diagnostic purposes.

The formation of thromboxane B2 (TxB2), 12L-hydroxy-5,8,10 heptadecatrienoic acid (HHT) and 12L-hydroxy-5,8,10,14 eicosatrienoic acid (HETE) was determined in the platelets of normal human males and of patients with disorders in which an abnormal platelet aggregation occurs. Platelets were labelled with [1-14C] arachidonic acid. After Aggregation and extraction the metabolites wee separated by TLC and determined. In the platelets of normal males, TxB2 values were in the range 4.4-12.4%, expressed as a percentage of total radioactivity. Curves were constructed for the following ratios: TxB2 :HHT, TxB2 :HETE and (TxB2 + HHT) :HETE. These ratios were fairly contant. A comparison was made with the ratios obtained in the platelets of a small number of patients with either an enhanced or a diminished aggregation.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1979

The use of essential fatty acid deficient rats to study pathophysiological roles of prostaglandins. Comparison of prostaglandin production with some parameters of deficiency.

In a retrospective study on essential fatty acid deficient (EFAD) rats used to study pathophysiological roles of prostaglandins (PGs), slight increases in the linoleic acid content of the diet were found to gradually restore the depressed growth rate and to increase the reduced endogenous PG production. These apparently poorly deficient animals had a serum triene tetraene (omega9:omega6) ratio much higher than the value of 0.4 used as a criterion for EFA deficiency by nutritionists. Changes in body weight, serum omega9:omega6 and platelet PG production were not correlated with each other. Feeding rats on a diet containing less than 0.1 mg/g/linoleic acid led to decreasing platelet PG production as the degree of EFA deficiency increased. At this high level of deficiency, a serum omega9:omega6 ratio of 6 or over was achieved. This high ratio may be taken as an indicator of the degree of EFA deficiency required for studies on PG deprivation, but PG production by the tissue investigated or by platelets should preferentially be measured.

Animals↗
PubMed1978

Accumulation of blood platelets in carrageenin rat paw oedema. Possible role in the inflammatory process.

The accumulation of blood platelets in the carrageenin-induced paw oedema in rats was studied, using 51Cr-labeled platelets. A maximum in the accumulation was seen after 4 hours, followed by a decline after 5--6 hours. During the first 6 hours of the oedema formation, change in blood volume were small. A comparison was made with the accumulation of both 125J-albumin as a measure of extravasation and 125J-fibrinogen as an indication of blood clotting. When platelet aggregation was measured during the first 6 hours of the oedema formation, the lag time between the addition of collagen and the beginning of the aggregation was increased. No change in platelet serotonin was seen. These data support the idea that platelets participate in the inflammatory process.

Animals↗