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Biomedical subjects

J E Vincent

Publications and source records attributed to J E Vincent.

14 recordsLinked to original sources
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↗
PubMed1977

Platelets and mediators in the carrageenin rat paw oedema.

A number of similarities exist between several aspects of the imflammation process and the changes occurring in platelets during aggregation. This has initiated the search for a specific role of platelets in inflammation. The aim of our experiments was to investigate firstly whether during an acute inflammatory process platelets accumulate in the inflamed area and secondly whether the inflammation has an effect on the properties of the platelets. Rat platelets were labeled with 51Cr and injected into the tail vein of rats with a carrageenin-induced edema in one of the hind paws. The amount of radioactivity was measured in the inflamed paw and compared to the control one in the 24 hr following the injection. An accumulation of platelets was found at 3-4 hr after the injection of the carrageenin which disappeared later. Maximal swelling occurred after 5 hr. The aggregability of the platelets was determined at different times of the inflammatory process. After 2 hr, a decrease was observed which was higher after 4 and 6 hr. This effect might be due to the release of mediators during the inflammation.

Animals↗
PubMed1977

Formation by phospholipase A2 of prostaglandins and thromboxane A2-like activity in the platelets of normal and essential fatty acid deficient rats. Comparison with effect on human and rabbit platelets.

When rat platelets are incubated with phospholipase A2, thromboxane A2-like activity and prostaglandins are formed. The amounts are approximately similar, whether aggregation is induced after the incubation or not. No aggregation is observed when the platelets are incubated with phospholipase A2. In the platelets of essential fatty acid deficient rats, only small amounts of thromboxane A2-like acitivity and prostaglandins are formed. No formation of these substances occurs when human and rabbit platelets are incubated with phospholipase A2. The results indicate that formation of thromboxane A2-like activity enhances aggregation in rat platelets, but that aggregation is not induced.

Animals↗
PubMed1977

Acute anti-inflammatory effects of aspirin and dexamethasone in rats deprived of endogenous prostaglandin precursors.

Paw oedema, induced by carrageenan, was potentiated in normal rats by arachidonic acid and bishomo-gamma-linoleic acid, but not by 5,8,11-eicosatrienoic acid. The latter is not an endogenous prostaglandin precursor, but replaces the other two in essential fatty acid deficient (EFAD) rats. Carrageenan oedema was partially suppressed in these EFAD rats. Aspirin exhibited equal suppression of carrageenan oedema in both normal and EFAD rats, despite the fact that, in the latter, prostaglandins are of negligible importance. The anti-inflammatory effect of dexamethasone was also identical in both normal and EFAD rats. The view that interference with the prostaglandin-system explains the acute anti-inflammatory effects of the two drugs, is discussed, in relation to the present results.

Animals↗
PubMed1976

Biphasic effects of phospholipase A2 on platelet aggregation. Effect of prostaglandin synthesis inhibitors and essential fatty acid deficiency.

Phospholipase A2 has a biphasic action upon the aggregation of rat platelets. In the first phase, occurring after shorter incubation periods with the enzyme, aggregation is enhanced. Longer incubation periods lead to an inhibition of the aggregation. The first phase disappears after the addition of indomethacin whereas the second phase persists. Incubation of platelets with phospholipase A2 leads to serotonin release. Prostaglandins are formed without platelet aggregation. Whereas the same effects occurred at the high dose of phospholipase A2 when platelets of essential fatty acid deficient rats were used, a difference was seen at the lower dose. It is concluded that in the first phase, arachidonic acid is liberated and transformed into aggregation inducing intermediates which are formed in the prostaglandin synthesis. In the second phase, changes may occur in the outer membrane which lead to diminished sensitivity to aggregating agents.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1975

The effect of non-steroid anti-inflammatory drugs, dibutyryl cyclic 3',5'-adenosine monophosphate and phosphodiesterase inhibitors on platelet aggregation and the platelet release reaction in normal and essential fatty acid deficient rats.

A comparison was made of the action of three classes of substances with platelet aggregation inhibiting effect in normal and essential fatty acid deficient rats. In the latter group, the effect of indomethacin was considerably reduced, whereas the difference was smaller with aspirin. Dibutyryl cyclic AMP had the same inhibiting effect in both groups. Of the phosphodiesterase inhibitors tested, dipyridamole was inactive, whereas the inhibiting effects of caffeine and papaverine are slightly reduced in the deficient animals. The same differences between the two groups were seen in the magnitude of the release reaction after 14C-serotonin labelling. These data support the idea that the non-steroid anti-inflammatory drugs act by inhibiting the formation of an aggregation-inducing substance from arachidonic acid.

Animals↗