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Biomedical subjects

M Lagarde

Publications and source records attributed to M Lagarde.

At least 253 records · Page 14Linked to original sources
PubMed1981

Refractoriness of diabetic platelets to inhibitory prostaglandins.

Inhibition of collagen-induced platelet aggregation by either endothelial extracts, prostacyclin, prostaglandin E1 or prostaglandin D2 was investigated. The inhibition was less efficient with diabetic platelets than with platelets from normal donors. The refractoriness of diabetic platelets to inhibitory prostaglandins was observed both with platelet-rich plasma and platelets isolated from their plasma. Moreover levels of cyclic AMP in resting platelets and after stimulation by either PGE1 or PGD2 were lower in diabetic platelets than in normal platelets. It is concluded that the weaker response of diabetic platelets to inhibitory prostaglandins could be related to their content in cyclic AMP.

Adolescent↗
PubMed1981

Constitutional thrombocytopathy with subnormal response to thromboxane A2.

A new type of congenital platelet dysfunction was found in a young woman presenting a life-long bleeding disorder. The known types of thrombopathia and von Willebrand's disease were excluded by appropriate investigations. The platelets were morphologically normal, underwent normal shape change and contraction and synthesized thromboxane A2 (TXA2) normally. The release reaction was abnormal and the aggregation response to ADP, adrenalin, collagen, thrombin, sodium arachidonate and vasopressin was depressed due to decreased sensitivity of the platelets to prostaglandin endoperoxides and TXA2. Platelet cAMP content was increased.

Adolescent↗
PubMed1980

15-Hydroperoxyeicosatetraenoic acid inhibits human platelet aggregation.

Using human platelets isolated from their plasma, we showed that 15-hydroperoxyu-eicosatetraenoic acid (15-HPETE) inhibits platelet aggregation induced either by arachidonic acid or prostaglandin H2 analog. 15-HPETE does not modify platelet prostaglandin and thromboxane formation from exogenous arachidonic acid but does decrease platelet lipoxygenase activity.

Arachidonic Acids↗
PubMed1980

Dihomogammalinolenic acid (20:3 omega 6) is more anti-aggregatory than eicosapentaenoic (20:5 omega 3) in a platelet-endothelial cell mixture.

The effect of 20:3 omega 6, the precursor of 1 series prostaglandins was to inhibit platelet aggregation more strongly than either 20:5 omega 3, the precursor of 3 series prostaglandins or 20:3 omega 3 which is not a substrate of prostaglandin synthetase. When platelets and dissociated endothelial cells were pretreated with 20:3 omega 6, platelet aggregation in the presence of endothelial cells was much more inhibited than after 20:5 omega 3 pretreatment.

8,11,14-Eicosatrienoic Acid↗
PubMed1980

Fatty acids bound to serumalbumin decrease the half-life of thromboxane A2.

The half-life of thromboxane A2 is increased in plasma as well as in a buffer containing serumalbumin. Moreover, the half-life of thromboxane A2 depends on the amount of unesterified fatty acids bound to albumin. When more fatty acids are bound, the half-life is shortened. This shortening is accompanied by a decrease of the aggregating activity of thromboxane A2.

Chemical Phenomena↗
PubMed1979

Effects of ticlopidine on platelet prostaglandin metabolism. Possible consequences for prostacyclin production.

Ticlopidine, known to inhibit the primary wave of ADP-induced platelet aggregation and to increase the bleeding time, can modify platelet prostaglandin metabolism. The basal level of platelet PGE1 is enhanced by the drug. Ticlopidine does not decrease biosynthesis of prostaglandin endoperoxides from arachidonic acid but increases production of primary prostaglandins, cheifly prostaglandin D2, and causes a slight diminution of thromboxane B2 formation. The excess of prostaglandin endoperoxides not converted to primary prostglandins may escape from platelets and produce more prostacyclin if endothelial cell microsomes are present in the incubate.

Adenosine Diphosphate↗
PubMed1979

Basal level of human platelet prostaglandins: PGE1 is more elevated than PGE2.

Radioimmunoassays of platelet prostaglandins E1 and F1 alpha in platelet rich plasma or platelet suspension, demonstrate that both PGE1 and PGF1 alpha are present at higher concentrations than prostaglandins E2 and F2 alpha. Gas chromatography--mass spectrometry determinations of prostaglandins E1 and E2 in resting washed platelets confirm this difference. Lastly, there is a greater incorporation of [1--14C] acetate into prostaglandins E1 and F1 alpha compared to that into prostaglandins E2 and F2 alpha.

Blood Platelets↗
PubMed1978

[Sterologic evaluation on in vitro thrombin-induced platelet degranulation and contraction (author's transl)].

Stereologic study of the in vitro release reaction from unstirred washed platelets provided quantitative information on the contractile wave induced by thrombin. Contraction was estimated from the reduction in the volume of both the granular compartment and the vacuoles of the surface connected canalicular system. Dibutyryl cyclic-AMP (10(-4) M) and dipyridamole (10(-3) M) inhibited degranulation, but they had no effect on the contraction produced by thrombin at high concentrations (0.1 UI/ml). Aspirin (10(-4) M) inhibited contraction induced by thrombin at concentration of 0.1 and 0.02 UI/ml (p less than 0.01 at each concentration). In two patients with hereditary cyclo-oxygenase deficiency, contraction produced by thrombin at low concentration (0.02 UI/ml) failed to induce contraction.

Aspirin↗
PubMed1978

Impairment of platelet thromboxane A2 generation and of the platelet release reaction in two patients with congenital deficiency of platelet cyclo-oxygenase.

Two cases of thrombocytopathia with congenital deficiency of platelet cyclo-oxygenase were investigated. The platelet release reaction was impaired. There was a marked decrease of aggregation with collagen and with adrenalin and a total absence of aggregation with sodium arachidonate. The platelet response to labile aggregation stimulating substance (LASS, mostly thromboxane A2) was normal. There was no biosynthesis of prostaglandin cyclic endoperoxides or of thromboxane A2 from arachidonic acid. Basal levels of platelet PGE1 were lowered although plasma levels were normal. Thrombin decreased the cyclic AMP content of patients' platelets and also that of control platelets pretreated with aspirin. The patients platelets showed no ultrastructural difference when compared with control platelets, except for a slight decrease of granule volume, but, in contrast to control platelets, thrombin (0.02 U/ml) did not provoke contraction of the patients' platelets.

Adult↗
PubMed1977

A simple radiochemical assay of thromboxane B2, 12-hydroxyeicosatetraenoic acid (HETE) and 12-hydroxyheptadecatrienoic acid (HHT) synthetized by human platelets.

A simple radiochemical assay of thromboxane B2, 12-hydroxyeicosatetraenoic acid (HETE) and 12-hydroxyheptadecatrienoic acid (HHT) produced by platelets from arachidonic acid has been described. Moreover, this assay is suitable for measuring thromboxane A2 trapped as 11-mono-O-methylthromboxane B2 and minor products such as prostaglandins E2, F2alpha and D2. The advantage of this technique is discussed as to its ease and specificity.

Arachidonic Acids↗