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J R Vane

Publications and source records attributed to J R Vane.

At least 235 records · Page 13Linked to original sources
PubMed1983

Synthesis of arachidonate cyclo-oxygenase products by rheumatoid and nonrheumatoid synovial lining in nonproliferative organ culture.

Specimens of human rheumatoid and nonrheumatoid synovial lining were maintained in nonproliferative organ culture for 20 hours. The culture fluids were then assayed for prostaglandin E(2) (PGE(2)), thromboxane B(2) (TXB(2)), and 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha)) by specific radioimmunoassay. The presence of each of these substances was confirmed by gas chromatography and mass spectrometry. Rheumatoid tissue produced significantly more of each cyclo-oxygenase product than nonrheumatoid tissue.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Prostacyclin.

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Animals↗
PubMed1981

Prostacyclin: its biosynthesis, actions and clinical potential.

Prostacyclin (PGI2) is the product of arachidonic acid metabolism generated by the vessel wall of all mammalian species studied, including man. Prostacyclin is a potent vasodilator and the most potent inhibitor of platelet aggregation so far described. Prostacyclin inhibits aggregation through stimulation of platelet adenyl cyclase leading to an increase in platelet cyclic AMP. In the vessel wall, the enzyme that synthesizes prostacyclin is concentrated in the endothelial layer. Prostacyclin can also be a circulating hormone released from the pulmonary circulation. Based on these observations we proposed that platelet aggregability in vivo is controlled via a prostacyclin mechanism. The discovery of prostacyclin has given a new insight into arachidonic acid metabolism and has led to a new hypothesis about mechanisms of haemostasis. Reductions in prostacyclin production in several diseases, including atherosclerosis and diabetes, have been described and implicated in the pathophysiology of these diseases. Additionally, since prostacyclin powerfully inhibits platelet aggregation and promotes their disaggregation, this agent could have an important use in the therapy of conditions in which increased platelet aggregation takes place and in which, perhaps, a prostacyclin deficiency exists. Prostacyclin has been used beneficially in humans during extracorporeal circulation procedures such as cardiopulmonary bypass, charcoal haemoperfusion and haemodialysis. Its possible use in other conditions such as peripheral vascular disease or transplant surgery is at present being investigated.

Angiotensin I↗
PubMed1981

Prostacyclin and blood coagulation.

Prostacyclin is a potent but unstable vasodilator, and inhibitor of platelet aggregation, which is produced by blood vessel walls. Platelet aggregability may be constantly conditioned in vivo by local or circulating prostacyclin. Prostacyclin is important in the maintenance of vascular homeostasis and may be implicated in certain disease states. The use of prostacyclin in antithrombotic therapy appears logical, considering its action in increasing platelet cyclic AMP and reducing aggregation; its potential in antithrombotic therapy is presently being explored.

Arteriosclerosis↗
PubMed1980

The effects of non-steroid anti-inflammatory drugs on leukocyte migration in carrageenin-induced inflammation.

Some non-steroid anti-inflammatory drugs which inhibit arachidonate cyclo-oxygenease have been examined for their effects on leukocyte migration, prostaglandin production and oedema formation in carrageenin-induced inflammation in the rat. At doses which inhibited oedema, all the drugs tested caused a dose-dependent reduction in numbers of leukocytes and prostaglandin concentrations in 24-h inflammatory exudates. At lower doses, indomethacin, aspirin, sodium salicylate, flurbiprofen and phenylbutazone significantly potentiated leukocyte migration by 20-70%. Ibuprofen, naproxen and BW755C reversed the indomethacin-induced increase in leukocyte accumulation. BW755C inhibits the generation of chemotactic lipoxygenase products and it is possible that the effects of all these drugs on leukocyte migration are mediated through the lipoxygenase pathway of arachidonic acid metabolism.

Animals↗