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Biomedical subjects

M Verstraete

Publications and source records attributed to M Verstraete.

At least 163 records · Page 9Linked to original sources
PubMed1982

A pharmacological approach to the inhibition of platelet adhesion and platelet aggregation. Wright-Schulte Lecture.

A first level of pharmacological interference with platelet function is located at the site of the agonist-receptor interaction (receptors for collagen, adenosine diphosphate, serotonin, fibrinogen). A second level of interaction is to prevent the mobilization of intracellular calcium ions which can be obtained by inhibition of phosphodiesterase, activation of cAMP (e.g. with prostacyclin analogues), inhibition of thromboxane A2 formation or blocking of its receptors. Compounds preventing the platelet contractile process or platelet secretion could theoretically also prevent some platelet functions.

Adenylyl Cyclases↗
PubMed1981

Thromboxane synthetase inhibition as antithrombotic strategy.

The imidazole derivative UK-37 248, a thromboxane synthetase inhibitor, reduces the in-vitro formation of thromboxane B2 and hydroxyheptadecatrienoic acid by washed platelets, and this is compensated for by an increased production of prostaglandins E2 and F2 alpha; arachidonic acid challenged platelets pretreated with UK-37 248 also stimulate the production of prostacyclin by aspirin pretreated cultured endothelial cells. In a double-blind placebo controlled study to examine the in vivo properties of UK-37 248, human volunteers ingested 200 mg of the compound. Their serum thromboxane B2 levels dropped and their plasma 6-keto-prostaglandin F1 alpha values rose. Arachidonic acid induced platelet aggregation was completely inhibited whereas that elicited by adenosine-5'-diphosphate was unaffected. By reducing formation of pro-aggregatory tromboxane A2 and increasing production of anti-aggregatory prostacyclin, thromboxane synthetase inhibitors may be better than aspirin as antithrombotic agents.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

[Problems and prospects for clinical heparin use].

The paper contains new data on the pharmacodynamics of heparin and its interaction with the Xa factor, antithrombin III and thrombin. A critical assessment of the clinical efficacy of different types of heparin treatment of thromboembolisms is given, including thromboembolism of the pulmonary artery.

Absorption↗
PubMed1981

[Actual state of thrombolytic treatment of recent vein thrombosis and pulmonary embolism (author's transl)].

Recent deep vein thrombosis of the iliofemoral segment often leads to pulmonary embolism and to impaired valve function. Although more common, occlusions in the calf veins are less dangerous, and often a self-limiting disorder as almost half of these thrombi lyse spontaneously. Approximately 70% of fresh deep venous thrombi dissolve under intensive and prolonged thrombolytic treatment with streptokinase and long-term follow-up studies indicate that normal valve function is preserved in those patients in whom thrombus clearance was obtained. Thrombosis with streptokinase or urokinase appears to be the current treatment of choice for most cases of massive and severe, life-threatening pulmonary embolism; those patients surviving more than an hour or so after massive infarction comprise a prognostically better group, in whom the chances of surviving embolectomy is today smaller than the probability of survival without surgery but with thrombolytic treatment. Obviously there are problems in the evaluation but also in the thrombolytic treatment with streptokinase and urokinase of deep venous thrombosis and pulmonary embolism. These problems do not concern the principle of thrombolysis, but are largely due to the fact that the drugs so far used also induce a systemic fibrinogenolysis resulting in a bleeding risk. There is already good evidence that tissue activator of plasminogen is highly specific for fibrin and can induce thrombolysis in experimental animals without inducing systemic fibrinogenolysis.

Animals↗