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Biomedical subjects

M Verstraete

Publications and source records attributed to M Verstraete.

At least 181 records · Page 10Linked to original sources
PubMed1979

Stimulation of prostacyclin release from vessel wall by Bay g 6575, an antithrombotic compound.

Ingestion of 1.2 g Bay g 6575 daily for 1 week by six healthy volunteers had no effect on blood-coagulation, fibrinolysis, or platelet aggregation in vitro, but it seemed to inhibit platelet aggregation in vivo (shown by a smaller reduction in the platelet aggregate ratio after venous occlusion). Plasma drawn from five volunteers after ingestion of a single dose of 1.2 g of the drug stimulated prostacyclin release from slices of rat aorta which had been washed until they stopped releasing anti-aggregating substances, whereas plasma from the same individuals before ingestion of the substance did not. Administration of either Bay g 6575 or dipyridamole alone had no effect on platelet aggregation in vitro, but combined administration resulted in a striking and prolonged inhibition of A.D.P.-induced platelet aggregation. It is proposed that the previously described antithrombotic properties of Bay g 6575 in animals are due to stimulation of prostacyclin release from the vessel wall, and that this effect is also demonstrable in man.

Adenosine Diphosphate↗
PubMed1979

Clinical trial of brinase and anticoagulants as a method of treatment for advanced limb ischemia.

A randomized, single-blind trial of repeated intravenous infusion of Brinase was carried out in 70 petients with severe chronic limb ischemia, who were candidates for lumbar sympathectomy or amputation. The enzyme caused s significant increase in calf and ankle pressure index. At six months follow-up, the clinical results were statistically significant in favour of Brinase when all patients were considered, but not if 10 patients with Buerger's disease were omitted from the analysis. Patients treated with a combination of Brinase and coumarins had a better clinical outcome than patients receiving either treatment on its own.

Aged↗
PubMed1979

Medical treatment in intermittent claudication.

A variety of measures advocated in the treatment of intermittent claudication are critically reviewed. Daily leg exercises increase the walking ability but the mechanism of this effect remains controversial. To date, doubt persists whether drugs, either vasodilating or antithrombotic, are of any clinical value in this condition.

Exercise Therapy↗
PubMed1978

Biochemical changes noted during intermittent administration of streptokinase.

An intermittent dosage scheme of streptokinase (standard initial dose 600,000 units SK infused over 30 min and repeated injections of 250,000 units SK at 24 hr intervals) was applied during 4 days in 9 patients with chronic obliterative arterial disease and in 8 patients with venous occlusion. Each dose of streptokinase produced an immediate fall in plasminogen to 17% (SEM 5.1) of the initial value, the level then rose to 50% (SEM 5.4) within 24 hr. Lowered levels of antiplasmin and fibrinogen (both less than 40% of the initial values) were maintained. This safe level of fibrinogen was maintained despite brief but high peaks of plasmin activity after each injection of SK. A parallel increase of the thrombin time and the fibrin (ogen) degradation products was obtained following each infusion. No bleeding was observed. The relative therapeutic effect of intermittent infusions of streptokinase has still to be compared with the continuous administration of streptokinase in controlled clinical trials.

Antibodies↗
PubMed1978

Inhibition of plasmin by antithrombin-heparin complex. II. During thrombolytic therapy in man.

The role of antithrombin as an inhibitor of plasmin in the presence and absence of heparin was studied during thrombolytic therapy in 12 patients with vascular occlusive disease. The extent of plasmin-antithrombin-(heparin) complex formation was studied by intravenous injection of iodine-labelled antithrombin (5-20 muCi) and quantitation of the amount of antithrombin bound to plasmin. In the absence of heparin, less than 0.8% of the labelled antithrombin was recovered in the plasmin-antithrombin complex but between 1.2 and 4.8% following injection of 5000 iu of heparin. Thus only between 3 and 11% of the in vivo formed plasmin is neutralized by antithrombin-heparin complex. Repeated activation of the fibrinolytic system resulted in a shortening of the plasma radioactivity half-life of labelled antithrombin from 2.45 to 2.03 d in the absence of heparin (three patients), and from 3.13 to 2.35 d following heparin administration (two patients). This increased turnover does not result in a decrease of the plasma antithrombin level.

Adult↗
PubMed1978

Turnover of radiolabelled plasminogen and prothrombin in cirrhosis of the liver.

The turnover of purified radiolabelled plasminogen was studied in four patients with cirrhosis of the liver, and that of radiolabelled prothrombin in six patients with cirrhosis of the liver. The cirrhotic patients showed an increased fractional catabolic rate and a decreased synthetic rate, resulting in subnormal plasma levels of plasminogen and prothrombin. The plasma concentration of the two proteins correlated with the synthetic rate, but not with the fractional catabolic rate. Heparin infusion prolonged the shortened half-life of plasminogen in two cirrhotics from 1.25 to 2.10 days and from 1.45 to 1.90 days, and the half-life of prothrombin in three cirrhotics from 2.25 to 2.70 days, from 2.35 to 2.80 days and from 2.40 to 3.70 days. These results indicate that the abnormal turnover of labelled plasminogen and prothrombin in cirrhosis of the liver is due to two mechanisms; increased breakdown, reversible by heparin administration, and impaired synthesis. The decreased plasma levels are, however, mainly caused by decreased synthesis.

Humans↗
PubMed1978

[The interaction between drugs and oral anticoagulants of the coumarin group].

The problem of drug interactions during prolonged use of coumarin anticoagulants is important for most patients receiving anticoagulants take several other drugs. Frequent interaction causes either potentialisation of the anticoagulant effect with risk of hemorrhage or inhibition of the anticoagulant effect with risk of thrombosis. The various mechanisms which may explain most interactions are reviewed and the authors propose a list of drugs which should not be administered with coumarin.

Albumins↗
PubMed1978

[Treatment of acute arterial occulusions with streptokinase].

Of the patients treated within the first week after thrombo-embolic occulusion of the arteries of the lower limb 45% achieve total disobliteration with thrombolytic therapy. The authors discuss the factors influencing disobliteration, as well as the mortality and complications of thrombolytic treatment using streptokinase. Surgical treatment (the Fogarty catheter) is complementary. Choice of treatment is made by a combination of factors which include the age of the patient, the site and extent of the block, the amount of neuro-muscular ischaemia, and the general condition of the patient.

Acute Disease↗