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Biomedical subjects

J Musiał

Publications and source records attributed to J Musiał.

59 records · Page 4Linked to original sources
PubMed1978

Arachidonic acid-induced platelet aggregation and thromboxane A2 generation in patients with coronary heart disease.

Arachidonic acid (AA)-induced platelet aggregation was studied in platelet-rich plasma of 32 male patients who survived myocardial infarction and in 32 healthy men of similar age. Only in three healthy subjects, but in 13 patient, irreversible platelet aggregation was induced consistently with concentrations of AA below 500 micrometer. The rate of conversion of AA to thromboxane A2 (TXA2) by platelets of these patients was augmented, although less endogenous TXA2 was required to trigger aggregation of their platelets as compared to the controls. The results indicate that among patients with coronary heart disease a subgroup can be distinguished which can possibly benefit from the secondary preventive treatment with aspirin and with other anti-platelet drugs which inhibit the generation of TXA2 in platelets.

Adult↗
PubMedDate not supplied

[Familial occurrence of Glanzmann thrombasthenia].

Glanzmann's thrombasthenia, known also as Glanzmann's disease, is an autosomally inherited hemorrhagic disease with unique abnormalities of platelet functions. Authors present a large family in which Glanzmann's disease was diagnosed in the father and two sons. An analysis of platelet membranes enabled diagnosis of Glanzmann's thrombasthenia type II. A decrease in clot contractibility, fibrinogen binding to blood platelets, and decreased glycoprotein IIb and IIIa levels with marked impairment of GP IIb and IIIa complexes formation were characteristic for affected family members. One daughter died 8 days after birth with the symptoms of hemorrhagic diathesis. Mother and remaining three sons are healthy without the signs of Glanzmann's disease.

Adolescent↗
PubMedDate not supplied

[Effect of thromboxane A2 synthetase inhibitor and prostacyclin analogue on arterial blood pressure, fibrinolysis and platelet function in patients with hypertension].

An effect of the specific thromboxane A2 synthetase inhibitor and stable prostacyclin analogue on arterial blood hypertension was investigated in 12 patients with spontaneous hypertension of II degree and in 12 healthy subjects. The patients were given a 3-hour intravenous infusion of Iloprost (Schering) in the dose of 2 ng/kg b.w. per minute and OKY-046 (ONO, Japan) in a single oral dose of 400 mg. Iloprost shortened euglobin fibrinolysis time without an effect on tissue plasminogen activator levels or blood pressure. OKY-046 decreased TBX2 to undetectable values, increased 6-keto-PGF1 alpha by 8-fold, and significantly reduced both systolic and diastolic blood pressures in hypertensive patients. Such effects may dependent upon an increase in the endogenous prostacyclin or an inhibition in thromboxane production in the affected arterial walls. If the present observations would be confirmed by double blind trial, they would constitute the base for new pharmacotherapy of hypertension.

Adult↗
PubMedDate not supplied

[Should hemostatic factors be considered in the prevention of cardiovascular disease?].

The relationship between thrombosis and atherosclerosis has been already suggested in the middle of the last century. More recently, in 1976 a hypothesis has been put forward which emphasize the leading role of chronic injury to endothelial cells followed by platelet attachment and the release of platelet derived growth factors in pathogenesis of atherosclerosis. There is also a growing body of evidence that cytokines, thrombin and the fibrinolytic system are involved in the initiation and progression of atherosclerotic lesions. Lipoprotein (a) is emerging as a link between atherogenic role of lipids and the haemostatic system. At the same time epidemiological data are pointing at the possible role of fibrinogen, factor VII and plasminogen activator inhibitor-1 as risk factors for ischemic heart disease. Thrombus formation is also responsible for the majority of acute coronary syndromes. On the other hand aspirin and other antiplatelet drugs seem to protect from vascular complications of atherosclerosis. Than the question which rather arises is: what is the best antithrombotic strategy in patients with cardiovascular diseases?

Animals↗