[The radioisotope labelling of thrombocytes using a monoclonal antibody against membrane glycoproteins IIb-IIIa and the measurement of thrombocyte adhesion/aggregation on the substrate surface].

A new method for platelet labeling based on binding of monoclonal antibody to human platelets has been suggested in this study. Monoclonal antibody VM16a against membrane glycoproteins IIb-IIIa was labeled by 125I and then incubated with platelets. About 70% of added antibody was bound when it was used at the concentrations corresponding to the linear part of the concentration curve (0.

[Adhesive activity of blood platelets in patients with stable or unstable angina pectoris and acute myocardial infarct].

Platelet adhesive activity was assayed in patients with stable angina (SA) or unstable angina (UA) and acute myocardial infarction (AMI). With scanning electron microscopy, platelet adhesions to Type IV collagen (C-IV) and plastic material, which had been stimulated by low-dose ADP, epinephrine and U-46 619, a stable thromboxane A2 analogue (agonist-induced adhesion) were determined. As compared with the control group, patients with SA or UA, showed significantly higher adhesion of platelets to the collagen substrate, whereas UA patients alone displayed a significantly increased agonist-induced adhesion when epinephrine was employed as an agonist.

[Agonist-induced platelet adhesion: use of the method in patients with myocardial infarction].

A new method of agonist-induced platelet adhesion has been developed for the evaluation of platelet activity. Platelet adhesion to plastic was stimulated by low doses of ADP, epinephrine and stable thromboxane analogue U46619. These inducers cause more than 3-fold increase of platelet adhesion in concentrations by 5-10 times lower than those necessary for stimulation of platelet aggregation in Born aggregometer.

[Intensity of free radical oxidation and the blood lipid fatty acid composition in ischemic heart disease].

A comprehensive study of the intensity of free radical oxydation of lipids, of changes in the total polyunsaturated free acids and antiradical activity of the blood lipids undertaken in 73 patients with different forms of ischaemic heart disease showed that in all forms of illness there exists intensification of peroxyde oxydation of lipids, more marked in acute myocardial infarction. Rise of antiradical activity of lipids is a sequel to activation of the compensatory mechanisms, directed at neutralization of the negative action of toxic lipid peroxydes. Correlation between the changes in the total polyunsaturated fatty acids and antiradical activity of the lipids permits one to consider that accumulation of polyene acids may be one of the factors helping the intensification of free radical processes.