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Biomedical subjects

E P Panchenko

Publications and source records attributed to E P Panchenko.

53 records · Page 3Linked to original sources
PubMed1987

[Thrombocyte function in physical exertion and induced myocardial ischemia in patients with ischemic heart disease].

Reaction to graded bicycle exercise in patients with newly developed angina pectoris, patients with chronic IHD and subjects without IHD with normal coronary arteries was studied. Platelet activation by physical exercise was significantly more often (35.7%) in patients with newly developed angina pectoris than in patients with chronic IHD (12.8%) and patients without IHD (13%). It is shown that myocardial ischemia during physical exercise does not influence the frequency of the platelet activation signs determination. Development of platelet activation in physical exercise was promoted by minor disease duration, lower basic platelet functional activity and more evident increase in haematocrite in physical exercise.

Adult↗
PubMed1987

[Phosphocreatine: thrombocyte aggregation in patients with stenocardia].

Phosphocreatine (Neoton produced by "Schapparelli Farmaceutici") was infused intravenously to 27 patients with CHD at a dose of 2000 mg: 13 patients with unstable and 10 patients with stable angina pectoris. Phosphocreatine blocked ADP-induced platelet aggregation in these patients, but had no significant effect on the platelet aggregation induced by collagen, platelet activating factor or serotonin.

Adenosine Diphosphate↗
PubMed1987

[Unstable stenocardia: functional activity and free cytoplasmic calcium of thrombocytes and vaso- and thrombocytoactive prostanoids].

Platelet function was studied in patients with diverse clinical patterns of unstable angina. In vasospastic angina, anginal attacks coincide with the highest increment in Ca2+ of platelets, and their high sensitivity to aggregation inductors, which declines as the condition stabilizes. Unstable angina without the vasospastic component is associated with reduced platelet sensitivity to aggregation inductors, particularly so in patients showing signs of intracoronary thrombosis. Spontaneous anginal attacks are accompanied with a rise of thromboxane B2 and a drop in the stable prostacyclin metabolite level.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Thromboxane and prostacyclin in patients with stenocardia in induced and spontaneous ischemia of the myocardium].

The levels of TxB2 and 6-keto-PGI alpha in the coronary sinus and thoracic aorta blood were determined in 14 patients with angina pectoris and signs of coronary atherosclerosis. 12 patients were involved in a dynamic study: before, during and 10 minutes after ischaemia-inducing atrial pacing. In all the patients atrial pacing resulted in a typical episode of angina, in 7 of them ST-segment depression of not less than 2 mm was seen on the ECG. In one patient arachidonic acid metabolites were evaluated during the control period and during a spontaneous episode of angina accompanied by ST-segment elevations. In 8 of 9 patients TxB2 was produced by the myocardium during atrial pacing. During monitored evaluation of arachidonic acid metabolites one patient with spontaneous angina demonstrated a gradual lowering of the 6-keto-PGI alpha, it being minimal by the beginning of the episode; TxB2 level increased more rapidly.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Unstable stenocardia: the results of the intracoronary administration of fibrinolytic agents].

Intracoronary thrombolytic infusions were used in 10 patients with unstable angina and high risk of myocardial infarction (MI). Streptokinase (500,000 units per hour) was used in 9 patients, and urokinase, in one. Vascular recanalization was achieved in 4 cases where angiography showed coronary arterial occlusion by a thrombus. Myocardial infarction developed in 8 patients (large-focal in 6 and small-focal in 2) within 1 to 16 days after the thrombolytic infusion. Therefore, short-term local thrombolytic infusion fails to prevent myocardial infarction in patients with unstable angina.

Adult↗
PubMed1986

[Free cytoplasmic calcium and thrombocyte aggregation in patients with ischemic heart disease. The effect of ADP, thrombocyte activation factor and serotonin].

Ca++ level in the platelets of patients with different forms of CHD (angina pectoris of new onset, including the spastic form, acute myocardial infarction) and of subjects without signs of CHD or coronary atherosclerosis was measured basally and after stimulation with ADP, platelet activation factor and serotonin. Simultaneously platelet aggregation induced by the same stimuli was studied. Basal platelet Ca++ did not differ significantly between the groups. Stimulation by ADP and serotonin increased Ca++ concentration, the change being greatest in patients with spastic angina pectoris. Augmentation of free platelet Ca++ in patients with acute myocardial infarction did not differ from that in subjects without CHD and coronary atherosclerosis, and in some cases it was even less pronounced. Free Ca++ level showed good correlation with platelet aggregation. It is suggested that the differences revealed are due to changes in the sensitivity of platelet receptors to the inductors used.

Adenosine Diphosphate↗
PubMed1984

[Fibronectin level in coronary sinus blood in myocardial ischemia caused by atrial stimulation].

Patients with coronary heart disease and angina pectoris were examined. The blood outflowing from the myocardium at the height of ischemia induced by atrial stimulation was found to have lower levels of fibronectin. Ten minutes after the stimulation discontinuation the concentration of fibronectin returned to baseline. A reduction in the fibronectin content during myocardial ischemia seems to be related to its consumption as a result of maintaining antithrombotic function.

Adult↗
PubMed1983

[Pulmonary artery thromboembolism: its clinical and coagulative diagnosis].

A total of 250 subjects were investigated using a diagnostic search flow-chart. Pulmonary artery thromboembolism (PATE) was diagnosed in 102 patients. The results have demonstrated the value of laboratory tests employed--markers of thrombin- and plasminemia and platelet activation--for PATE diagnosis. To diagnose PATE, levels of fibrinogen-fibrin and beta-thromboglobulin degradation products should be measured in myocardial infarction patients, and plasma soluble fibrin measurement should be added to those in patients with circulatory insufficiency. In recurrent PATE, continuous increase of plasma beta-thromboglobulin and soluble fibrin levels, antithrombin III exhaustion and reduced levels of fibrinogen-fibrin degradation products are of diagnostic value.

Antithrombins↗
PubMed1981

[Characteristics of the disseminated intravascular coagulation syndrome in ischemic heart disease patients with congestive circulatory failure].

Patients with ischaemic heart disease of severe forms with congested insufficiency of the circulation have chronic latent disseminated intravascular blood coagulation, which is confirmed by the increased level of soluble fibrin, products of breakdown of fibrinogen-fibrin, decreased activity of antithrombin III, marked sludging of erythrocytes at the microcirculatory level. A high degree of the correlation between the content of soluble fibrin and the marked sludge-phenomenon was found. Thromboembolic complications arising in this group of patients were accompanied by marked progress of the disorders found, which permitted one to isolate a limited as the the number of parameters coagulogram for the diagnosis of acute intravascular thrombosis in the patients with ischaemic heart diseases with congested insufficiency of the circulation. The important role of a preserved plasmin system for the prognosis in patients with congested insufficiency of the circulation with thromboembolic complications is shown.

Aged↗
PubMed1979

[State of hemostasis and blood rheology in congestive circulatory insufficiency].

One hundred and ninety-eight patients with congestive circulatory insufficiency were examined; 54 had stage IIA, 88 stage IIB, and 56 stage III of the disease. Blood viscosity, blood platelet and erythrocyte aggregation, fibrinogen disintegration products, and soluble fibrin were determined and the protamine sulfate test was performed. Statistically significant reduction of hematocrit, increase of erythrocyte aggregation, dysfunction of blood platelets, and increase in the content of products of fibrinogen and fibrin disintegration were revealed with progression of congestive circulatory insufficiency. These changes are evidence of disseminated intravascular coagulation in such patients and are important in prognostication.

Blood Viscosity↗
PubMed1979

[Content of fibrinogen degradation products, soluble fibrin and the fibrinolytic activity of blood in myocardial infarct].

The blood content of soluble fibrin and D and E fibrinogen fragments, the protamine sulfate test and the activity of plasmin and plasminogen activator were studied in patients with macrofocal myocardial infarction. It was established that the content of soluble fibrin in blood considerably increases in the first days of the disease, and the level of products of fibrinogen D and E disintegrationand the value of the protamine sulfate test increase in the 2nd--3rd week of the disease. The appearance in the blood of fibrinogen derivates was attended by low activity of plasmin and plasminogen activator in blood. The highest content of fibrinogen derivates and low activity of plasmin and plasminogen activator were noted in patients with arrhythmias and congestive circulatory insufficiency. It is suggested that the appearance in circulation of high-molecular fibrinogen compounds is important in the development of rheological disorders.

Adult↗