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Biomedical subjects

G V Andreenko

Publications and source records attributed to G V Andreenko.

At least 19 recordsLinked to original sources
PubMed2005

[The fibrinolytic system in uric acid dysmetabolism].

The subjects of the study were 50 first-degree relatives of patients with uric acid (UA) dysmetabolism. The subjects were divided into three groups: 15 with hyperuricosuria and normal UA blood level (group 1), 17--with hyperuricosuria and hyperuricemia (group 2), and 18--with hyperuricemia and lowered UA clearance (group 3). All of them displayed inhibited urine fibrinolytic activity (UFA) and reduced urokinase activity. The degree of UFA inhibition correlated with urokinase activity (r = 0.60) and grew from group 1 to group 3; the subjects in the latter had maximal manifestations of tubulointerstitial nephritis, which suggests that disorder of the local fibrinolytic mechanisms plays an important role in the development and progress of urate tubulointerstitial renal lesion. No changes of blood fibrinolysis were observed.

Diabetes Mellitus↗
PubMed2003

[Effect of diet therapy on status of hemocoagulation and fibrinolysis in type 2 diabetes patients].

The changes in parameters of blood coagulation and the fibrinolytic system in 60 patients with type 2 diabetes mellitus was studied. We conclude what the non insulin depended diabetes mellitus is associated with disturbances in hemostatic and fibrinolytic systems that could contribute to the development of diabetic vascular disease. Besides favorable influence to a clinical picture of disease universal normalizing influence of traditional diet therapy on parameters of coagulation and the fibrinolytic system. Our results show that diet therapy improve metabolic control in type 2 diabetic patients could reflect a reduces thrombotic potential and decreased cardiovascular risk.

Adult↗
PubMed2000

Coagulation and fibrinolysis in rats after surgery with monopolar electrical scalpel.

Blood coagulation, fibrinolysis in plasma and peritoneal fluid, and activity of tissue plasminogen activator in the peritoneum and uterine horns were studied in albino rats after surgery on the uterine horns with a monopolar electrical scalpel. This instrument induced severe inflammatory reaction and disturbances in the fibrinolysis and coagulation systems.

Animals↗
PubMed1999

[Urokinase as a blood and urine plasminogen activator in chronic glomerulonephritis and amyloidosis].

To estimate the individual role of the plasminogen activators (PA) urokinase (u-PA) and tissue (t-PA) in the development of two renal diseases (the nephrotic forms of chronic glomerulonephritis (CGN) and amyloidosis, the baseline plasma and urine levels of u-PA and t-PA antigens, their functional activity (FPAA), and changes in these parameters were determined after protein loading test (0.7 g/kg). In healthy individuals and patients with amyloidosis, the baseline FPAA changes from 0 to the maximum were caused only by the alterations of u-PA levels, in those with CGN, they were induced by the changes in the content of u-PA and t-AP antigens. The functional loading test revealed PA reserves solely in patients having a high baseline FPAA for both nephropathies: u-PA in amyloidosis and t-PA in CGN. In all the patients, the urine levels of u-PA antigens were 20-40 times more than those of t-PA antigens and 5-6 times less than those plasma u-PA. The findings suggest that urokinase may be regarded as the major plasminogen activator involved in CGN and amyloidosis.

Amyloidosis↗
PubMed1995

[Tissue-type plasminogen activator in patients with lupus nephritis].

ELISA was used to measure tissue plasminogen activator antigen in blood plasma and urine of 42 patients with active lupus nephritis (16 with isolated urinary syndrome, 13 with nephrotic syndrome, 13 with rapidly progressive LN). Control groups consisted of 17 patients with inactive LN and 15 healthy subjects. Inhibition of fibrinolysis in vascular system correlating with the disease severity was found in patients with active LN. This may result from both defective synthesis of tissue plasminogen activator and neutralizing action of antiactivator. Urinary fibrinolytic activity was inhibited only in patients with rapidly progressive LN because of hyperactive synthesis of antiactivator. The above changes occur as endothelial cell dysfunction due to activating and damaging action of immune complexes, antibodies, cytokines on vascular endothelium. Zero activator activity of plasma and urine in patients with active LN reflects severe dysfunction of endothelial cell caused by its structural disorganization.

Adolescent↗
PubMed1995

[The venous occlusion test in assessing the fibrinolytic activity of the vascular endothelium in lupus nephritis patients].

A venous occlusion test was used to evaluate the reserves of the kidneys and that of vascular endothelium fibrinolytic activity (VEFA) in patients with lupus nephritis (LN). Prior to and following venous occlusion functional activity of plasminogen activators in plasma and urine (PAPU), plasma activity of antiactivator (PAAA), urokinase urine activity (UUA) were measured by fibrin plate lysis test in 24 patients with active LN, 6 SLE patients with intact kidneys, 10 healthy subjects. Venous occlusion test revealed normal reserve of plasma activator activity in mild LN and depletion of this reserve in LN patients with nephrotic syndrome and rapidly progressive LN. In the latter patients PAPU and PAAA were suppressed. PAPU reserve existed in all the patients, but those with rapidly progressive LN. UUA in LN was close to normal and did not change significantly after venous occlusion. The data obtained suggest that patients with severe LN had reduced reserves of VEFA, while in those with progressive LN there were also diminished reserves of renal fibrinolytic activity reflecting the severity of endothelial lesion.

Adolescent↗
PubMed1994

[The functional activity of plasminogen activators in the blood plasma and urine of patients with lupus nephritis].

A fibrin plate technique was employed to study functional activity of plasminogen activators in plasma and urine (FAAP, FAAU), activity of antiactivator in plasma (AAAP), urokinase urine activity (UUA) in 35 lupus nephritis (LN) patients. The latter comprise 3 groups by the disease severity: 22 patients with active LN attended by urinary syndrome (group 1), 7 patients with LN associated with nephrotic syndrome (group 2), 6 patients with rapidly progressing LN (group 3). Control groups included 5 SLE patients with unaffected kidneys and 25 healthy subjects. FAAP proved heterogeneous both in SLE and healthy subjects. SLE patients with progressive LN had diminishing FAAP which was accompanied by growing AAAP. The latter reached maximal values in groups 2 and 3. UUA declined with LN aggravation. The relation of low FAAP in LN patients to affection of vascular endothelium and binding of plasminogen activators with the inhibitors to form inactive complexes is considered.

Adolescent↗
PubMed1992

[The effect of a protein loading test on the fibrinolytic system in patients with chronic glomerulonephritis and amyloidosis].

Investigation of the reserves of the fibrinolytic system with the aid of protein stimulation was carried out in 10 patients with chronic glomerulonephritis and in 10 patients suffering from amyloidosis. All the patients manifested proteinuria exceeding 3.5 g/day and other symptoms of nephrotic syndrome of varying intensity. Renal function was preserved in all the patients. The reserves of the fibrinolytic system were measured by analyzing blood plasma and urine before and after beef protein stimulation. The data revealed reciprocal responses of activator activity in blood plasma and urine in patients suffering from chronic glomerulonephritis and amyloidosis. In patients with amyloidosis, the test revealed complete depletion of activator activity in urine while its considerable reserves were preserved in blood plasma of the systemic channel.

Amyloidosis↗
PubMed1991

[The fibrinolysis system in recurrent myocardial infarction].

Studies of blood fibrinolytic activity in 112 patients with repeated acute myocardial infarction or injury to the myocardium have revealed reduced fibrinolytic activity on non-heated fibrin plates, decreased plasmin activity and euglobulin+ fraction lysis, lowered levels of plasminogen activator, total nonenzymic fibrinolysis, antithrombin III, ++FFDP, and elevated soluble complexes of fibrin-monomer level. Complications of myocardial infarction presenting as thromboembolism; ciliary arrhythmia, chronic aneurysm with thrombosis are associated with still more marked disorders of the fibrinolysis system.

Adult↗
PubMed1991

[Newly developed stenocardia: effect of intensive physical training on the indicators of the blood coagulation system and fibrinolysis].

The impact of 6-week strenuous exercise training (SET) on blood coagulative and fibrinolytic parameters (levels of fibrinogen, soluble fibrin, fibrinogen-fibrin degradation products, activities of plasminogen and plasmin) was studied in 28 patients with first angina pectoris, in 16 of whom in the first 3 months of onset of the disease, but angina pectoris lasting 3-4 prior to SET. The 6-week strenuous exercises in patients with first angina were found to cause a decrease in fibrinogen levels, exert no action on thrombin and fibrin formation. They did not diminish plasminogen activator release during exercise in patients with pre-exercise unstable angina.

Adult↗
PubMed1988

Plasminogen activator in nephrotic syndrome.

Plasminogen activators were studied in blood urine in 207 patients with nephrotic syndrome of different etiological forms. The blood plasminogen activator activity was decreased in chronic glomerulonephritis, SLE, systemic vasculities as result of great level of inhibitors (L2M), penetration of enzymes to abdominal and pleural transudates, excretion to urine. The blood plasminogen activator activity and urokinase level in chronic glomerulonephritis was dependent on the degree of nephrotic syndrome. The plasminogen activator in amyloidosis was sharply elevated because of permanent irritability of endothelial wall by amyloid mass. Venous occlusion caused the release of plasminogen activator to blood only in more favourable clinical course of nephrotic syndrome.

Adolescent↗
PubMed1988

Depletion of fibrinolysis activators as a result of continuous stress.

The dynamics of disorders in haemostasis and fibrinolysis upon continuous stress was studied in model experiments with rats exposed to emotional-pain-stress. It was shown that the plasminogen activator (PA) is released into the blood within the first few minutes of exposure to stress. Four hours after cessation of continuous stress (6 hours) the enzyme depletion and fibrinolysis depression occurred. Such stress-induced changes in the blood system function can be regarded as a risk factor in the development of thrombosis.

Animals↗