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Biomedical subjects

R Rółkowski

Publications and source records attributed to R Rółkowski.

17 recordsLinked to original sources

Antithrombotic activity of losartan in two kidney, one clip hypertensive rats. A study on the mechanism of action.

The potential antithrombotic action of losartan, an AT1 receptor antagonist, administered to two-kidney, one-clip rats (2K1C) in an experimental model of venous thrombosis was evaluated. The involvement of nitric oxide (NO) in this effect was also studied. Venous stasis was induced by ligation of the vena cava. Losartan after single dose (10 mg/kg, p.o.) significantly reduced the venous thrombus growth. The antithrombotic action of losartan in 2K1C rats was abolished by N(G)-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg s.c.) and restored by L-arginine (1000 mg/kg s.c.). Platelet adhesion to fibrillar collagen significantly decreased after administration of losartan. No changes in primary hemostasis and platelet aggregation were observed. Moreover, coagulation parameters such as activated partial thromboplastin time, prothrombin time and euglobulin clot lysis time were found unchanged after losartan administration either in systemic circulation or at the place of thrombus formation. Our results indicate that antithrombotic activity of losartan in 2K1C rats is NO--dependent; observed inhibition of platelet adhesion could also play a role in this phenomenon.

Angiotensin Receptor Antagonists↗

Losartan inhibits experimental venous thrombosis in spontaneously hypertensive rats.

The potential antithrombotic action of losartan, the AT1 receptor antagonist, in an experimental model of venous thrombosis in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) was tested. The involvement of nitric oxide and prostacyclin in this effect was also studied. Venous stasis was induced by ligation of the vena cava. Losartan, after administration of a single, hypotensive dose (10 mg/kg, p.o.), significantly reduced the thrombus weight in SHR but not in WKY. The antithrombotic activity of losartan in SHR was abolished by NG-nitro L-arginine methyl ester (L-NAME) (30 mg/kg s.c.) but not by indomethacin (2.5 mg/kg s.c.). No changes in primary hemostasis, platelet aggregation, coagulation parameters such as activated partial thromboplastin time, prothrombin time, euglobulin clot lysis time, and fibrinogen level, either in SHR or in WKY rats, were found. Our results indicate the NO-dependent mechanism in the antithrombotic effect of losartan on venous thrombosis in SHR.

Analysis of Variance↗

Cyclophosphamide in diffuse lung damage.

Some cyclophosphamide toxic effects on lung tissue are presented. Cyclophosphamide metabolism, pathogenesis of lung damage and morphological lung tissue changes caused by that agent were characterized. Attention was focused on BAL evaluation as a useful method in the monitoring of lung tissue damage degree.

Animals↗

Influence of captopril on some haemostatic parameters in rats with ongoing process of venous thrombosis.

Recent laboratory findings strongly suggest that renin-angiotensin system plays an important role in regulation of haemostasis and fibrinolysis. In our previous study we showed that captopril exerts antithrombotic effect in venous thrombosis in rats. In this study we demonstrated that this effect is not a result of changes in platelet count, fibrinogen level alterations in blood coagulation pathways and fibrinolytic activity of the plasma. Further investigations are necessary to elucidate the mechanism of antithrombotic action of captopril.

Animals↗

Complexoproductive and antiheparin properties of low density lipoproteins (LDL). III. Interaction of low density lipoproteins (LDL) with synthetic polyanionic compounds.

Low density lipoprotein (LDL) form insoluble complex bonds with polymetacrylic and polyvinylsulphonic acids in the presence of calcium chloride. Quantity of arising complexes depends on the concentrations of LDL, acids and calcium chloride and on pH. These complexes dissociate solutions of sodium chloride, urea and guanidine hydrochloride.

Calcium Chloride↗

Complexoproductive and antiheparin properties of low density lipoproteins (LDL). V. Optimum conditions of the coagulation method to determine antiheparin activity in the blood plasma.

It was found that storing the plasma in the temperature 0 degree C, 4 degrees C and 20 degrees C and especially in 37 degrees C increases pH and decreases antiheparin activity estimated by the heparin-thrombin test. Measurements of the heparin-thrombin time should be carried out directly after obtaining the plasma or after reducing the plasma to pH 7.40.

Adult↗

Complexoproductive and antiheparin properties of low density lipoproteins (LDL). VI. Antiheparin activity in blood plasma of different species of vertebrates.

Antiheparin activity of plasma of different species of vertebrates depends to a large extent on contents of low density lipoproteins (LDL). High antiheparin activity of the blood plasma of chicken and human corresponds to high contents of LDL and low antiheparin activity of the blood plasma of horse, cow, sheep, dog and pig corresponds to decreased contents of these proteins. Differences in the contents of fibrinogen, acid alfa1-glycoproteins, globulins, alkaline proteins and antithrombin III activity have smaller influence on antiheparin activity in the blood plasma of the examined animals.

Animals↗

Complexoproductive and antiheparin properties of low density lipoproteins (LDL). I. Interaction of isolated low density lipoproteins with heparin of different molecular weight.

Low density lipoproteins/LDL/ form unsoluble complexes with heparin of different molecular weight in the presence of CaCl2. Quantity of the complexes depends on molecular weight of heparin, concentration of reagents and pH of the reacting medium. The biggest quantity of complexes result from LDL-heparin of the molecular weight 16000, the quantity is smaller with heparin of the molecular weight 5100 and the quantity is smallest with heparin of the molecular weight 3700. Components of LDL--heparin complexes are bound by means of ion and hydrogen bonds.

Calcium Chloride↗

Complexoproductive and antiheparin properties of low density lipoproteins (LDL). II. Interaction of serum low density lipoproteins (LDL) with heparin of different molecular weight.

Quantity of unsoluble LDL complexes with heparin of different molecular weight in hypo-, normo-, and hyperlipemic blood serum in the presence of CaCl2 was estimated. At the same weight concentration the biggest quantity of LDL complexes are formed with heparin with heparin of the molecular weight 16000, the quantity is smaller with heparin of the molecular weight 5100, and it is the smallest with heparin of molecular weight 3700.

Calcium Chloride↗

[Role of low-density lipoproteins of the blood plasma during labor in heparin neutralization].

It was shown that increased antiheparin activity of the blood plasma of women in labour is evoked by increased level of low density lipoproteids (LDL). This activity does not depend on changes neither of the level of other compounds neutralizing heparin (fibrinogen, acid alpha 1-glycoproteid, globulins, basic proteins) nor conditioning its action (antithrombin-III). The intensity of antiheparin action of LDL increases in the presence of calcium ions.

Antithrombin III↗

[Anti-heparin activity of plasma with various low density lipoprotein content].

Anti-heparin activity correlated with LDL concentration in the plasma. Blood plasma of women in labour is characterized by the high antiheparin activity and low LDL levels. Anti-heparin activity is low and LDL levels are low in blood plasma in childhood. An effect of other factors neutralizing heparin (e.g. fibrinogen, platelet factor 4, acid alpha 1-glycoprotein, globulins, basic proteins) and differences of anti-thrombin III on plasma anti-heparin activity has been excluded. Neutralization of heparin anticoagulation activity by LDL is of clinical value. Blood LDL level should be considered, while heparin therapeutical doses are under scrutiny.

Adult↗