The Effect of Erythropoietin on Platelet Function and Fibrinolysis in Chronic Renal Failure

1994 ◽  
Vol 17 (3) ◽  
pp. 141-145 ◽  
Author(s):  
D. Stenver ◽  
L. Jeppesen ◽  
B. Nielsen ◽  
J. Dalsgaard Nielsen ◽  
C. Hædersdal ◽  
...  
Keyword(s):  
Platelet Function ◽  
Clot Lysis ◽  
Platelet Activity ◽  
Platelet Factor ◽  
Human Erythropoietin ◽  
Lysis Time ◽  
Euglobulin Clot Lysis Time ◽  
Erythropoietin Treatment

The influence of erythropoietin therapy on platelet function and fibrinolysis was evaluated in 12 anemic hemodialysis patients. Six months of therapy with human erythropoietin (50 to 80 IU/kg initially) raised the hemoglobin level to 10.8 g/dl but did not increase platelet activity in vivo as measured by beta-thromboglobulin or platelet factor 4. There was no change in the platelet aggregation thresholds in vitro for ADP, adrenaline, thrombin or collagen during treatment. Platelet number and volume were also unaffected. Fibrinolytic activity intensified as erythropoietin treatment proceeded, with a fall of euglobulin clot lysis time and rise in the activity of t-PA. PAI-1 levels also showed a downward trend, without reaching significance. Thus erythropoietin treatment in modest doses does not seem to adversely influence the hemostatic system in patients on hemodialysis.

A Comparison of Pentosan Polysulphate and Heparin II: Effects of Subcutaneous Injection

1982 ◽  
Vol 47 (02) ◽  
pp. 109-113 ◽  
Author(s):  
A-M Fischer ◽  
R E Merton ◽  
N A Marsh ◽  
S Williams ◽  
P J Gaffney ◽  
...  
Keyword(s):  
Subcutaneous Injection ◽  
Factor Xa ◽  
Coagulation System ◽  
Clot Lysis ◽  
Lysis Time ◽  
At Iii ◽  
Euglobulin Clot Lysis Time ◽  
Pentosan Polysulphate

SummaryA comparison has been made between the effects of pentosan polysulphate (SP54) and mucosal heparin following subcutaneous injection in man. Unlike heparin, pentosan polysulphate has relatively little effect in vivo as measured by anti-factor Xa clotting assay and none by an anti-Xa amidolytic assay (S-2222). However, pentosan polysulphate is at least as potent as heparin on a weight basis in producing activation of lipoprotein lipase, shortening of the euglobulin clot lysis time and impairing the generation of factor Xa. Our data indicate that pentosan polysulphate has more marked effects in vivo than in vitro, that the action of the drug on clotting is mediated mainly via an At III-independent pathway, and that its effects are not confined to the coagulation system.

scholarly journals ‘In Vivo’ and ‘In Vitro’ Effects of Some Vasoactive Drugs on Platelet Function and on Coagulation/Fibrinolysis System

1977 ◽  
Author(s):  
A.G. Dettori ◽  
O. Ponari ◽  
C. Manotti ◽  
A. Megha ◽  
M. Pini
Keyword(s):  
Platelet Function ◽  
Vasoactive Drugs ◽  
Platelet Function Tests ◽  
Lysis Time ◽  
Low Concentrations ◽  
Euglobulin Lysis Time ◽  
In Vitro Effects ◽  
Induced Aggregation

Three substances widely used as vasoactive drugs are known to have an inhibiting effect on platelet aggregation ‘in vitro’. We investigated the changes induced on thrombelastogram, routine clotting tests, euglobulin lysis time (ELT), platelet count, aggregation, and adhesiveness by i, v. administration of these drugs to man. The same indices were also studied ‘in vitro’ by adding comparable concentrations of the substances to human blood or plasma.Aminophilline did not produce any significant variation in ADP-or collagen-induced aggregation either ‘in vitro’ (50 to 200 μg/ml) or ‘in vivo’ (240 mg). A trend to disaggregation was seen only in a few cases. Shorter ELT were found 30 and 120 minutes after injection.A papaverine derivative (Metaverinum, 150 mg) showed a similar ‘in vivo’ pattern: minor changes in platelet function tests and a moderate activation of fibrinolysis were seen. The drug acted ‘in vitro’ as a powerful inhibitor of aggregation (from 30 µg/ml)while fibrinolysis was only activated at the highest concentration (120 µg/ml).Bencyclan, capable of inhibiting platelet function ‘in vitro’ at very low concentrations (0.25µM) did not show similar effects ‘in vivo’ (50 mg) apart from a reduced platelet adhesiveness to glass.

scholarly journals A preliminary investigation of in vitro anti-thrombotic and anti-platelet activity of Pinus Gerardiana

2017 ◽  
Vol 4 (1) ◽  
pp. 1098 ◽  
Author(s):  
Atta-ur Rehman ◽  
Sara Naz ◽  
Muhammad Zaman ◽  
Syed Saeed-ul-Hassan ◽  
Javed Iqbal ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Clot ◽  
Preliminary Investigation ◽  
Circulatory System ◽  
Clot Lysis ◽  
Platelet Activity ◽  
In Vivo Models ◽  
The Stability

Introduction: Hemostasis is a process which preserves the stability of a closed and high-pressure circulatory system after any vascular injury. Circulating platelets are recruited to the site of injury, where they develop a major component of the developing thrombus, blood clotting, started by tissue factor, concludes in the generation of thrombin and fibrin. Thrombosis is a serious event in the arterial diseases and a major cause in the development of myocardial infarction, stroke and venous thrombo-embolism which justify prominent morbidity and mortality rate. The knowledge of molecular and cellular mechanism of the formation of thrombus has developed considerably in the recent studies by using different in-vitro and in-vivo models of diseases. P. gerardiana nut oil has been reported to possess anti-bacterial, anti-fungal, anti-viral, anti-septic, anti-neuralgic, diuretic, expectorant, hypertensive properties. However, hardly, any data is available regarding effects of nut oil on platelet function. In this study, fibrinolytic activity and effect on platelet aggregation were investigated. Method: P. gerardiana nut oil was extracted by using n-Hexane and then concentrated by rotary evaporator. Anti-thrombotic and fibrinolytic activities were evaluated on blood clot formation. Effects on platelet aggregation of the oil were determined based on collagen or epinephrine induced platelet aggregation. Results: P. gerardiana caused blood clot lysis in-vitro. P. gerardiana nut oil inhibited collagen dependent platelet aggregation while accelerated the epinephrine dependent platelet aggregation. In vitro whole blood coagulation was also reduced. In vivo P. gerardiana nut oil has no significant effect on blood cell indices. Conclusion: P. gerardiana nuts oil can be an effective therapy for the treatment of cardiovascular disorders and thromboembolism.

Changes in Platelet Function, Blood Coagulation and Fibrinolysis During Insulin-Induced Hypoglycaemia in Juvenile Diabetics and Normal Subjects

1982 ◽  
Vol 47 (03) ◽  
pp. 254-258 ◽  
Author(s):  
J Dalsgaard-Nielsen ◽  
S Madsbad ◽  
J Hilsted
Keyword(s):  
Insulin Infusion ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Clot Lysis ◽  
Control Group ◽  
Lysis Time ◽  
Euglobulin Clot Lysis Time ◽  
Juvenile Diabetics ◽  
Clot Lysis Time

SummaryHaemostatic parameters were assessed before insulin induced hypoglycaemia and 0, 1 and 2 fu after discontinuation of insulin infusion in 7 non-diabetics, aged 28 (22-31) years (mean and range), and 8 juvenile diabetics, aged 3L (27-35) years, with a mean duration of diabetes of 4 years. The patients were normoglycaemic for at least L0 hr before the study.Platelet aggregation in vitro was induced by lower adenosine diphosphate (ADP) concentrations in the diabetics than in the controls before hypoglycaemia and 0 and 60 min after insulin infusion. Platelet counts decreased significantly in the diabetics after hypoglycaemia, whereas no changes were seen in the control group. The activated partial thromboplastin time (APTT) was reduced in both groups and significantly lower in the diabetics than in the controls 120 min after insulin infusion.Fibrinogen and factor VIII R: Ag increased after insulin infusion; highest values were seen in the diabetics. The euglobulin clot lysis time (ELT) was reduced in both groups during insulin infusion; L20 min after end of insulin infusion ELT was significantly longer in the diabetics than in the control group.

Correlation of in Vivo Clot Lysis with other Thrombolytic Variables Following Administration of abbokinase ®(Tissue Culture Urokinase), to Anesthetized Dogs

1979 ◽  
Author(s):  
D. Martin ◽  
J. Cain ◽  
J. Chmiel ◽  
S.E. El Masry
Keyword(s):  
Mathematical Model ◽  
Tissue Culture ◽  
Plasma Levels ◽  
Half Life ◽  
Clot Lysis ◽  
Lysis Time ◽  
Euglobulin Lysis Time ◽  
Anesthetized Dogs

An anesthetized dog model, using an extracorporeal loop containing an autologous radioactive clot, was utilized to test the effects of various doses of ABBOKINASE® on the rate of clot lysis and on plasma levels of urokinase, plasmin, antiplasmin, plasminogen and fibrinogen. The effects of ABBOKINASE® on hematocrit, euglobulin lysis time and125 I-clot lysis, in vitro, were also determined. Correlations were sought between plasma urokinase, plasmin, antiplasmin and the rate of clot lysis. Kinetic evaluations of half-lives of urokinase and plasmin and of the rate of regeneration of antiplasmin were made. Some of the conclusions reached were: 1) plasma fibrinogen does not decrease until antiplasmin is depleted and free plasmin appears in blood. 2) plasma urokinase levels are related to the dose infused and decrease with a half-life of about 8 minutes following infusion. 3) the rate of clot lysis in the loop is proportional to the dose of ABBOKINASE® over a defined range of doses and can be fitted to a mathematical model. 4) at lower doses, clot lysis occurs in the absence of measurable free plasmin.

Kinetics and In Vivo Distribution of In-111-Labelled Platelets and Platelet Function in Familial Hypercholesterolaemia

1987 ◽  
Vol 58 (03) ◽  
pp. 811-816 ◽  
Author(s):  
P Wessels ◽  
A du P Heyns ◽  
A J Esterhuysen ◽  
P N Badenhorst ◽  
M G Lötter ◽  
...  
Keyword(s):  
Platelet Function ◽  
Familial Hypercholesterolaemia ◽  
Reticuloendothelial System ◽  
Platelet Factor ◽  
In Vivo Distribution ◽  
Normal Limits ◽  
Platelet Aggregate ◽  
Thrombotic Complications

SummaryThe kinetics, in vivo distribution and sites of sequestration of autologous In-111-labelled platelets and other platelet function parameters were studied in ten patients with type IIa or IIb familial hypercholesterolaemia and thrombotic complications of atherosclerosis. The in vitro platelet aggregation response to ADP (P = 0.50) and collagen (P = 0.46); binding of fibrinogen to platelets (P = 0.61); and plasma beta-thromboglobulin levels (P = 0.42) of the patients and normal reference subjects did not differ significantly. The in vivo distribution of In-111-labelled platelets at equilibrium was within normal limits, and at the end of platelet life-span the sequestration pattern of labelled platelets in the reticuloendothelial system was also normal (spleen P = 0.31; liver P = 0.54). There was minimal evidence of in vivo platelet activation: only mean platelet lifespan (MPLS), 195±57 hours (difference between mean MPLS of patients and controls was 25 hours, with a 95% confidence interval from 23 to 31 hours; P = 0.02); mean platelet platelet turnover, 2298±824 platelets/μl/hour (P = 0.005); plasma platelet factor 4 (P = 0.02); and the mean circulating platelet aggregate ratio, 0.8±0.1 (P = 0.02); differed significantly from normal. These results suggest that abnormalities of platelet function and kinetics observed in type II hyperlipoproteinaemia cannot be ascribed wholly to the hyperlipidaemia, but may be induced by the associated atherosclerosis.

Clot Lysis in a Perfusion System

1966 ◽  
Vol 15 (01/02) ◽  
pp. 205-219
Author(s):  
C. A Bouvier ◽  
J Gruendlinger ◽  
S Berthoud
Keyword(s):  
Aminocaproic Acid ◽  
Clot Lysis ◽  
Fibrin Gel ◽  
Standard Size ◽  
Lysis Time ◽  
Therapeutic Thrombolysis ◽  
And Diffusion ◽  
Diffusion Problems

SummaryMost information on clot lysis is derived from in vitro methods whereby various components of the clotting and fibrinolytic systems are mixed before an actual clot is formed. This situation bears little relationship to thrombolysis in vivo. Therefore several techniques have been recently proposed, in which pre-formed clots are exposed to the effects of active agents by contact and diffusion rather than by intimate mixing prior to clotting. We describe an apparatus whereby a perfusion is delivered at controlled rates to clots of standard size and volume formed in calibrated tubes. The composition of the clots can be varied as well as the rate of perfusion and the content of perfusate. The surface of contact between the fluid and the fibrin gel is kept constant throughout and the clot-perfusate relationship is as close as possible to the in vivo situation during thrombolytic therapy. Under these conditions clot lysis by Streptokinase appears as a linear function of time, and the rate of lysis is directly related to kinase concentration. Since the clot intrinsic plasminogen-proactivator content is sufficient to ensure lysis, the lysis time finally depends upon the rate of diffusion of the kinase into the gel. Inhibition obtained with various amounts of E-aminocaproic acid incorporated to the clots or added to the perfusion fluid also suggests that diffusion problems are of major importance in physiological and therapeutic thrombolysis.

Effect of a Selective Thrombin Inhibitor MCI-9038 on Fibrinolysis In Vitro and In Vivo

1986 ◽  
Vol 56 (01) ◽  
pp. 028-034 ◽  
Author(s):  
Y Tamao ◽  
T Yamamoto ◽  
R Kikumoto ◽  
H Hara ◽  
J Itoh ◽  
...  
Keyword(s):  
Cell Injury ◽  
Factor Xiiia ◽  
Thrombin Inhibitor ◽  
Clot Lysis ◽  
Plasma Clot ◽  
Lysis Time ◽  
Combined Use ◽  
Lower Effect

SummaryThe effect of a selective thrombin inhibitor, (2R, 4R)-4-methyl-1- [N2- [(3-methyl-1,2,3,4-tetrahydro-8-quinolinyl)sulfo-nyl]-L-arginyl]-2-piperidinecarboxylic acid (MCI-9038), on the fibrinolysis induced by t-PA and u-PA was studied in vitro and in vivo. MCI-9038 remarkably reduced the lysis time of the plasma clot generated by the addition of calcium chloride to the plasma at the concentration ranging from 0.01 to 0.3 μM. Heparin also reduced the plasma clot lysis time with a lower effect than MCI-9038. The fibrin crosslinkage in the plasma clot was inhibited by MCI-9038 or heparin. MCI-9038 potently inhibited the factor XIIIa generation from factor XIII by thrombin.The effect on the in vivo thrombolysis was studied on the arterial thrombosis generated by the endothelial cell injury of the rabbit carotid artery by acetic acid. t-PA dissolved the thrombi with the infusion at 0.96 mg/kg over 2 h without a significant activation of a systemic fibrinolysis. u-PA dissolved the thrombi with the infusion at 180,000 and 360,000 IU/kg over 2 h. At a dose of 0.48 mg/kg t-PA or 90,000 IU/kg u-PA, the thrombi were not dissolved, but the combined use of MCI-9038 at 1.2 mg/kg over 2 h effectively dissolved the thrombi. Thus, combination of MCI-9038 with plasminogen activators accelerated thrombolysis of an experimental thrombosis in rabbits.

Platelet Activity In Vivo in Hyperlipoproteinemia – Importance of Combined Hyperlipidemia

1998 ◽  
Vol 79 (02) ◽  
pp. 268-275 ◽  
Author(s):  
Anders Bröijersén ◽  
Anders Hamsten ◽  
Mats Eriksson ◽  
Bo Angelin ◽  
Paul Hjemdahl
Keyword(s):  
Urinary Excretion ◽  
Platelet Function ◽  
Mental Stress ◽  
Ex Vivo ◽  
Platelet Activity ◽  
Leukocyte Counts ◽  
Artery Disease ◽  
Platelet Secretion

SummaryPlatelet hyperactivity in vitro is found in patients with isolated hypercholesterolemia. It is, however, less well established if platelet activity in vivo is enhanced, and if there are differences between various types of hyperlipoproteinemia.Platelet function in vivo was studied at rest and during mental stress in men with isolated hypercholesterolemia (phenotype IIa; n = 21) or combined hyperlipidemia (phenotype IIb; n = 29), and age-matched normolipidemic controls (n = 41). The urinary excretion of 11-dehydrothromboxane B2 was elevated in patients compared to controls (IIa, p <0.05; IIb, p <0.001), and higher in type IIb than in IIa patients (p <0.05). Platelet secretion, assessed as plasma β-thromboglobulin levels, was higher in type IIb patients compared to controls (p <0.01) and type IIa patients (p <0.05) during mental stress. The urinary excretion of β-thromboglobulin was also elevated in type IIb patients compared to controls (p <0.05). Platelet aggregability at rest, as measured by filtragometry ex vivo was, however, reduced in both patient groups compared to controls (p <0.05). No correlations were found between plasma lipoprotein levels and markers of platelet function in vivo. Type IIb patients had higher plasma fibrinogen levels and higher leukocyte counts than controls (p <0.05 and p <0.001) and type IIa patients (p <0.05 and p = 0.06). Thromboxane excretion was positively related to fibrinogen levels and leukocyte counts (p <0.01 for both). Preliminary data regarding serum TNF-α also indicated an elevation of this inflammatory cytokine in type IIb patients (p <0.05 vs controls).In conclusion, thromboxane generation and platelet secretion in vivo are enhanced in patients with hypercholesterolemia, and particularly so among patients with concomitant elevation of plasma triglycerides. The mechanism is unknown, but inflammatory mediators may be involved. The present findings are of interest in relation to the role of triglycerides in coronary artery disease.

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