Blood Coagulation and Platelet-function Parameters before and during Parenteral Administration of Medroxyprogesterone Acetate as a Contraceptive Agent

1974 ◽  
Vol 31 (02) ◽  
pp. 346-353 ◽  
Author(s):  
G Baele ◽  
A Vermeulen ◽  
M Thiery

SummaryThe effects of medroxyprogesterone acetate on blood coagulation and platelet collagen aggregation were studied in nineteen women. After parenteral administration of the compound for 4 and 7 months, the activated partial thromboplastin time showed a significant decrease. The percentage of the prothrombin time test rose after 4 months, but not significantly after 7 months ; factor II decreased after 7 months of treatment. The reaction time during which no aggregation occurred after addition of a collagen suspension to a stirred platelet-rich plasma, was shorter after both 4 and 7 months of treatment. Other coagulation and platelet-function parameters were not altered. Although a trend toward hypercoagulability was detected, the changes were not the same as those reported for combined oral contraceptives.

1984 ◽  
Vol 12 (01n04) ◽  
pp. 116-123 ◽  
Author(s):  
Jih-Pyang Wang ◽  
Mei-Feng Hsu ◽  
Che-Ming Teng

Bleeding time in rats was markedly prolonged after the adminstration of the water extract of Hsien-Ho-T'sao. This antihemostatic effect was more marked in the group of i.p. injection of the drug than in the group of p.o. administration for 2 to 7 consecutive days. Blood coagulation studies showed that plasma prothrombin time, activated partial thromboplastin time and stypven time were prolonged, while thrombin time adnd fibrinogen level were not changed. The thromboelastographic recording showed that reation time was prolonged and maximal elasticity of clot was decreased. In addition, ADP- and collagen- induced aggregations of platelet-rich plasma was suppressed. In conclusion, the prolongation of the bleeding time might be due to both anticoagulant and antiplatelet action of the drug.


1973 ◽  
Vol 30 (03) ◽  
pp. 494-498 ◽  
Author(s):  
G de Gaetano ◽  
J Vermylen

SummaryThrombelastograms of both native blood and re-calcified platelet-rich plasma samples taken from subjects given a single oral dose of aspirin (1 gram) were not significantly different from the pretreatment recordings. Aspirin also did not modify the thrombelastogram when preincubated in vitro with platelet-rich plasma at concentrations inhibiting the platelet “release reaction” by collagen. Thrombelastography therefore cannot evaluate the effect of aspirin on platelet function.


1980 ◽  
Vol 44 (03) ◽  
pp. 143-145 ◽  
Author(s):  
J Dalsgaard-Nielsen ◽  
J Gormsen

SummaryHuman platelets in platelet rich plasma (PRP) incubated at 37° C with 0.3–2% halothane for 5–10 min lost the ability to aggregate with ADP, epinephrine and collagen.At the same time uptake and release of 14C-serotonin was inhibited. When halothane supply was removed, platelet functions rapidly returned to normal. However, after high concentrations of halothane, the inhibition of platelet aggregation was irreversible or only partially reversible.The results suggest that halothane anaesthesia produces a transient impairment of platelet function.


1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard

SummarySodium pentobarbital (SPB) and three other barbituric acid derivatives were found to inhibit platelet function in vitro. SPB had no effect on the primary response to ADP of platelets in platelet-rich plasma (PRP) or washed platelets but inhibited secondary aggregation induced by ADP in human PRP. The drug inhibited both phases of aggregation induced by epinephrine. SPB suppressed aggregation and the release reaction induced by collagen or low concentrations of thrombin, and platelet adherence to collagen-coated glass tubes. The inhibition by SPB of platelet aggregation was readily reversible and isotopically labeled SPB did not become firmly bound to platelets. No inhibitory effect on platelet aggregation induced by ADP, collagen, or thrombin could be detected in PRP obtained from rabbits after induction of SPB-anesthesia.


1963 ◽  
Vol 10 (02) ◽  
pp. 295-308 ◽  
Author(s):  
Clarence Merskey ◽  
Herbert Wohl

Summary1. Groups of rats were fed thrombogenic diets and the effects on blood coagulation and fibrinolysis assessed.2. Animals fed a diet containing cholesterol, thiouracil and cholic acid developed high levels of coagulation factors I, II, V, VII—X, VIII, IX and X.3. Animals fed a similar diet with additional 40% beef fat developed even greater elevation of V, VII—X, VIII and X, similar elevation of factor II, and lesser (but still significant) elevation of factors I and IX. In addition marked elevation of blood platelets occurred.4. Euglobulin lysis time of the group not fed the additional fat was longer than in controls. Significant prolongation of euglobulin lysis time was not found in the group fed additional fat.5. If the increased levels of plasma fibrinogen were taken into account, it was found that a larger amount of fibrin was lysed per unit time in the euglobulin lysis test with plasma from rats fed either atherogenic diet compared with controls.6. Defective thromboplastin generation was present in both groups of rats fed an atherogenic diet. The defect was present in the serum and was not due to lack of a factor required for thromboplastin generation. An inhibitor was present in the serum which was capable of preventing the action of normal serum.7. No good correlation was found between the occurrence of changes in blood coagulation or fibrinolysis and the presence or absence of thrombosis and infarction.8. The exact cause of these anomalies remains unexplained, as does the cause of the thrombosis in these animals. Starvation per se does not account for these abnormal findings. They could not adequately be explained on the basis of “hypercoagulability” of the blood.


1995 ◽  
Vol 73 (03) ◽  
pp. 472-477 ◽  
Author(s):  
H R Lijnen ◽  
B Van Hoef ◽  
D Collen

SummaryThe interactions of recombinant staphylokinase (SakSTAR) with human platelets were investigated in a buffer milieu, in a human plasma milieu in vitro, and in plasma from patients with acute myocardial infarction (AMI) treated with SakSTAR.In a buffer milieu, the activation rate of plasminogen by SakSTAR or streptokinase (SK) was not significantly altered by addition of platelets. Specific binding of SakSTAR or SK to either resting or thrombin- activated platelets was very low. ADP-induced or collagen-induced platelet aggregation in platelet-rich plasma (PRP) was 94 ± 2.7% or 101 ± 1.7% of control in the presence of 0.1 to 20 μM SakSTAR, with corresponding values of 95 ± 2.8% or 90 ± 4.6% of control in the presence of 0.1 to 4 μM SK. No effects were observed on platelet disaggregation. ATP secretion following collagen-induced platelet aggregation was 4.3 ± 0.26 μM for SakSTAR (at concentrations of 0.1 to 20 μM) and 4.4 ± 0.35 μM for SK (at concentrations of 0.1 to 4 μM), as compared to 3.4 ± 0.70 μM in the absence of plasminogen activator.Fifty % lysis in 2 h (C50) of 60 μl 125I-fibrin labeled platelet-poor plasma (PPP) clots prepared from normal plasma or from plasma of patients with Glanzmann thrombasthenia and immersed in 0.5 ml normal plasma, was obtained with 12 or 16 nM SakSTAR and with 49 or 40 nM SK, respectively. C50 values for lysis of 60 μl PRP clots prepared from normal or patient plasma were also comparable for SakSTAR (19 or 21 nM), whereas SK was 2-fold more potent toward PRP clots prepared from Glanzmann plasma as compared to normal plasma (C50 of 130 versus 270 nM).No significant effect of SakSTAR on platelet function was observed in plasma from patients with AMI treated with SakSTAR, as revealed by unaltered platelet count, platelet aggregation and ATP secretion.Thus, no effects of high SakSTAR concentrations were observed on human platelets in vitro, nor of therapeutic SakSTAR concentrations on platelet function in plasma.


1979 ◽  
Vol 42 (05) ◽  
pp. 1615-1619 ◽  
Author(s):  
Martin J Smith ◽  
Boyd Braem ◽  
Kent D Davis

SummaryPlatelet acetylcholinesterase (AChE) activity was measured in gel-filtered platelet preparations. Three different anticholinesteratic agents (eserine, neostigmine, and diiso- propylphosphorofluoridate) at final concentrations of 10 μM caused complete inhibition of AChE activity after 30 min incubation at room temperature with either platelet-rich plasma or gel-filtered platelets. Complete inhibition of platelet AChE had no effect on platelet aggregation, factor-3 availability, and plasma clot retraction. We conclude that platelet membrane AChE activity is not required for normal platelet function as measured by these in vitro parameters.


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