The Effect of Warfarin Sodium on the Duration of Platelet Aggregation

1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler
Keyword(s):  
Platelet Count ◽  
Placebo Group ◽  
Platelet Aggregation ◽  
Prothrombin Time ◽  
Platelet Rich Plasma ◽  
Healthy Adults ◽  
Double Blind Study ◽  
Double Blind ◽  
Warfarin Sodium

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.

Enhancement of ADP-induced Platelet Aggregation by Adrenaline in Vivo and Its Prevention

1973 ◽  
Vol 29 (02) ◽  
pp. 490-498 ◽  
Author(s):  
Hiroh Yamazaki ◽  
Itsuro Kobayashi ◽  
Tadahiro Sano ◽  
Takio Shimamoto
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Endothelial Surface ◽  
Important Interaction ◽  
Blood Coagulability ◽  
The Difference

SummaryThe authors previously reported a transient decrease in adhesive platelet count and an enhancement of blood coagulability after administration of a small amount of adrenaline (0.1-1 µg per Kg, i. v.) in man and rabbit. In such circumstances, the sensitivity of platelets to aggregation induced by ADP was studied by an optical density method. Five minutes after i. v. injection of 1 µg per Kg of adrenaline in 10 rabbits, intensity of platelet aggregation increased to 115.1 ± 4.9% (mean ± S. E.) by 10∼5 molar, 121.8 ± 7.8% by 3 × 10-6 molar and 129.4 ± 12.8% of the value before the injection by 10”6 molar ADP. The difference was statistically significant (P<0.01-0.05). The above change was not observed in each group of rabbits injected with saline, 1 µg per Kg of 1-noradrenaline or 0.1 and 10 µg per Kg of adrenaline. Also, it was prevented by oral administration of 10 mg per Kg of phenoxybenzamine or propranolol or aspirin or pyridinolcarbamate 3 hours before the challenge. On the other hand, the enhancement of ADP-induced platelet aggregation was not observed in vitro, when 10-5 or 3 × 10-6 molar and 129.4 ± 12.8% of the value before 10∼6 molar ADP was added to citrated platelet rich plasma (CPRP) of rabbit after incubation at 37°C for 30 second with 0.01, 0.1, 1, 10 or 100 µg per ml of adrenaline or noradrenaline. These results suggest an important interaction between endothelial surface and platelets in connection with the enhancement of ADP-induced platelet aggregation by adrenaline in vivo.

Montreal Platelet Syndrome (MPS):Ultrastructural, Biochemical And Functional Studies

1981 ◽  
Author(s):  
M M Frojmovie ◽  
J G Milton ◽  
S S Tang
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Shape Change ◽  
Protein Profile ◽  
Peripheral Blood Smear ◽  
Ionophore A23187 ◽  
Clot Retraction ◽  
Platelet Counts

MPS is characterized by autosomal dominant inheritance thrombocytopenia (5,000-120,000 μl-1), abnormally large platelets on peripheral blood smear, spontaneous aggregation (SA), normal clot retraction and thromboplastin formation, nypervolumetric shape change and normal amounts of plasma membrane. Here we describe further characteristics of MPS for 3 siblings /5 affected family members. The ultrastructural features of MPS platelets were normal except for the high frequency of giant granules. Platelet aggregation (PA) was studied in citrated platelet-rich plasma at platelet counts of 5,000-40,000 μl-1 and was quantitated microscopically from the decrease in single platelet count. PA could be increased over that due to SA alone by the addition of ADP, adrenalin, collagen, ionophore A23187, arachidonic acid and ristocetin, suggesting that the response to these agents may be normal. The ristocetin-induced increase in PA was completely blocked by an IgG specific for BSS. In contrast, over a 4 year period, thrombin (0.2 units/ml) either did not or only slightly increased PA over SA for 3/3 donors. However, MPS platelets pelleted from ACD-PRP and resuspended in Tyrodes’, pH 7.4 at a platelet count of ~ 200,000 μ1-1 showed a normal response to thrombin by aggregometry. Only one donor’s platelets had both reduced sialic acid and glycoprotein (G.P.) 1 reduction/abnormality with otherwise normal G.P. and protein profile, while the other 2 siblings’ platelets showed no such abnormalities. The above results indicate that biochemical variability exists for MPS platelets from different affected siblings. Moreover, our observations raise the possibility that platelet aggregation abnormalities in thrombobytopenic disorders (may be obscured by (1) preparation artefacts and/or (2) artificially increasing platelet counts for in vitro studies.

Effects of Astaxanthin Supplementation on Lipid Peroxidation

2007 ◽  
Vol 77 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Karppi ◽  
Rissanen ◽  
Nyyssönen ◽  
Kaikkonen ◽  
Olsson ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Placebo Group ◽  
Intervention Group ◽  
Control Group ◽  
Double Blind Study ◽  
Carotenoid Pigment ◽  
Double Blind

Astaxanthin, the main carotenoid pigment in aquatic animals, has greater antioxidant activity in vitro (protecting against lipid peroxidation) and a more polar configuration than other carotenoids. We investigated the effect of three-month astaxanthin supplementation on lipid peroxidation in healthy non-smoking Finnish men, aged 19–33 years by using a randomized double-blind study design. Also absorption of astaxanthin from capsules into bloodstream and its safety were evaluated. The intervention group received two 4-mg astaxanthin (Astaxin®) capsules daily, and the control group two identical-looking placebo capsules. Astaxanthin supplementation elevated plasma astaxanthin levels to 0.032 μmol/L (p < 0.001 for the change compared with the placebo group). We observed that levels of plasma 12- and 15-hydroxy fatty acids were reduced statistically significantly in the astaxanthin group (p = 0.048 and p = 0.047 respectively) during supplementation, but not in the placebo group and the change of 15-hydroxy fatty acid was almost significantly greater (p = 0.056) in the astaxanthin group, as compared with the placebo group. The present study suggests that intestinal absorption of astaxanthin delivered as capsules is adequate, and well tolerated. Supplementation with astaxanthin may decrease in vivo oxidation of fatty acids in healthy men.

Platelet Aggregation Evoked In Vitro and In Vivo by Phosphatidic Acids and Lysoderivatives: Identity with Substances in Aged Serum (DAS)

1979 ◽  
Vol 42 (02) ◽  
pp. 631-640 ◽  
Author(s):  
K A Schumacher ◽  
H G Classen ◽  
M Späth
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Guinea Pig ◽  
Pulmonary Vascular Resistance ◽  
Platelet Rich Plasma ◽  
Human Platelets ◽  
Active Components ◽  
Phosphatidic Acids

SummaryIn serum incubated at 36° C for 18-24 hours a factor (DAS) develops which on intravenous injection into cats evokes platelet aggregation followed by an increase in pulmonary vascular resistance (PVR). This change in PVR is mediated via the platelets since it significantly correlates with the preinjection platelet count. There is evidence that phosphatidic acids (PA) and lysophosphatidic acids (LPA) are the active components of DAS. Investigations performed on platelet-rich plasma from man, cat, pig, dog, rabbit, guinea pig, and rat demonstrate that only human and feline platelets exposed to PA or to LPA are aggregated. Feline platelets are more sensitive to either compound than are the platelets from men; however, human platelets exhibit two exceptional properties, a) the sensitivity rapidly declines with time, b) pretreatment with subthreshold concentrations of LPA or PA induces a specific tachyphylaxis.

DECREASE OF PLATELET AGGREGATION AFTER INTAKE OF SMALL AMOUNTS OF PURIFIED EICOSAPENTAENOIC ACID IN ELDERLY PEOPLE. POSSIBLE ROLE OF VITAMIN E

1987 ◽  
Author(s):  
M Croset ◽  
E Vericel ◽  
M Rigaud ◽  
Ph Coupron ◽  
M Dechavanne ◽  
...  
Keyword(s):  
Vitamin E ◽  
Platelet Aggregation ◽  
Eicosapentaenoic Acid ◽  
Elderly People ◽  
Platelet Rich Plasma ◽  
Daily Intake ◽  
Double Blind Study ◽  
Double Blind ◽  
Thrombotic Complications ◽  
Normal Humans

Platelet hyperactivity is believed to be involvedin the thrombotic complications of elderly people.Since it has been proposed that eicosapentaenoic acid(EPA) can reduce platelet functions in normal humans,we have investigated its effect in elderly people. The daily intake (100 mg EPA) was at least 20 fold lower than usually tested. In a randomized, double blind study, eight people ingested EPA given as a pure triglyceride (1,3-didecanoyl,2-eicosapentaenoyl-glycerol) for 2 months and eight people ingested a placebo containing the same amount of vitamin E than in EPA preparation. Platelet aggregation, the oxygenatedmetabolism of arachidonic acid (AA), and vitamin E content of both plasma and platelets were investigated. Ingestion of EPA resulted in a slight but significant reduction of platelet-rich plasma aggregation in response to epinephrine and AA. The same decrease was observed with washed platelets when triggered bythrombin or collagen. EPA intake failed to affect the oxygenated metabolism of AA, measured by the formation of TXB2, HHT and 12-HETE from either exogenous or endogenous (thrombin stimulation) AA. Formation of AA oxygenated products including 6-keto-PGFla in clotted blood was unaffected. Excretion of urinary TXB2, 6-keto-PGFlα and their 2,3-dinor metabolites wasleft unchanged by ingestion of EPA. Platelet, but not plasma α- and γ-tocopherols were significantly increased by EPA intake. We conclude that, in our experiment, the reduction of platelet aggregation could not be explained by modification of AA metabolism. Since vitamin E has been associated with a decrease ofplatelet aggregation, at least in vitamin E deficiency, and platelet vitamin E being reduced with age, we speculate that the decreased platelet aggregation after EPA intake might be related to the increased platelet tocopherols.

scholarly journals Heparin-induced thrombocytopenia: confirmation of diagnosis with in vitro methods

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 395-401 ◽  
Author(s):  
JC Fratantoni ◽  
R Pollet ◽  
HR Gralnick
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Venous Thrombosis ◽  
Platelet Rich Plasma ◽  
Control Population ◽  
Immune Mechanism ◽  
Heparin Induced Thrombocytopenia ◽  
In Vitro Methods ◽  
Heparin Administration

Profound thrombocytopenia developed in a patient during treatment with heparin for venous thrombosis. The platelet count increased toward normal when heparin administration was stopped, but fell abruptly when the drug was again given. Platelet aggregation occurred when heparin was added to the patient's platelet-rich plasma, or to normal platelets plus the patient's serum. This serum also effected release of 3H- serotonin from normal platelets. This pattern of aggregation was clearly different from that occasionally caused by heparin in a control population. The data is consistent with an effect of heparin on platelets, possibly mediated by on immune mechanism.

scholarly journals Heparin-induced thrombocytopenia: confirmation of diagnosis with in vitro methods

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 395-401 ◽  
Author(s):  
JC Fratantoni ◽  
R Pollet ◽  
HR Gralnick
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Venous Thrombosis ◽  
Platelet Rich Plasma ◽  
Control Population ◽  
Immune Mechanism ◽  
Heparin Induced Thrombocytopenia ◽  
In Vitro Methods ◽  
Heparin Administration

Abstract Profound thrombocytopenia developed in a patient during treatment with heparin for venous thrombosis. The platelet count increased toward normal when heparin administration was stopped, but fell abruptly when the drug was again given. Platelet aggregation occurred when heparin was added to the patient's platelet-rich plasma, or to normal platelets plus the patient's serum. This serum also effected release of 3H- serotonin from normal platelets. This pattern of aggregation was clearly different from that occasionally caused by heparin in a control population. The data is consistent with an effect of heparin on platelets, possibly mediated by on immune mechanism.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

Stimulated Platelet Aggregation, Thromboxane B2 Formation and Platelet Sensitivity to Prostacyclin - A Critical Evaluation

1981 ◽  
Vol 45 (03) ◽  
pp. 204-207 ◽  
Author(s):  
Wolfgang Siess ◽  
Peter Roth ◽  
Peter C Weber
Keyword(s):  
Arachidonic Acid ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Reliable Method ◽  
Platelet Rich Plasma ◽  
Critical Evaluation ◽  
Vascular Diseases ◽  
Thromboxane B2 ◽  
Test Time ◽  
Stimulation Of

SummaryPlatelets have been implicated in the development of atherosclerotic and thrombotic vascular diseases. Evaluation of platelet aggregation in relation to endogenously formed compounds which affect platelet function may provide information of clinical and pharmacological relevance. We describe a method in which thromboxane B2 (TXB2) formation was analyzed following stimulation of platelet-rich plasma (PRP) with ADP, 1-epinephrine, collagen, and arachidonic acid. In addition, we determined platelet sensitivity to prostacyclin following ADP- and collagen-induced platelet aggregation. The parameters under study were found to depend on the platelet count in PRP, on the type and dose of the aggregating agent used, and on the test time after blood sampling. By standardization of these variables, a reliable method was established which can be used in clinical and pharmacological trials.

Reaction of Acetaldehyde with Human Platelets

1992 ◽  
Vol 67 (01) ◽  
pp. 126-130 ◽  
Author(s):  
Olivier Spertini ◽  
Jacques Hauert ◽  
Fedor Bachmann
Keyword(s):  
Platelet Aggregation ◽  
Inhibitory Action ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
Shape Change ◽  
Reaction Medium ◽  
Human Platelets ◽  
Membrane Glycoproteins ◽  
Neutral Ph

SummaryPlatelet function defects observed in chronic alcoholics are not wholly explained by the inhibitory action of ethanol on platelet aggregation; they are not completely reproduced either in vivo by short-term ethanol perfusion into volunteers or in vitro by the addition of ethanol to platelet-rich plasma. As acetaldehyde (AcH) binds to many proteins and impairs cellular activities, we investigated the effect of this early degradation product of ethanol on platelets. AcH formed adducts with human platelets at neutral pH at 37° C which were stable to extensive washing, trichloracetic acid hydrolysis and heating at 100° C, and were not reduced by sodium borohydride. The amount of platelet adducts formed was a function of the incubation time and of the concentration of AcH in the reaction medium. At low AcH concentrations (<0.2 mM), platelet bound AcH was directly proportional to the concentration of AcH in the reaction medium. At higher concentrations (≥0.2 mM), AcH uptake by platelets tended to reach a plateau. The amount of adducts was also proportional to the number of exposures of platelets to pulses of 20 pM AcH.AcH adducts formation severely impaired platelet aggregation and shape change induced by ADP, collagen and thrombin. A positive correlation was established between platelet-bound AcH and inhibition of aggregation.SDS-PAGE analysis of AcH adducts at neutral pH demonstrated the binding of [14C]acetaldehyde to many platelet proteins. AcH adduct formation with membrane glycoproteins, cytoskeleton and enzymes might interfere with several steps of platelet activation and impair platelet aggregation.This in vitro study shows that AcH has a major inhibitory action on platelet aggregation and may account for the prolonged ex vivo inhibition of aggregation observed in chronic alcoholics even in the absence of alcoholemia.

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