scholarly journals Changes of the Antiheparin Activity of the Blood Plasma After Irradiation

1978 ◽  
Vol 19 (3) ◽  
pp. 181-188 ◽  
Author(s):  
Z. DIENSTBIER ◽  
P. KLIR ◽  
J. POSPISIL ◽  
E. SKALA
Keyword(s):  
Blood Plasma ◽  
Antiheparin Activity

An iron-binding component in human blood plasma

2001 ◽  
Vol 14 (2) ◽  
pp. 111-113
Author(s):  
Arthur L. Schade ◽  
Liona Caroline
Keyword(s):  
Blood Plasma ◽  
Human Blood ◽  
Human Blood Plasma ◽  
Iron Binding ◽  
Binding Component

The Effect of Lysed Platelets on Neutralization of Heparin In Vitro with Protamine as Measured by the Activated Coagulation Time (ACT)

1991 ◽  
Vol 66 (02) ◽  
pp. 213-217 ◽  
Author(s):  
Arthur P Bode ◽  
William J Castellani ◽  
Edna D Hodges ◽  
Susan Yelverton
Keyword(s):  
Platelet Rich Plasma ◽  
Coagulation Time ◽  
Platelet Factor ◽  
Platelet Suspension ◽  
Antiheparin Activity ◽  
Unit Increase ◽  
Heparin Anticoagulation ◽  
Heparin Activity ◽  
Activated Coagulation Time

SummaryThe effect of lysed platelets on the activated coagulation time (ACT) was studied in heparinized whole blood during titration with protamine. Frozen-thawed washed platelet suspension, or a chromatography fraction thereof, or autologous frozen-thawed platelet-rich plasma was added in various dilutions to freshly drawn blood anticoagulated with 3,000 USP units/1 heparin. After a 10 min incubation, the amount of protamine needed to restore the ACT to baseline ("protamine titration dose") was determined. We found that the protamine titration dose decreased in proportion to the amount of lysed platelet material added; expressed as a percentage of the total number of platelets present, each unit increase in lysed platelets produced a 1.7% ±0.8 (SD) reduction in the protamine dose needed to normalize the ACT. A heparin activity assay showed that this effect was not due to antiheparin activity of lysed platelets such as platelet factor 4 (PF4). Our data indicate that the procoagulant activity of platelet membranes reduced the sensitivity of the ACT to heparin. These findings suggest that membranous platelet microparticles may cause an inaccurate calculation, based on the ACT, of a protamine dose to reverse heparin anticoagulation in cardiopulmonary bypass procedures.

Plasma Antiheparin Activity, Soluble Fibrin Monomer Complexes and Fibrinolysis in Plasma of Patients after Surgery

1969 ◽  
Vol 22 (02) ◽  
pp. 408-410 ◽  
Author(s):  
R Farbiszewski ◽  
B Lipiński ◽  
W Lebenstein
Keyword(s):  
Soluble Fibrin ◽  
Antiheparin Activity ◽  
Fibrin Monomer

Antiheparin Activity of Human Serum and Platelet Factor 4

1973 ◽  
Vol 30 (01) ◽  
pp. 093-105 ◽  
Author(s):  
C.H.J Sear ◽  
L Poller ◽  
F.R.C Path
Keyword(s):  
Molecular Weight ◽  
Ionic Strength ◽  
Blood Serum ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Gel Filtration ◽  
Normal Serum ◽  
Platelet Factor ◽  
Mean Values ◽  
Antiheparin Activity

SummaryThe antiheparin activity of normal serum has been studied by comparing the antiheparin activities of sera obtained from normal whole blood, platelet-rich plasma and platelet-’free’ plasma with a purified platelet extract during differential isoelectric precipitation and by gel filtration chromatography.The mean values for the activity of PRP-serum and PFP-serum were 106% (S.D. 11) and 10% (S.D. 3) of untreated whole blood respectively. The activity of whole blood serum, PRP serum and whole blood serum plus platelet extract precipitated under identical physical conditions, i.e. pH 7.0, I =0.008, indicating that the activities of the three samples are probably associated with PF4. PF4 precipitated from human platelet extract at pH 4.0, but this is probably due to the difference in the two biochemical environments investigated, i.e. serum and platelet extract.The gel filtration experiments revealed striking similarities between the major antiheparin activities of serum and platelet extract. At physiological pH and ionic strength both activities were associated with high molecular weight material, but at physiological pH and elevated ionic strength both activities behaved as much smaller entities of molecular weight between 25,000 and 30,000 daltons and it seems very likely that both activities are associated with the same molecule, i.e. PF4.

Protection from Hg-Inactivation of Factor XIII by Mercaptalbumin

1970 ◽  
Vol 24 (03/04) ◽  
pp. 352-355 ◽  
Author(s):  
P Fantl
Keyword(s):  
Blood Plasma ◽  
Factor Xiii ◽  
Active Component ◽  
Plasma Albumin ◽  
Plasma Factor ◽  
Mercuric Ions

SummaryThe blood plasma factor XIII (fibrin stabilizing factor) is inactivated by mercuric ions and can be reactivated by serum - or plasma albumin of which the active component is mercaptalbumin. A relation between mercaptalbumin concentration and factor XIII activity is pointed out.

Neutralization of Antithrombin VI (Fibrinogen Breakdown Products) with Platelet Antiheparin Factor (Platelet Factor 4)*

1965 ◽  
Vol 14 (03/04) ◽  
pp. 490-499 ◽  
Author(s):  
S Niewiarowski ◽  
R Farbiszewski ◽  
A Popławski
Keyword(s):  
Zinc Acetate ◽  
Antithrombin Iii ◽  
Platelet Factor 4 ◽  
Breakdown Product ◽  
Platelet Factor ◽  
Chromatography Column ◽  
Antiheparin Activity

SummaryIt has been found that fibrinogen breakdown product – antithrombin VI – is neutralized by the purified preparation of platelet factor 4, obtained by means of zinc acetate precipitation and DEAE chromatography column. It has been suggested that antiheparin activity of platelet factor 4 and its ability to neutralize antithrombin VI may be related to the same protein.The purified preparation of platelet factor 4 does not influence the fibrinogen – fibrin conversion by thrombin. This means that platelet factor 2 and platelet factor 4 are not the same substance.Crude platelet extracts neutralize antithrombin III and V. However, the purified product did not interferes with the action of these antithrombins.

Coagulation Disorders in Thrombocythaemia, a Study of Seven Cases

1962 ◽  
Vol 07 (01) ◽  
pp. 114-128 ◽  
Author(s):  
Stefan Niewiarowski ◽  
Halina Zywicka ◽  
Zbigniew Latałło
Keyword(s):  
Liver Parenchyma ◽  
Platelet Factor 4 ◽  
Coagulation System ◽  
Severe Bleeding ◽  
Clotting Factors ◽  
Platelet Factor ◽  
Antiheparin Activity ◽  
Thromboplastic Activity ◽  
Bleeding Episodes ◽  
Routine Coagulation

SummaryThe blood coagulation system has been studied in 7 patients with thrombocythaemia. 4 of these patients had thrombocythaemia after splenectomy, 2 of them had thrombocythaemia associated with myeloid leukemia, and 1 thrombocythaemia associated with polycythaemia. Severe bleeding episodes were noted in 5 cases, 2 patients had only mild bleeding symptoms.Each patient was examined several times. The period of observations varied from 2 months to 3 years. Platelet count varied from 350 000 to 3 800 000 per mm3.Bleeding time and tourniquet test were normal in all cases. Routine coagulation and fibrinolysis studies did not reveale characteristic abnormalities in plasma clotting factors. A decrease of prothrombin complex components was observed in 4 cases. This disturbance was due to the coexisting injury of liver parenchyma or myeloid changes but not to an increase of platelets or to the abnormalities in the platelet system.An increase of antiheparin activity was found in the plasma of 4 patients. This activity is probably due to the escape of platelet factor 4 from destroyed or qualitatively changed platelets into plasma.Platelet clotting factors were investigated in isolated platelet suspensions, A significant decrease of platelet factor 1 was observed in all patients and a decrease of platelet factor 4 in 5 patients. In 2 cases platelet factor 4 increased. Platelet thromboplastic activity showed a great variety of disturbances in conformity with other workers observations.Recent views on the pathogenesis of bleedings in thrombocythaemia are discussed. On the basis of their own investigations the authors suggest that the significant disturbances of platelet function may contribute to the development of bleeding, and that the increase of antiheparin activity in plasma may produce hypercoagulability and favorize the formation of thrombi.

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