Effect of High Plasma-Estrogen Level on Blood Coagulation Parameters

1979 ◽  
Author(s):  
H.C. Kim ◽  
E. Kemmann ◽  
R. Shelden ◽  
P. Saidi
Keyword(s):  
Factor Viii ◽  
Blood Coagulation ◽  
Antithrombin Iii ◽  
Fibrinogen Level ◽  
High Plasma ◽  
Base Line ◽  
Coagulation Parameters ◽  
Estrogen Level ◽  
Line Level ◽  
Gonadotropin Therapy

Administration of gonadotrophin (human FSH and LH) raises plasma estrogen level, while progesteron level remains unchanged. We studied the effect of high plasma estrogen level on the blood coagulation parameters. Coagulation parameters were measured on seven anovulatory women of ages between 26-33 years, who were undergoing daily gonadotropin therapy to induce an ovulation. Plasma 17-beta estradiol (E2) level increased 5 fold of base-line level during the treatment (fron 114 ± 28 pg/ml to 553 ± 217 pg/ml). Fibrinogen levels increased from 248 ± 38 mg% of base-line to 353 + 78 mg% during the treatment (t=3.17, P < .025). There was a significant positive correlation between E2 and fibrinogen level (r =.762, a=239.99, b=.23). However, there were no significant changes in prothrombin time (P.T.), activated partial thromboplastin time (A.P.T.T.), Factor VIII procoagulant activity (VIII. C), Factor VIII-related antigen (VIIIR:Ag), platelet retention by glass bead columns, or antithrombin III level during gonadotropin therapy. This study indicates that the acute endogenous rise of ovarian estrogen increases fibrinogen level, similar to pregnancy; but it does not have significant effect on the factorVIII-associated activities (FVIII:C & FVIIIR:Ag).

Effects of Human Antithrombin III on Mortality and Blood Coagulation Induced in Rabbits by Endotoxin

1984 ◽  
Vol 51 (02) ◽  
pp. 232-235 ◽  
Author(s):  
D C Triantaphyllopoulos
Keyword(s):  
Blood Coagulation ◽  
Bolus Dose ◽  
Antithrombin Iii ◽  
Coagulation Parameters ◽  
E Coli ◽  
At Iii ◽  
Baseline Values

SummaryTwenty-one rabbits were infused with 20μg/kg/hr of E. coli endotoxin for 6 hr. Eight of the animals were preinjected immediately before the infusion of endotoxin, with a bolus dose of human AT III calculated to increase the antithrombin content of the plasma by about 4 units/ml. All eight animals which were preinjected with AT III survived, while 5 of the 13 control rabbits infused with endotoxin alone died. The changes in coagulation parameters from the baseline values, between the 8 control rabbits which survived and the 8 animals which were preinjected with AT III were compared. The concentration of the preinjected human AT III declined significantly faster (P: <0.01) than that of the native rabbit AT III. AT III prevented the decline of F.XII throughout the infusion of the endotoxin. However, the decline in F.V, fibrinogen, prothrombin and platelets was not affected (P: >0.5) by the injection of AT III.

Serial Changes in the Coagulation System Following Clotting Factor Concentrate Infusion

1975 ◽  
Vol 34 (02) ◽  
pp. 475-482 ◽  
Author(s):  
F. E Preston ◽  
D. A Winfield ◽  
R. G Malia ◽  
E. K Blackburn
Keyword(s):  
Liver Disease ◽  
Factor Viii ◽  
Antithrombin Iii ◽  
Fibrinogen Level ◽  
Plasma Fibrinogen ◽  
Coagulation System ◽  
Clotting Factor ◽  
Plasma Fibrinogen Level ◽  
Clotting Factor Concentrates ◽  
Factor Concentrate

SummaryVarious parameters of the coagulation system have been monitored in patients with Christmas disease following the infusion of clotting factor concentrates. Significant reduction of clotting factor VIII and serum antithrombin III were observed in each of the five studies, whilst the plasma fibrinogen level fell in four subjects. The induced abnormalities were shortlived and there were no clinical sequelae. Further studies are required to assess the effects of similar concentrates in patients with liver disease.

scholarly journals Localization of the Inhibitory Site(s) of Pentosan Polysulphate in Blood Coagulation

1988 ◽  
Vol 60 (02) ◽  
pp. 220-225 ◽  
Author(s):  
R Wagenvoord ◽  
H Hendrix ◽  
C Soria ◽  
H C Hemker
Keyword(s):  
Factor Viii ◽  
Blood Coagulation ◽  
Antithrombin Iii ◽  
Inhibitory Effect ◽  
Independent Effect ◽  
Factor V ◽  
Factor X ◽  
Enzymatic Function ◽  
Factor Viiia ◽  
Pentosan Polysulphate

SummaryWe studied the inhibitory effect of pentosan polysulphate (PPS, Hémoclar®) on thrombin formation in blood coagulation. In contrast to a current hypothesis (1) the anti thrombin III independent effect of PPS on blood coagulation is not caused by preventing the binding of the factors IX, IXa, X, Xa, VIII, V, Va and II onto procoagulant phospholipids.We investigated the activation by thrombin of factors I, V and VIII. A strong inhibitory effect of PPS on factor VIII activation could be observed. Inhibition of the activation of factor V to the same extent requires about 30-fold higher concentrations of PPS, whereas the activation (clotting) of fibrinogen is not inhibited. The effect of PPS on factor VIIIa is two-fold: A) it inhibits its formation and B) it inhibits its function probably by the formation of a factor VIIIa-PPS complex.Prothrombinase, constituted of purified factors Xa, Va and phospholipids was not inhibited by PPS, neither were incomplete forms of this enzyme, lacking phospholipids or factor Va. The complete factor X activating enzyme (factors IXa, VIIIa and phospholipids), however, was strongly inhibited, but incomplete forms, lacking factor VIII, were not. The inhibition of the complete enzyme can be explained by reversible binding of PPS to factor VIIIa (causing an inhibition of its function) and it is not an effect on the enzymatic function of the complete enzyme. On saturation of the enzyme with an excess of factor VIIIa no inhibition by PPS is noticed.We postulate therefore that the antithrombin III independent inhibitory effect of PPS on thrombin generation on blood coagulation is by interaction with factor VIIIa. This effect is additional to the heparin-like action of PPS, i.e. potentiation of the activity of antithrombin III and/or heparin cofactor II. At concentrations attained during therapeutic use the action of pentosan polysulphate on factor VIIIa is the only one that will significantly inhibit the coagulation mechanism.

The Natural Course of Defibrination Syndrome Caused by Echis Colorata Venom in Man

1974 ◽  
Vol 31 (03) ◽  
pp. 420-428 ◽  
Author(s):  
M Fainaru ◽  
S Eisenberg ◽  
N Manny ◽  
C Hershko
Keyword(s):  
Factor Viii ◽  
Blood Coagulation ◽  
Major Bleeding ◽  
Renal Damage ◽  
Specific Treatment ◽  
Natural Course ◽  
Factor V ◽  
Thrombocyte Count

SummaryThe natural course of defibrination syndrome caused by Echis colorata venom (ECV) in five patients is reported. All patients developed afibrinogenemia within six hours after the bite. Concomitantly a depression in factor V was recorded. Factor VIII and thrombocyte count in blood were normal in most patients. In the light of the known effects of ECV on blood coagulation in vivo and in vitro it is concluded that the afibrinogenemia is due to intravascular clotting.Four patients had transient renal damage, manifested by oliguria, azotemia, albuminuria and cylindruria, ascribed to microthrombi in the renal glomeruli.After the bite, the natural course was benign, no major bleeding was observed, and all signs of coagulopathy reverted to normal within 7 days. Therefore we recommend no specific treatment for this condition. In the case of heavily bleeding patients, administration of antiserum against ECV and/or heparin should be considered.

Natural Oestrogen in the Female Climacteric - Influence on Blood Coagulation and Fibrinolysis

1978 ◽  
Vol 40 (02) ◽  
pp. 532-541 ◽  
Author(s):  
Anders Lagrelius ◽  
Nils-Olov Lunell ◽  
Margareta Blombäck
Keyword(s):  
Blood Coagulation ◽  
Antithrombin Iii ◽  
Coagulation Factors ◽  
Control Group ◽  
Blood Coagulation Factors ◽  
Excessive Bleeding ◽  
Oestrone Sulphate ◽  
Menopausal Women ◽  
History Of ◽  
Coagulation And Fibrinolysis

SummaryThe aim of the present study was to investigate the effect on blood coagulation and fibrinolysis of a natural oestrogen preparation, piperazine oestrone sulphate, prospectively in menopausal women. Scopolamine was given to the control group.The women were investigated before and during treatment with regard to factors VIII, VII, X, V, fibrinopeptide A, antithrombin III, plasminogen, rapid antiplasmin and α1-antitrypsin. There was no significant change towards hypercoagulability or decreased fibrinolysis in any group. In the oestrogen group, however, a tendency towards an increased level of plasminogen and a decreased level of antiplasmin was demonstrated. In the scopolamine group there was an unexpected fall in factors X and V and also in plasminogen and α1,-antitrypsin. A low level of some blood coagulation factors in some of the women before treatment is somewhat astonishing; none of them had any history of excessive bleeding.

Respective Roles of Antithrombin III and Alpha 2 Macroglobulin in Thrombin Inactivation

1981 ◽  
Vol 45 (01) ◽  
pp. 051-054 ◽  
Author(s):  
A M Fischer ◽  
J Tapon-Bretaudiere ◽  
A Bros ◽  
F Josso
Keyword(s):  
Antithrombin Iii ◽  
Practical Interest ◽  
High Plasma ◽  
At Iii ◽  
Human Material ◽  
Cofactor Activity

SummaryIn order to investigate the mechanism of thrombin inactivation in the presence of both antithrombin III (AT III) and α 2-macroglobulin (α 2 M), thrombin and the inhibitors have been purified from human material and thrombin inactivation studied using purified reagents either alone or added to defibrinated plasma. Comparison of clotting and amidolytic activities of residual thrombin allowed to measure the amount of thrombin bound to α 2 M. In a purified reagent system as well as in plasma, part of exogenous thrombin is bound to α 2 M. The amount of bound thrombin is related to α 2 M concentration. Conversely, previous plasma α 2 M depletion by immunoabsorption increases the consumption of heparin-cofactor activity by exogenous thrombin. Thus AT III and α 2 M compete for thrombin inactivation. This finding could be of practical interest in clinical situations associating high plasma α 2 M levels and a decrease of AT III concentration.

Prevention of massive intraoperative bleedings associated with heparin with the systemic use of fibrin monomer in the experiment

2019 ◽  
pp. 48-55
Author(s):  
А.П. Момот ◽  
В.М. Вдовин ◽  
Д.А. Орехов ◽  
Н.А. Лычёва ◽  
И.Г. Толстокоров ◽  
...  
Keyword(s):  
Liver Injury ◽  
Blood Loss ◽  
Unfractionated Heparin ◽  
Loss Rate ◽  
Antithrombin Iii ◽  
Fibrinogen Level ◽  
Circulating Blood Volume ◽  
Intraoperative Bleeding ◽  
Fibrin Monomer ◽  
Antithrombin Iii Activity

Цель исследования - изучение способности фибрин-мономера предупреждать тяжелую интраоперационную кровопотерю, ассоциированную с введением нефракционированного гепарина, при дозированной травме печени. Методика. На кроликах «Шиншилла» индуцировали гипокоагуляцию нефракционированным гепарином (150 ед/кг). Профилактику интраоперационных кровотечений осуществляли внутривенным введением фибрин-мономера (0,25 мг/кг) за 1 ч до травмы или протамина сульфата (1,5 мг/кг) за 10 мин до травмы. После нанесения стандартной травмы печени оценивали объем (в % ОЦК) и темп (мг/с) кровопотери. Анализировали число тромбоцитов, активированное парциальное тромбопластиновое время, протромбиновое и тромбиновое время свертывания, уровень фибриногена и активность антитромбина III, параметры ротационной тромбоэластометрии крови. Результаты. Объем кровопотери в группах животных после в/в введения фибрин-мономера и протамина сульфата на фоне гепаринизации был, соответственно, в 5,1 и 4,0 раза меньше по сравнению с группой плацебо, получавшей тот же антикоагулянт. Вместе с тем, фибрин-мономер не влиял на параметры коагулограммы (отсутствие видимого гемостазиологического эффекта) и тромбоэластограммы, тогда как применение протамина сульфата в качестве антидота гепарина сопровождалось нормализацией данных тромбоэластометрии и коррекцией гипокоагуляционного сдвига по активированному парциальному тромбопластиновому времени, протромбиновому и тромбиновому времени. Заключение. Установлено, что фибрин-мономер (0,25 мг/кг) снижает посттравматическое кровотечение в условиях блокады свертывания крови гепарином без видимых признаков восстановления гемостатического равновесия. The research objective was to study the ability of fibrin monomer to prevent severe intraoperative blood loss associated with administration of unfractionated heparin in controlled liver injury. Methods. Hypocoagulation was induced in chinchilla rabbits with unfractionated heparin (150 U/kg). Intraoperative bleeding was prevented by administration of fibrin monomer (FM, 0.25 mg/kg, i.v.) one hour prior to the injury and of protamine sulfate (PS, 1.5 mg/kg, i.v.) 10 min prior to the injury. Following the liver injury, blood loss was assessed as percentage of circulating blood volume and the blood loss rate (mg/s). Platelet counts, aPTT, PT, TT, fibrinogen level, antithrombin III activity, and parameters of blood rotation thromboelastometry were analyzed. Results. The volume of blood loss was 5.1 times and 4.0 times less, respectively, after the FM and PS administration during heparinization compared to the placebo group treated with the same anticoagulant. However, FM affected neither coagulogram indexes (no visible hemostasiological effect) nor thromboelastogram while the use of PS as an antidote for heparin was associated with normalization of thromboelastometric data and correction of hypercoagulative changes in aPTT, PT, TT. Conclusion. FM at a dose of 0.25 mg/kg reduced severity of posttraumatic bleeding induced by heparin inhibition of coagulation with no visible signs of hemostatic balance recovery.

EXPRESSION IN ONTOGENESIS OF HUMAN BLOOD COAGULATION FACTORS

1987 ◽  
Author(s):  
H J Hassan ◽  
A Leonardi ◽  
C Chelucci ◽  
R Guerriero ◽  
P M Mannucci ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Protein C ◽  
Antithrombin Iii ◽  
Liver Homogenate ◽  
Coagulation Factor ◽  
Coagulation Factors ◽  
Factor Ix ◽  
Adult Liver ◽  
Blood Coagulation Factors ◽  
Guanidine Isothiocyanate

We have analyzed the expression of several blood coagulation factors (IX, VIII, X, fibrinogen chains) and inhibitors (antithrombin III, protein C) in human embryonic and fetal livers, obtained from legal abortions at 6-11 week post-conception. The age was established by morphologic staging and particularly crown-rump lenght measurement.Total cellular RNA was isolated from partially purified hepatocytes or total liver homogenate using the guanidine isothiocyanate method. Poly(A)+ RNA was selected by oligodT cellulose chromatography. The size and the number of the embryonic and fetal transcripts are equivalent to those observed in adult liver, as evaluated by Northern blot analysis of total or poly(A)+ RNA hybridized to human cDNA probes.The level of coagulation factor transcripts in embryonic and fetal liver was evaluated by dot hybridization of total RNA (0.5-10 ug), as compared to RNA extracted from normal adult liver biopsies. The expression of blood coagulation factors in embryos is generally reduced for all factors, but at a different degree. In 5-11 wk liver, the level of factor IX is 5-10% of that observed in adults, while fibrinogen, protein C, antithrombin III RNA level rises from 25 to 50% and factor X is expressed at a level comparable to that observed in adult liver.We conclude that during these stages of development blood coagulation factors are expressed according to three different time, curves, possibly due to the effect of different types of regulatory mechanisms.

Sign in / Sign up

Export Citation Format

Share Document