Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During normal pregnancy, the concentrations of many of the clotting factors rise, thereby increasing the potential to generate fibrin. There is also evidence of increased thrombin activity during normal pregnancy which sharply increases during placental separation. Antithrombin III, the main inhibitor of thrombin and activated factor X, shows no compensatory rise during pregnancy but increases during the puerperium. Plasminogen and antiplasmin concentrations rise during pregnancy but systemic fibrinolytic activity, as measured by the euglobulin lysis time, is markedly depressed during pregnancy; the reduced fibrinolytic activity returns to non-pregnant values very soon after delivery. The loss of fibrinolytic activity is presumed to be loss of plasminogen activator, because when this is added in excess in the urokinase sensitivity test, the fibrinolytic response is normal. The capacity for localized fibrinolytic activity is not lost, however, because fibrinolytic degradation products are slightly raised during pregnancy. The overall pattern is one of increased coagulant and reduced fibrinolytic capacity during pregnancy which may protect the pregnant woman against the haemostatic challenge of placental separation.
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PMID:Blood clotting and fibrinolysis in pregnancy. 38 69

With the use of cohort labeling with 75Se-selenomethionine, simultaneous platelet, fibrinogen, and plasminogen survival studies were carried out in 8 patients with chronic alcoholic liver disease and in 5 normal subjects. Clinical features, liver function tests, coagulation and fibrinolytic system activities, and platelet function were also assessed. On the basis of platelet survival, the patients could be divided into two groups. Three patients had shortened platelet survival; they were all thrombocytopenic and had greater prolongation of the prothrombin time (PT) and activated partial thromboplastin time (PTT) than the other 5 patients. However, platelet turnover was decreased in all the patients, and there was no difference between the two groups with regard to fibrinogen or plasminogen survival nor in the in vitro evidence of disseminated intravascular coagulation (DIC). Fibrinogen survival was increased in 5 of the 8 patients. Plasminogen survival was normal in 6 patients and prolonged in 2 patients with very low plasminogen levels. The absence of increased fibrinogen turnover in the patients studied indicates that the abnormalities in coagulation tests were not due to consumption coagulopathy. The authors' studies suggest that, at least for patients with chronic stable alcoholic liver disease, the concept that the coagulopathy of liver disease is due to increased utilization of clotting factors should be revised with caution.
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PMID:The hemostatic defect of chronic liver disease. Kinetic studies using 75Se-selenomethionine. 42 8

The amount of procoagulative and fibrinolytic agents in cellular organoids was studied in the cat n. ischiadicus. All cellular fractions revealed high thromboplastic activity. Plasminogen, its activator, and proactivator were discovered in the ischiadic nerve. In dogs, the changes of functional state of nerves were accompanied by discharging of tissue thromboplastin and stimulators of fibrinolysis into the external medium with stimulaneous changes of intracellular contents of hemocoagulating factors. Thus, electric stimulation of the nerve intensified its thromboplastic activity, increased concentration of analogs of the plasma factors (II, VII, IX) and stimulation of fibrinolytic agents. The data obtained suggest presence of close enough interaction between the changes of functional condition of cells and dynamics of their procoagulative and fibrinolytic power.
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PMID:[Dynamics of peripheral nerve procoagulant and fibrinolytic activity upon electrical stimulation]. 45 59

The results of this paper indicate that cattle infected with B. bovis (argentina) have a markedly altered and activated coagulation system. A degree of thrombin activation occurs due partly to release of thromboplastin-like substances from lysed erythrocytes but due primarily to activation of kallikrein by babesial proteases. This produces a hyperfibrinogenaemia, particularly in intact cattle, with soluble fibrin complexes constituting up to one-third of the total fibrinogen concentration. High molecular weight non-coagulable fibrinogen-like proteins are detected terminally but more so in splenectomized cattle. Plasminogen concentration decreases in splenectomized but not intact cattle while low molecular weight fibrinogen degradation products are not easily detected. It is suggested that a hypercoagulable intermediate state with little or no fibrin deposition occurs rather than terminal disseminated intravascular coagulation.
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PMID:Babesia bovis (argentina): observations of coagulation parameters, fibrinogen catabolism and fibrinolysis in intact and splenectomized cattle. 60 70

An asymptomatic woman (Ms. Williams) was found to have a severe abnormality in the surface-activated intrinsic coagulation, fibrinolytic, and kinin-generating pathways. Assays for known coagulation factors were nromal while Fletcher factor (pre-kallikrein) was 45%, insufficient to account for the observed markedly prolonged partial thromboplastin time. Plasminogen proactivator was present at 20% of normal levels and addition of highly purified plasminogen proactivator containing 10% plasminogen activator partially corrected the coagulation and fibrinolytic abnormalities but not the kinin-generating defect. This effect was due to its plasminogen activator content. In addition, Williams trait plasma failed to convert prekallilrein to lakkilrein or release kinin upon incubation with kaolin. Kininogen antigen was undetectable. When normal plasma was fractionated to identify the factor that corrects all the abnormalities in Williams trait plasma, the Williams factor was identified as a form of kininogen by its behavior on ion exchange chromatography, gel filtration, disc gel electrophoresis, and elution from an anti-low molecular weight kininogen immunoadsorbent. High molecular weight kininogen as well as a subfraction of low molecular weight kininogen, possessed this corrective activity while the bulk of low molecular weight kininogen functioned only as a kallikrein substrate. Kininogen therefore is a critical factor required for the functioning of Hageman factor-dependent coagulation and fibrinolysis and for the activation of prekallikrein.
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PMID:Williams trait. Human kininogen deficiency with diminished levels of plasminogen proactivator and prekallikrein associated with abnormalities of the Hageman factor-dependent pathways. 120 89

The effects of a contraceptive with a low estrogen content (Neogynon), the estrogen component (50 mcg ethinyl estradiol) and consecutively the gestagen component (250 mcg D-Norgestrel) of the contraceptive on blood coagulation and fibrinolysis were studied in 8 women. Each treatment cycle was followed by a control cylce. At various times of the control and therapy cycles coagulation and fibrinolytic parameters were investigated. Statistical analyses were performed using multivariate 2-factorial analysis of variance. Plasminogen exhibited a statistically significant increase during the treatment with ethinyl estradiol and the combination of this steroid with D-norgestrel. No significant changes were found for all other parameters, including partial thromboplastin time, fibrinogen, Factors X, IX, VIII, Factor VIII-related antigen, antithrombin III, and fibrin(ogen)degradation products.
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PMID:[Blood coagulation and fibrinolysis in women receiving estrogen, gestagen and estrogen-gestagen-contraceptives (author's transl)]. 127 96

Procoagulant, anticoagulant, and fibrinolytic activities are associated with endothelial cells and involve the production, secretion, and receptor mediated binding of proteins involved in these processes. The procoagulant aspect of endothelial cells function involves the production and release of von Willebrand Factor(vWF), the production of tissue factor, and the presence of Factor IX/IXa receptors on the cell surface. Secretion of vWf will promote the initial steps in thrombus formation by supporting platelet-platelet interaction and platelet-subendothelial matrix adhesion. Tissue factor which is undetectable in resting cells appears after exposure to various cytokines and initiates factor VIIa activation of factors IX and X. Receptors of Factor IX/IXa are also present and mediate the assembly of the prothrombinase complex on the endothelial cell surface. The anticoagulant pathway involves the cell surface protein thrombomodulin, protein C and its cofactor protein S. Thrombomodulin binds thrombin which activates protein C which in the presence of protein S cleaves and inactivates Factors V and VIII. Inactivation of these two coagulation cofactors halts the coagulation. Finally, endothelial cells also play a pivotal role in the fibrinolytic system. Production and regulated secretion of tissue plasminogen activator creates a profibrinolytic state in the endothelial cell environment. In addition, receptors for plasminogen and urokinase are also present, constituting a cell surface mediated fibrinolytic pathway. Plasminogen activator inhibitor type I, the primary inhibitor of tPA, is also produced by endothelial cells. Thus endothelial cells can promote and inhibit fibrinolysis, depending on the prevailing environmental conditions.
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PMID:[Endothelial cells and vascular hemostasis]. 131 12

Activation and inhibition of the haemostatic system was reviewed including the interaction between the four biological systems involved in haemostasis: the vessel wall, the platelets, the coagulation system and the fibrinolytic system. The haemostatic mechanism is initiated at the site of injury through local activation of surfaces and release of tissue thromboplastin, resulting in formation and deposition of fibrin. The coagulation process is regulated by physiological anticoagulants. Activation of fibrinolysis is triggered by the presence of fibrin, and the role of tissue-type plasminogen activators (t-PA) at the site of fibrin formation in particular is emphasized. The process is regulated by physiological inhibitors, of which alpha 2-antiplasmin, histidine-rich glycoprotein and plasminogen activator inhibitor are reported to be of major physiological significance. The role of fibrinolysis in the regulation of the dynamic haemostatic balance is discussed, elucidated through examples of congenital deficiencies of the coagulation and the fibrinoytic system. Pharmacological inhibitors of fibrinolysis (i.e. epsilon-aminocaproic acid and tranexamic acid) and their possible effect on the haemostatic system are described. The systemic effects on the fibrinolytic system of surgery and oral surgery is reviewed, and it is concluded, that oral surgery has insignificant effects on blood fibrinolysis. In contrast, oral surgery induces changes of fibrinolysis in the oral environment; initially the fibrinolytic activity of saliva is reduced, due to the presence of inhibitors of fibrinolysis originating from the blood and the wound exudate. When bleeding and exudation cease, the fibrinolytic activity of the saliva will increase. Plasminogen and plasminogen activator, identified as t-PA are present in the oral environment under physiological conditions. Plasminogen is secreted in the saliva and the sources of t-PA include oral epithelial cells and gingival crevicular fluid. The presence of plasminogen and t-PA in the oral environment implies that when fibrin is present (i.e. after surgery), fibrinolysis is triggered. Haemorrhagic complications to oral surgery in patients without known defects of the coagulation system is reviewed. It is concluded that the investigations conducted to the present day do not permit final conclusions with respect to the pathophysiological role of defects in the coagulation and the fibrinolytic systems for the development of bleeding after oral surgery. Further investigations are necessary in order to clarify these aspects, and should include extensive laboratory analyses to reveal rare congenital defects such as factor XIII- and alpha 2-antiplasmin deficiencies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Haemostasis in oral surgery--the possible pathogenetic implications of oral fibrinolysis on bleeding. Experimental and clinical studies of the haemostatic balance in the oral cavity, with particular reference to patients with acquired and congenital defects of the coagulation system. 180 33

Fluid cadaveric blood is generally known as a characteristic of sudden death. However, it has been reported that soft blood clots have been observed in a number of cases of sudden death after alcohol drinking. Such a tendency was also recognized on autopsy cases in our laboratory. This study was carried out to reveal the effects on clotting and fibrinolytic system in golden hamsters under acute alcohol intoxication. Furthermore, the influences of ether anaesthesia were also observed. Activities of clotting and fibrinolytic factors were measured with fluorogenic peptide substrate. Prothrombin and factor X activities began to decrease 1 hr after administration of alcohol. But thrombin-like and factor Xa-like activities significantly increased after 1 hr and then returned to the initial value 4 hr after administration. Plasminogen activity began to decrease 1 hr after administration, whereas plasmin-like and t-PA-like activities increased after 1 hr and returned to the initial values or decreased after 4 hr. These results show that under acute alcohol intoxication clotting and fibrinolytic factors (prothrombin, factor X and plasminogen) in golden hamsters were converted temporarily to their active forms (thrombin, factor Xa and plasmin). No influence of only ether anaesthesia on clotting and fibrinolytic activities was observed. At 1 hr after administration of alcohol some effects of ether anaesthesia on prothrombin, prekallikrein and kallikrein were observed and then were not observed after 4 hr. But it seems that the influence of ether anaesthesia on clotting and fibrinolytic activities was negligible in the process after alcohol consumption.
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PMID:[Clotting and fibrinolytic activities in acute alcoholic golden hamsters with or without ether anaesthesia]. 192 Sep 21

Thirty-six young, healthy, nonsmoking women have been selected to check the effect of low-dose oral contraceptives on hemostasis. Two identical groups were treated by Marvelon (a monophasic oral contraceptive containing ethinyl estradiol and desogestrel) or Trigynon (a triphasic oral contraceptive containing ethinyl estradiol and levonorgestrel) for a 6-month period. In the absence, previously controlled, of substantial differences between the effects of each treatment on hemostasis, all the results were pooled at the third and sixth month of the study. The effects of oral contraceptive treatment were as follows: (1) platelet number, platelet aggregating ratio, and plasma beta-thromboglobulin level were not significantly altered, and (2) antithrombin III activity was not reduced despite a slight decrease or antigen concentration. The von Willebrand factor parameters, factor VIII:C, factor VII:C, and clottable fibrinogen were significantly increased. Plasminogen (activity and antigen concentrates) and alpha 2-antiplasmin levels were also significantly increased. Activated partial thromboplastin time and euglobulin lysis time measured after venous occlusion were significantly shortened. Although statistical analysis did not show dramatic changes in all these parameters, some individual extreme values were substantially altered. Therefore we believe that these later values are worthy of cautious consideration for weighing the role that hemostasis factors might play in individual thrombotic risk.
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PMID:Hemostasis profile in women taking low-dose oral contraceptives. 214 79


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