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PubMed1984

Involvement of hemostasis during an autoimmune glomerulonephritis induced by mercuric chloride in brown Norway rats.

Mercuric chloride (HgCl2) induces in Brown Norway (BN) rats an autoimmune disease characterized by a biphasic glomerulonephritis (GN). A transient nephrotic syndrome occurs during the third and fourth weeks after the first HgCl2 injection. Related to nephrotic syndrome, an hypercoagulable state develops with decreased factor XII and anti-thrombin III (AT III) levels and increased factor V activity and fibrinogen concentration. Moreover, during the same period, most of the rats were found thrombocytopenic. The presence of soluble fibrin monomer complexes and of fibrin degradation products (FDP) in the plasma of these rats associated with fibrin thrombi in glomerular capillary lumen proved the occurrence of disseminated intravascular coagulation (DIC). DIC was responsible for the death of several rats but most of these survived and clotting abnormalities were no longer found. Numerous factors can explain the occurrence of DIC in this model: anti glomerular basement membrane antibodies, circulating immune complexes, complement activation and/or glomerular endothelial cell detachment. The HgCl2 induced autoimmune disease appears as a good experimental model to study the relation between coagulation process and glomerulonephritis.

Animals↗
PubMed1992

[Changes in the blood coagulation and fibrinolysis system in the course of normal pregnancy].

In the present study we investigated several factors of hemostasis and fibrinolysis during the normal pregnancy in 52 women. Whereas the Thrombin-Time did not show any change, the increase of the Hepato-Quick and the decrease of the Partial Thromboplastin-Time was significant. During pregnancy we observed a significant increase of the activity of fibrinogen, factor XII and prekallikrein as well as of the von-Willebrand-factor-antigen (VIIIR:Ag). The activity of factor II and X remained constantly. The increased activity of factors of hemostasis was accompanied by an increase of activity and concentration of antithrombin-III. In contrast to the activity of the hemostatic system we could not find any significant alteration of the fibrinolytic system. The cause must be searched in the observed increase of plasminogen-activator-inhibitor (PAI)--likly in combination with a decrease of the tissue-type plasminogen activator (t-PA). Our data indicate, that the highest risk for thrombosis already might exist in week 24 of pregnancy, because a distinct increase of hemostatic activity is combined with a nearly unchanged fibrinolytic activity.

Adult↗
PubMed1981

Platelets and coagulation proteins.

Platelets participate in hemostasis in part by their complex interrelationships with coagulation proteins. Several intrinsic platelet proteins are present in alpha-granules (fibrinogen, factor V, factor VIII antigen, platelet factor 4), in the cytosol (factor XIII), or in the membrane fraction (factor XI). Platelets also contribute to surface-mediated zymogen activations of plasma factors XII, XI, X, and prothrombin and bind several coagulation proteins including factor Xa, thrombin, and fibrinogen. Finally, platelets can protect coagulation enzymes (factors XIa and Xa) from inactivation by plasma proteinase inhibitors. Thereby intrinsic coagulation reactions occur preferentially on the platelet surface leading to fibrin formation within and around platelet plugs.

Blood Coagulation Factors↗
PubMed1986

Effects of intravenous radiographic contrast media on the blood pressure and on factors of the contact activation system in the rat.

Blood pressure (BP), plasma prekallikrein (PK), and the extent of activation of factor XII (XII-ACT) were studied after the intravenous injection into rats of dextran (Macrodex), the ionic radiographic contrast substance iodipamide (Biligrafin), or the non-ionic contrast substance iohexol (Omnipaque). After acetone activation plasma kallikrein was assayed as plasminogen activator, BAEe esterase or S-2302 amidase, and factor XIIa was assayed as kaolin-activated prekallikrein activator. Dextran induced a strong and lasting hypotension, preceded by significant lowerings in PK and XII-ACT. Iodipamide induced a rapid and dose dependent BP fall, no change in plasma PK, but a slightly reduced XII-ACT. Iohexol induced no significant alterations, neither in BP, nor in plasma parameters. Pretreatments of the rats with iodipamide abolished the dextran-induced reductions in PK and XII-ACT, and almost blocked the fall in BP. We conclude that the ionic contrast substance iodipamide is capable of blocking dextran shock in the rat by preventing an activation of the contact activating system in plasma.

Anaphylaxis↗
PubMed1994

Hemostatic abnormalities in acute myocardial infarction as detected by specific blood markers.

In order to elucidate the mechanism of thrombus formation in acute myocardial infarction (AMI), coagulation and fibrinolytic and inhibitory proteins were systemically examined in 12 patients with AMI and 29 normal subjects. Activities of factor XII, II and V and concentration of high molecular weight kininogen and Factor II were significantly lower in AMI patients than in normal control subjects. Factor XI activity was also increased in AMI patients as compared with normal controls. Von Willebrand Factor and fibrinogen levels were increased in patients with AMI. Plasma D-dimer concentration was also significantly higher in AMI patients than in controls. Activation of the intrinsic pathway, thrombin generation, fibrin formation and fibrin degradation may be present in patients with AMI just after the onset of coronary thrombus formation.

Aged↗
PubMed1993

Coagulation and inhibitory and fibrinolytic proteins in essential hypertension.

Arterial hypertension (HTN) increases the risk of cerebral coronary, and other vascular complications that frequently involve platelet activation and blood coagulation. Several key proteins in the blood coagulation, fibrinolytic and inhibitory systems were studied in 29 men with HTN (aged 45 +/- 3 yr) and 15 normal men of the same age. Plasma levels of high-molecular-weight kininogen and factors XII, IX, VII, X, II, and XIII, as well as von Willebrand factor (vWF), fibrinogen, fibronectin, alpha 2-antiplasmin, tissue-plasminogen activator, D-dimer, platelet factor-4, and protein C were measured by the use of appropriate functional and immunologic assays before and after a cardiopulmonary exercise stress test. The concentrations of vWF, alpha 2-antiplasmin, and D-dimer were significantly (P < 0.02) higher in the HTN group as compared with the control group. The exercise stress test resulted in significant rises in the plasma vWF, alpha 2-antiplasmin, and tissue-plasminogen activator levels in the two groups. The concentrations of vWF and D-dimer were related to diastolic blood pressure (r = 0.44 and 0.40, respectively; P < 0.02). Levels of vWF also were related to left ventricular mass index and left ventricular posterior wall and septal thickness (r = 0.34, 0.43, and 0.34, respectively; P < 0.05). The constellation of these findings suggests a low-grade fibrin formation and degradation, the magnitude of which is related to the diastolic blood pressure. The observed abnormalities can potentially contribute to the cardiovascular complications of untreated HTN.

Adult↗
PubMed1991

Factor XI activation in a revised model of blood coagulation.

Coagulation factor XI is activated in vitro by factor XIIa in the presence of high molecular weight kininogen (HMWK) and a negatively charged surface. Factor XII deficiency is not associated with bleeding, which suggests that another mechanism for factor XI activation exists in vivo. A revised model of coagulation is proposed in which factor XI is activated by thrombin. In the absence of cofactors, thrombin is more effective (kcat/Km = 1.6 x 10(5)) than factor XIIa (1.7 x 10(4)) in activating factor XI. Dextran sulfate enhances activation of factor XI by thrombin 2000-fold; part of this effect is due to autoactivation of factor XI by activated factor XI.

Blood Coagulation↗
PubMed2005

Local bradykinin formation is controlled by glycosaminoglycans.

Bradykinin is a potent inflammatory mediator that induces vasodilation, vascular leakage, and pain sensations. This short-lived peptide hormone is liberated from its large precursor protein high molecular weight kininogen (HK) through the contact system cascade involving coagulation factor XII and plasma kallikrein. Although bradykinin release is well established in vitro, the factors and mechanisms controlling bradykinin generation in vivo are still incompletely understood. In this study we demonstrate that binding of HK to glycosaminoglycans (GAGs) of the heparan and chondroitin sulfate type efficiently interferes with bradykinin release in plasma and on endothelial surfaces. Proteolytic bradykinin production on endothelial cells is restored following degradation of cell surface GAG through heparinase. Alternatively, application of HK fragments D3 or light chain, which compete with uncleaved HK for cell binding, promote kininogen proteolysis and bradykinin release. Intravital microscopy revealed that HK fragments increase bradykinin-mediated mesentery microvascular leakage. Topical application of D3 or light chain enhanced bradykinin generation and edema formation in the mouse skin. Our results demonstrate that bradykinin formation is controlled by HK binding to and detachment from GAGs. Separation of the precursor from cell surfaces is a prerequisite for its efficient proteolytic processing. By this means, fragments arising from HK processing propagate bradykinin generation, revealing a novel regulatory level for the kallikrein-kinin system.

Animals↗
PubMedDate not supplied

[Effects of various adsorbants on coagulation factors (author's transl)].

Adsorption of clotting factors by various adsorbants is studied (tricalcium phosphate, baryum sulfate or carbonate or citrate, calcium oxalate, aluminium hydroxyde and several silicate such as: kaolin, celite, bentonite, attapulgite, beidellite, asbestos). The main properties of each adsorbant are listed as well as several applications such as: selective adsorption of fibrinogen, separation between fibrinogen and factor VIII, separation of factor II from the other components of the prothrombin complex. Activation of factors XII and XI by the various silicates, as well as the activation of factor V by attapulgite are studied. Finally, the action of such adsorbants on the fibrinolytic system is summarized.

Adsorption↗
PubMed1989

The activation of the contact phase of coagulation by physiologic surfaces in plasma: the effect of large negatively charged liposomal vesicles.

The endogenous, negatively charged surface that induces activation of the contact coagulation factors was investigated in plasmas taken from women in late pregnancy and control subjects of child-bearing age. The plasmas from the two groups of subjects were incubated at 4 degrees C for 24 hours either in plastic or in glass tubes and the factor VII coagulant activity (VIIc) was assayed in the treated plasmas. The activation of factor VII under these conditions involves the generation of enzymes derived from factor XII (XIIa). The contact surface is rate-limiting for the activation of factor VII in the plasmas in both groups of subjects and can be supplemented by large multilamellar liposomal vesicles carrying the appropriate density of negative charge. The size of these vesicles is within the range of sizes of the large lipoprotein particles (chylomicrons, very low and intermediate-density lipoproteins). The relationship between the density of negative charge on the liposomal vesicles and VIIc was similar in the late pregnancy and the control plasmas incubated in plastic tubes. At a saturating density of negative charge the observed relative VIIc was similar in both sets of plasmas. The incubation of late pregnancy or control plasma in plastic tubes in the presence of sodium stearate caused VIIc to increase with increasing concentration of the added fatty acid. These results suggest that large lipoprotein particles carrying the appropriate free fatty acid at a sufficient density of negative charge could provide the contact surface that induces the generation of factor XIIa and the subsequent activation of factor VII. Moreover, plasmas from women in late pregnancy have a higher concentration of potential surface and a higher density of negative charge than the plasmas from nonpregnant women.

Anions↗
PubMed1977

Deficiency of coagulation factors VII and XII in a patient with Hodgkin's disease.

A patient with Hodgkin's disease is described in whom deficiencies of coagulation factors VII and XII were discovered. Depressed levels of these factors appear to reflect increased Hodgkin's disease activity and returned to normal when chemotherapy was instituted. There was no evidence of accelerated fibrinolysis, intravascular coagulation, or circulating anticoagulants in the patient. Possible mechanisms for the abnormality include impaired production and/or increased consumption of coagulation factors. This observation suggests that all patients with lymphoreticular neoplasms should be screened carefully for clotting disturbances prior to treatment.

Adolescent↗
PubMed1998

Postprandial lipaemia and haemostatic factors.

Factor VII activity (FVIIc), a reported risk factor for fatal coronary heart disease, increases transiently after a fat-rich meal. The response shows dose-response characteristics and peak FVIIc and triglyceride concentrations above fasting levels tend to be positively associated. The mechanism is incompletely understood, but appears to require factor IX and the presence in plasma of lipoprotein products of lipolytic activity. Factor XII is not apparently essential. The increase in FVIIc is due to raised activated factor VII (FVIIa) activity, but is not associated with increased thrombin production or changes in fibrinolytic activity. The response of FVIIa appears independent of the proportions of saturated, monounsaturated and polyunsaturated fatty acids in the dietary fat, although dietary stearic acid may be less effective than myristic acid. However, in one study in which deliberate efforts were made to force an increase in plasma free stearic acid, its plasma level was positively associated with postprandial FVIIc. Because FVIIa initiates the thrombotic response to rupture of an atheromatous plaque, a raised postprandial level may represent a transient rise in the likelihood of a clinically significant coronary thrombosis.

Animals↗
PubMed1989

A comparison of two APTT reagents which use silica activators.

The Ortho activated partial thromboplastin time (APTT) reagent, Thrombosil 1 (TS), was compared to the General Diagnostics automated APTT reagent (GD). TS produced more precise results over a 38-day period of testing a normal control plasma, indicating that the upper limit of the normal range could be more precisely set with TS. This normal range was better represented if the normal values with both reagents were logarithmically transformed before calculating the mean +/- 2 SD. TS was more sensitive to plasma which had been heparinized in vitro. This was also demonstrated in vivo by the testing of 100 plasmas from heparinized patients. On testing of in-vitro dilutions of normal plasma with factor-deficient plasmas, TS was more sensitive to decreasing levels of factors VIII, IX and XI but less sensitive to decreasing factor XII. This was demonstrable in vivo in 71% of cases with plasmas from factor-deficient patients. GD was more sensitive to the lupus anticoagulant in most cases.

Blood Coagulation Factors↗
PubMedDate not supplied

[Method of determining factor IX activity].

Modification of the method for factor IX activity determination was proposed. A mixture of chicken plasma and human plasma was used as factor IX-deficient substrate plasma. Moreover determinations were performed in the lack of kaolin-activator of factor XII. This allowed simplifying the assay performance. The described modification may be used to determine factor IX activity in its concentrates with the aim of diagnosis of haemophilia B and control of the disease treatment.

Animals↗
PubMed1992

Young infarct patients with single-vessel occlusion do not have an underlying prothrombotic state to explain their coronary occlusion.

To determine the importance of a prothrombotic state in the pathogenesis of coronary occlusion in young infarct patients, assessment of risk factor profile and thrombotic tendency was undertaken in 25 young male patients (age less than 45 yr) who were shown at angiography, following myocardial infarction, to have occlusion of a single coronary. Comparison was made with a control group of symptomatic males aged greater than 55 yr, who at angiography had significant disease in two or more coronary arteries (multi-vessel disease control group). At the time of the study more patients in the single-vessel disease study group smoked cigarettes (n = 12) compared to the control group (n = 5) (p less than 0.01). Serum cholesterol and triglycerides were higher, and high density lipoprotein-cholesterol lower, in the single-vessel disease group but the difference reached significance only with the high density lipoprotein-cholesterol. Quantitative platelet aggregability was similar in the two groups. Although the level of beta-thromboglobulin, was higher in the single-vessel disease study group the difference was not significant. There were also no significant differences between these groups in levels of fibrinogen, Factor XII and alpha-2 antiplasmin. Patients in the multi-vessel disease group, however, had increased Factor VII levels (p less than 0.01). There were no significant differences between the two groups in fibrinolytic potential or in levels of antithrombin III. Coronary occlusion in the young appears likely to be due primarily to an arterial (plaque) related event as opposed to an abnormal coagulation response to minor arterial plaque damage.

Adult↗
PubMed2006

Contact activation prolongs clot lysis time in human plasma: role of thrombin-activatable fibrinolysis inhibitor and Factor XIII.

BACKGROUND: Contact activation system proteins (e.g., Factor XII, kallikrein) have been implicated as direct or indirect activators of plasminogen. However, contact activation and Factor XI have enhanced thrombin-activatable fibrinolysis inhibitor (TAFI) activation and decreased fibrinolysis, and Factor XIII (FXIII) also delays fibrinolysis via alpha(2)-anti-plasmin deposition on fibrin polymers. Thus, the goals of this study were to define how fibrinolysis is modulated in human plasma by contact or tissue factor (TF) activation, and what role TAFI and FXIII plays in this system. METHODS: Normal, TAFI-deficient and TAFI-deficient/FXIII-supplemented plasma was exposed to tissue-type plasminogen activator and activated with either celite or TF. Clot growth/disintegration kinetics were documented with thrombelastography. RESULTS: Normal plasma activated with celite had significantly prolonged onset and duration of clot lysis compared with samples activated with TF. TAFI-deficient plasma activated with celite was noted to have a duration of clot lysis not different from samples activated with TF, but a significant difference in time to onset of lysis persisted. Celite activation of TAFI-deficient/FXIII-supplemented plasma showed significantly prolonged onset and duration of clot lysis compared with samples activated with TF. CONCLUSIONS: Primarily TAFI, and to a lesser extent FXIII, contributed to contact system protein-mediated attenuation of fibrinolysis. Clinical investigation of these phenomena is warranted in clinical settings involving contact activation (e.g., intra-aortic balloon pumps and ventricular assist devices) to determine whether these devices modulate fibrinolysis and perhaps contribute to thromboembolic morbidity.

Carboxypeptidase B2↗
PubMed2003

The evolution of vertebrate blood coagulation as viewed from a comparison of puffer fish and sea squirt genomes.

The blood coagulation scheme for the puffer fish, Fugu rubripes, has been reconstructed on the basis of orthologs of genes for mammalian blood clotting factors being present in its genome. As expected, clotting follows the same fundamental pattern as has been observed in other vertebrates, even though genes for some clotting factors found in mammals are absent and some others are present in more than one gene copy. All told, 26 different proteins involved in clotting or fibrinolysis were searched against the puffer fish genome. Of these, orthologs were found for 21. Genes for the "contact system" factors (factor XI, factor XII, and prekallikrein) could not be identified. On the other hand, two genes were found for factor IX and four for factor VII. It was evident that not all four factor VII genes are functional, essential active-site residues having been replaced in two of them. A search of the genome of a urochordate, the sea squirt, Ciona intestinalis, did not turn up any genuine orthologs for these 26 factors, although paralogs and/or constituent domains were evident for virtually all of them.

Amino Acid Sequence↗