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PubMed2005

Coagulation under flow: the influence of flow-mediated transport on the initiation and inhibition of coagulation.

A mathematical model of intravascular coagulation is presented; it encompasses the biochemistry of the tissue factor pathway, platelet activation and deposition on the subendothelium, and flow- and diffusion-mediated transport of coagulation proteins and platelets. Simulation experiments carried out with the model indicate the predominant role played by the physical processes of platelet deposition and flow-mediated removal of enzymes in inhibiting coagulation in the vicinity of vascular injury. Sufficiently rapid production of factors IXa and Xa by the TF:VIIa complex can overcome this inhibition and lead to formation of significant amounts of the tenase complex on the surface of activated platelets and, as a consequence, to substantial thrombin production. Chemical inhibitors are seen to play almost no (TFPI) or little (AT-III and APC) role in determining whether substantial thrombin production will occur. The role of APC is limited by the necessity for diffusion of thrombin from the site of injury to nearby endothelial cells to form the thrombomodulin-thrombin complex and for diffusion in the reverse direction of the APC made by this complex. TFPI plays an insignificant part in inhibiting the TF:VIIa complex under the conditions studied whether its action involves sequential binding of TFPI to Xa and then TFPI:Xa to TF:VIIa, or direct binding of TFPI to Xa already bound to the TF:VIIa complex.

Binding Sites↗

PubMed1987

[The effects of FUT-175 (nafamostat mesilate) on blood coagulation and experimental disseminated intravascular coagulation (DIC)].

FUT-175 is a newly synthesized serine protease inhibitor. In the present study, we investigated the effects of FUT-175 on blood coagulation and experimental DIC. The effects on coagulation were examined in vitro by measuring the activated partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT) of rat plasma in the presence of FUT-175. FUT-175 exhibited remarkable anticoagulative effects to prolong APTT at a plasma concentration of 3 x 10(-7) M, PT at 1 x 10(-5) M and TT at 3 x 10(-5) M. The anticoagulative effect of FUT-175 at 1 x 10(-6) M on APTT was almost similar to that of heparin at 0.3 U/ml or that of gabexate mesilate at 1 x 10(-3) M. Experimental DIC was induced by a four-hr sustained intravenous infusion of endotoxin. FUT-175 was administered intraperitoneally prior to the injection of endotoxin or infused intravenously with endotoxin. As a result, the prolongation of APTT and PT, the decreases of fibrinogen level, platelet counts and complement level, and the increase of FDP were remarkably improved by FUT-175. Furthermore, glomerular fibrin deposits were reduced by the infusion of FUT-175. These results indicate that FUT-175, having a potent inhibitory effect on blood coagulation, is clinically applicable to therapy for DIC.

Animals↗

PubMed1991

[Coagulation abnormalities in stroke--disseminated intravascular coagulation as a complication of subarachnoid hemorrhage].

To determine the pathogenesis of the symptomatic vasospasm (SV) following subarachnoid hemorrhage (SAH), we compared the difference in coagulation activity between 52 aneurysmal patients with SV and 20 patients without SV. The hypercoagulable state was scored according to the Disseminated Intravascular Coagulation (DIC) scoring system. Our clinical studies showed that severe SAH following aneurysmal rupture caused the hypercoagulable state and there was a good correlation between the degree of the hypercoagulable state, the severity of SV and outcome of the aneurysmal patients. We stressed in this report that the monitoring of the blood coagulation and fibrinolytic activities is very important in severe SAH and that the hypercoagulable state after SAH plays an important role on the occurrence of SV.

Aged↗

PubMed1985

[General mechanisms of coagulation and their physiological inhibition. I. General mechanisms of blood coagulation].

Blood coagulation results from a sequence of enzymatic reactions, which involve 12 plasma proteins (coagulation factors), platelets, a tissue lipoprotein (tissue factor), vascular components and calcium ions. These reactions are induced by vascular lesions, and are promoted by blood contact with sub-endothelial structures and by the release of tissue factor into the circulation; they result in the formation of an hemostatic plug constituted of platelets and fibrin. The enzymatic reactions consist of proteolytic reactions, in which zymogens are converted to proteinases. These reactions are accelerated by both proteins-proteins interactions and by proteins-membrane surface (vascular wall, platelets) interactions, responsible for the amplification of the activation process, and its localization at the site of injury. The coagulation process is regulated by positive and negative feed-backs and by physiological inhibitors.

Animals↗

PubMed1991

A quartz crystal viscosity sensor for monitoring coagulation reaction and its application to a multichannel coagulation detector.

A quartz crystal viscosity sensor was applied to a coagulation reaction monitoring system. The system consists of 16 oscillating circuits, a channel selector, a frequency counter, a temperature controller and a microcomputer. The system is named the Quartz Chemical Analyzer (QCA). AT-cut quartz crystals (9 MHz) were used as viscosity detectors and were attached to a cell in order to expose only one side of the quartz plate. The system was applied to the detection of the blood coagulation factors VIII (F VIII) and IX (F IX). The activity of these factors was assayed by a single-stage method. A linear relationship was obtained in a double-logarithmic diagram of concentration versus coagulation time with respect to F VIII and F IX in the range 0.05-0.4 unit cm-3 and 0.025-0.2 unit cm-3, respectively.

Biosensing Techniques↗

PubMed1997

Heparin detection by the activated coagulation time: a comparison of the sensitivity of coagulation tests and heparin assays.

OBJECTIVE: Laboratory and point-of-care coagulation tests are frequently obtained to determine the presence of heparin after surgical procedures. The objective of this study was (1) to compare the sensitivity of the activated coagulation time (ACT), activated partial thromboplastin time (aPTT), protamine titration (Hepcon; HMS Medtronic, Hemotec, Englewood, CO), and thromboelastography (TEG) with heparin anticoagulation and (2) to determine how frequently residual heparin is present in the 24-hour period after heparin neutralization in cardiopulmonary bypass (CPB) patients. DESIGN: A prospective study. SETTING: A tertiary care university teaching center that performs more than 15,000 surgical procedures per year. PARTICIPANTS: Vascular surgical (n = 17) and CPB (n = 29). INTERVENTIONS: In vascular surgical patients, coagulation tests (ACT, protamine titration [Hepcon], and TEG) were obtained before and 90 minutes after heparin (50 to 60 U/kg IV) and compared with heparin concentration determined by factor Xa inhibition assay. In cardiac surgical patients, ACT and heparin concentrations were measured after anesthesia induction, during CPB, after protamine neutralization, and 3 as well as 6 hours after CPB. In addition to heparin concentrations and ACT measures, platelet counts, fibrinogen levels, and bleeding times were determined before and 3 and 24 hours after CPB. MEASUREMENTS AND MAIN RESULTS: Ninety minutes after heparin, significant heparin concentrations were present in all vascular surgical patients, but ACT was elevated in only 4 of 17 patients. Protamine titration (Hepcon) correlated with the factor Xa inhibitory assay for heparin (r2 = 0.76). All 17 patients had an abnormal TEG (mean "R" time = 81 +/- 39 minutes) and a marked elevation of aPTT (135 +/- 35 sec [normal 22 to 33 seconds]) 90 minutes after heparin. In CPB patients, ACT did not correlate with heparin assays. After protamine neutralization of heparin in CPB patients, ACT returned to baseline despite the presence of heparin in 3 of 29 patients (0.22, 0.18, and 0.33 U/mL). CONCLUSIONS: ACT was less sensitive to residual heparin anticoagulation than aPTT, TEG, and whole blood heparin assay. The whole blood heparin assay (Hepcon) provided sensitive and specific data about the presence of residual heparin. Despite the limitation of ACT in detecting heparin, the investigators found that residual heparin was not common in the period after uncomplicated CPB.

Aged↗

PubMed2002

Advanced prostate cancer activates coagulation: a controlled study of activation markers of coagulation in ambulatory patients with localized and advanced prostate cancer.

Cancer and increased age are risk factors for coagulation activation. Patients with advanced prostate cancer, which usually presents in the seventh to eighth decade of life, are likely to be at increased risk for thrombosis. We report results of a controlled study of changes in specific and sensitive markers of coagulation activation in patients with prostate cancer. Complete blood count, prothrombin time, partial thromboplastin time, prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin complex (TAT) and quantitative D-dimers (DD) were measured in 30 patients of advanced prostate cancer (androgen ablated), in 30 newly diagnosed localized prostate cancer patients, in 30 healthy age-matched volunteers, and in 20 healthy young volunteers. Plasma F1 + 2 (P < 0.05) and DD (P < 0.05), but not TAT, were significantly elevated in healthy elderly males (mean age, 77 years) when compared with healthy young volunteers (mean age, 35 years). F1 + 2, TAT and DD were significantly elevated in advanced prostate cancer when compared with healthy age-matched controls (P < 0.001). In conclusion, advanced prostate cancer patients have significantly increased levels of sensitive markers of coagulation activation compared with healthy age-matched controls. This data can be used to plan studies to determine the risk of clinically significant coagulopathy and the role of primary prophylaxis in patients with advanced prostate cancer.

Adult↗

PubMed2001

An enhanced fibrinolysis prevents the development of multiple organ failure in disseminated intravascular coagulation in spite of much activation of blood coagulation.

OBJECTIVES: To investigate the relationship between fibrinolytic enhancement and the development of multiple organ failure (MOF) in disseminated intravascular coagulation (DIC). To detect the useful prognostic index for outcome in DIC. DESIGN: Case-control study. SETTING: A department of internal medicine in a university hospital, a clinical division for diagnosis and treatment, mainly of respiratory diseases, hematologic diseases, DIC, and other diseases requiring critical care medicine. PATIENTS: A total of 69 DIC patients, 31 with MOF. INTERVENTIONS: None. MEASUREMENT AND MAIN RESULTS: The DIC patients with MOF had more elevated levels of tissue plasminogen activator antigen (t-PA) and plasminogen activator inhibitor antigen (PAI), and more depressed levels of plasmin-alpha2 plasmin inhibitor complex (PIC) and fibrin/fibrinogen degradation products than those without MOF, although no significant difference in thrombin-antithrombin complex (TAT) levels was observed. A fibrinolytic enhancement (shown by PIC) was parallel to an activation of blood coagulation (shown by TAT) in DIC patients without MOF, although no such fibrinolytic enhancement was provoked even by much activation of blood coagulation in DIC patients with MOF. Whereas all the patients without MOF were restored from DIC, 14 of 31 patients with MOF were unable to be restored from DIC and died. A significant increase in plasma levels of t-PA and PAI under the condition of sustained hemostatic activation was observed in the patients who died. CONCLUSION: Enhanced fibrinolysis was considered to be the important defense mechanism in preventing the development of MOF in DIC. The increases in plasma levels of t-PA and PAI were poor prognostic markers in DIC. Further careful study may be useful to clarify whether the fibrinolytic therapy is beneficial in clinical DIC patients with MOF.

Antifibrinolytic Agents↗

PubMed1985

Abnormal factor VIII coagulant antigen in patients with renal dysfunction and in those with disseminated intravascular coagulation.

Factor VIII antigen (VIII:CAg) exhibits molecular weight heterogeneity in normal plasma. We have compared the relative quantities of VIII:CAg forms present in normal individuals (n = 22) with VIII:CAg forms in renal dysfunction patients (n = 19) and in patients with disseminated intravascular coagulation (DIC; n = 7). In normal plasma, the predominant VIII: CAg form, detectable by sodium dodecyl sulfate polyacrylamide gel electrophoresis, was of molecular weight 2.4 X 10(5), with minor forms ranging from 8 X 10(4) to 2.6 X 10(5) D. A high proportion of VIII:CAg in renal dysfunction patients, in contrast, was of 1 X 10(5) mol wt. The patients' high 1 X 10(5) mol wt VIII: CAg level correlated with increased concentrations of serum creatinine, F1+2 (a polypeptide released upon prothrombin activation), and with von Willebrand factor. Despite the high proportion of the 1 X 10(5) mol wt VIII:CAg form, which suggests VIII:CAg proteolysis, the ratio of Factor VIII coagulant activity to total VIII:CAg concentration was normal in renal dysfunction patients. These results could be simulated in vitro by thrombin treatment of normal plasma, which yielded similar VIII:CAg gel patterns and Factor VIII coagulant activity to antigen ratios. DIC patients with high F1+2 levels but no evidence of renal dysfunction had an VIII:CAg gel pattern distinct from renal dysfunction patients. DIC patients had elevated concentrations of both the 1 X 10(5) and 8 X 10(4) mol wt VIII:CAg forms. We conclude that an increase in a particular VIII:CAg form correlates with the severity of renal dysfunction. The antigen abnormality may be the result of VIII:CAg proteolysis by a thrombinlike enzyme and/or prolonged retention of proteolyzed VIII:CAg fragments.

Aged↗

PubMed1991

[Intravascular coagulation in acute promyelocytic leukemia: analysis of coagulation and fibrinolysis parameters].

Eight pts with acute myeloid leukemia were studied to assess coagulation and fibrinolysis disturbances as a cause of hemorrhages associated to thrombopenia. Fibrinogen, products of fibrinogen to fibrin degradation, D-dimer, antithrombin III, protein C, plasminogen and alpha-2 antiplasmin determinations were performed at admission, during and after chemotherapy. All pts were on heparin during induction chemotherapy. Coagulation activation, which increased with the onset of chemotherapy (increases in D-dimer) and a decreasing trend at the end of the antileukemic therapy (normalization of fibrinogen levels) was observed. During the whole observation period alpha-2 antiplasmin levels remained very low. No significant changes were observed in antithrombin III or protein C levels. In conclusion, disseminated intravascular coagulation with associated thrombopenia is an important event in acute leukemia and an increased fibrinolytic activity due to low alpha-2 antiplasmin levels may take part in the genesis of hemorrhage. These data suggest that both heparin administration and the use of antifibrinolytic drugs may have a therapeutic effect.

Adolescent↗

PubMed1991

[Infective morbidity of replacement therapy in congenital coagulation deficiencies and its effects on demand of coagulation factors].

BACKGROUND: Analysis of the infective morbidity and mortality secondary to replacement hemotherapy in the population with congenital coagulation deficiencies (CCD) and their consequences on the demand for coagulation factors. METHODS: The 46 patients with CCD diagnosed in the autonomous community (AC) of the Balearic Islands (32 with hemophilia A, 6 with hemophilia B, 4 with von Willebrand's disease 2 with factor VII, 1 with factor X, and 1 with factor XII deficiencies) were investigated for infective morbidity and use of blood products from 1982 to 1987. RESULTS: 97% of the patients had some hepatitis marker, 77% had antibodies against human immunodeficiency virus (HIV) and 17% fulfilled the criteria for the acquired immunodeficiency syndrome (AIDS). There were 7 deaths (15%). The morbidity and mortality increased with age and use of blood products. There was a 46% reduction in factor VIII use between 1982 and 1986, from a mean yearly consumption per hemophiliac patient of 33444 international units (IU) to 18080 IU. CONCLUSIONS: The study results show a high prevalence of hepatitis and HIV, an important reduction in the demand of manufactured coagulation factors and a 15% reduction in the population with CCD during the study years.

Acquired Immunodeficiency Syndrome↗

PubMed1989

[Modification of blood coagulation by antihypertensive therapy? Effect of enalapril and hydrochlorothiazide on blood coagulation parameters in patients with essential hypertension].

An increased tendency of the blood to clot in patients with arterial hypertension is not desirable, since cardiovascular and cerebrovascular sequelae may be aggravated. Recently, activation of coagulation under ACE inhibition with captopril has been described. In an open, randomized study, we compared the influence of enalapril on various coagulation parameters with that of hydrochlorothiazide. In contrast to the latter, we detected no unfavorable influence of enalapril on the coagulation factors investigated. A transient increase in fibrin monomeres was observed in one patient each on enalapril and hydrochlorothiazide.

Adult↗

PubMed1989

[The effect of liver cirrhosis on activation of the coagulation and fibrinolysis system and on coagulation inhibitors].

The activation of coagulation and fibrinolysis as well as coagulation inhibitors in the blood of patients with compensated (n = 25) and decompensated (n = 25) liver cirrhosis were studied. Protein C (PC) was decreased in a more pronounced manner than antithrombin III (AT III) in liver cirrhosis. Thereby, PC proved to be a highly sensible indicator of liver cell dysfunction. Decreased levels of PC activity (PC ratio activity/antigen 0.82) in decompensated liver cirrhosis suggest production of dysfunctional, undercarboxylated PC. We observed increased blood concentrations of fibrinopeptide A (FPA) (p less than 0.05) in both groups of patients compared to healthy volunteers (n = 25), while D-Dimer was increased only in patients with decompensated liver cirrhosis (p less than 0.01). Comparing both groups of patients. D-Dimer was significantly different with higher levels in decompensated liver cirrhosis (p less than 0.01). The ratio D-Dimer/FPA was significantly increased in decompensated liver cirrhosis compared to both other groups. These observations indicate that efflux from the extravascular space, e.g. ascitic fluid, contributes to the high contents of fibrin degradation products (D-Dimer) in patients with decompensated liver cirrhosis. In summary we conclude that patients with liver cirrhosis have enhanced activation of both coagulation and fibrinolysis but that the balance is not significantly displaced.

Aged↗

PubMed1985

[General mechanisms of coagulation and their physiological inhibition. II. The regulation of coagulation by physiological inhibitors].

Inopportune coagulation of blood in vessels is prevented by defense mechanisms, in which plasma inhibitors play an important role. The inhibitors are glycoproteins and belong to two different groups, according to their mechanism of action. The first group consists of the inhibitors of serine proteases, which form inactive complexes with various coagulation enzymes; it includes antithrombin III, heparin cofactor II, alpha 2-macroglobulin, alpha 1-antitrypsin and C1S-inhibitor. The second group includes protein C and its cofactor, protein S. Protein C, activated by thrombin complexed with a protein cofactor present on the endothelial cell surface (thrombomodulin), is responsible for the proteolytic degradation of two coagulation cofactors (Va and VIII: Ca). The clinical importance of both antithrombin III, protein C and protein S is attested by the strong association between recurrent venous thromboembolic manifestations and inherited deficiencies of one or the other of these proteins.

Antithrombin III↗

PubMed1984

[Treatment of the injured spleen with fibrin glue, infrared contact coagulation and laser coagulation. An experimental study].

Experimental studies of hemostasis of the traumatised spleen are reported. After experimental trauma, rapid intraoperative hemostasis and subsequent preservation of the spleen was achieved by the use of a homologous fibrin glue system. A collagen fleece or an autologous fascial flap was used as a carrier for the adhesive mixture. Moreover hemostasis was also attempted with an infrared contact coagulation device and a Neodym-YAG-Laser. After fibrin gluing all the substances used are quickly absorbed by the organism. This is one of the major advantages of the fibrin adhesive method. When the bleeding surface was covered with a collagen fleece or a fascial flap, hemostasis was attained quickly. The collagen fleece has an absorptive effect which improves the hemostatic quality. Hemostasis with infrared coagulation is based on infrared light and on mechanical tissue compression. Possible pools of blood can be managed by compressing the contact surface. With this method, too, hemostasis can quickly be achieved. It was impossible to attain equally positive results with the contact-free laser device. Hemostasis is caused by a burn necrosis with the coagulation methods. The tissue healing process lasts until the necrotic tissue has been absorbed.

Blood Coagulation↗

PubMed1980

[Coagulation properties of the extravascular fluid. I. Coagulation factors in thoracic-duct lymph].

All coagulation factors could be found in the thoracic duct lymph of dogs, but the coagulation activities are significantly lower than that of plasma. Analysis of thoracic duct lymph shows that the activity components are significantly lower for factors I (30%), II (60%), V (20%), VII (50%), VIII (30%), IX (25%), X (70%) and factor XIII (30%). With global (TEG) and group test (PTT, thrombin time) various coagulation properties could be detected in blood and lymph. Antithrombin III reached two third of the plasma concentration. The prothrombin consumption in lymph was markedly reduced. The most remarkable result appears to be a certain quantitative modification of the individual factors in the lymph in comparison to those in blood. Although the lymph does not contain any thrombocytes, thromboplastin formation is sufficient for clot formation.

Animals↗

PubMed1994

[Multicenter prospective study of retinopathy of prematurity--III. Timing of the coagulation therapy and the course of retinopathy of prematurity after coagulation].

We reviewed the records of 360 cases of retinopathy of prematurity (ROP) in 12 institutions in Japan, and investigated the timing of the coagulation therapy and the course of ROP after coagulation. The first coagulation therapy was performed at 9.6 weeks after birth and 35.9 weeks of postconceptional age on the average. The severity index in individual infants also showed that the disease became worse during the period from 32 to 36 weeks of postconceptional age. However, the fundus was clearly visible and there was no primary hazy media during this period. On the basis of the results of the timing of the first treatment, the visibility of the fundus, and the severity index in individual infants, we concluded that an ophthalmological examination with special care should be performed during the period from 32 to 36 weeks of postconceptional age.

Humans↗

PubMed2005

Effects of coagulation factor deficiency on plasma coagulation kinetics determined via thrombelastography: critical roles of fibrinogen and factors II, VII, X and XII.

BACKGROUND: Thrombelastography (TEG) is used to assess coagulopathy. However, a comprehensive characterization of the effects of specific coagulation factor deficiencies and mode of activation on TEG data does not exist. METHODS: Thrombelastography was performed for 15 min with control plasma and plasmas deficient (<1% activity) in Factors II, V, VII, VIII, IX, X, XI, XII, or XIII activated with celite (0.28 mg ml(-1)) or tissue factor (TF, 0.1%) (n = 6 per condition). Additional fibrinogen concentration activity (75-345 mg dl(-1)) and Factor II, VII, X and XII activity-response relationships (1%, 6.25%, 12.5%, 25%, 50% and 100% activity) were obtained (n = 8 per condition). Thrombelastography parameters included reaction time (R), angle (alpha), and clot strength (A, amplitude; G, elastic modulus). RESULTS: Celite activation of FXII-deficient plasma, TF activation of FVII-deficient and FX-deficient plasma, and celite or TF activation of FII-deficient plasma resulted in an almost undetectable clot. Compared to control values, celite activation of plasmas deficient in FXI, FIX and FVIII resulted in prolonged R and decreased alpha values, whereas TF activation resulted in decreased alpha values. Celite and TF activation of FV-deficient plasma resulted in prolonged R and decreased alpha values, whereas FXIII-deficient plasma had decreased alpha, A and G-values compared to control values. CONCLUSIONS: The fundamental finding of this study is that coagulation factor deficiencies affect TEG parameters in both a factor-dependent and activation-dependent fashion. Utilizing both celite and TF activation improves the diagnostic power of TEG. Based on such TEG data, more targeted administration of blood products could potentially help improve perioperative hemostatic outcomes.

Blood Coagulation↗