Changes Occurring During Coagulation in Glass. I. Normal Human Blood

1960 ◽  
Vol 4 (01) ◽  
pp. 001-016
Author(s):  
Jessica H. Lewis ◽  
Paul Didisheim ◽  
John H. Ferguson ◽  
Kenichi Hattori

SummaryNormal whole blood was allowed to stand in glass tubes at 37° C, and the clotting process stopped at various intervals by the addition of sodium oxalate. During the first 15 minutes a marked acceleration of clotting activity was found. Study of the individual coagulation factors showed the following changes: a sustained and rapid fall in platelet count, a sustained and rapid rise in PTC (factor IX), a steady fall in fibrinogen, a more gradual fall in AHF (factor VIII), a rapid rise and subsequent fall in proaccelerin (factor V) activity, a somewhat lesser and slower rise and fall in proconvertin (factor VII) activity, and a slow fall in prothrombin concentration. No changes were noted in Hageman factor or PTA activities.

1959 ◽  
Vol 03 (04) ◽  
pp. 578-587
Author(s):  
Cecil Hougie

SummaryIn a mild case of Stuart factor (SF) deficiency and in a patient with hemophilia B (factor IX deficiency) consumption of AHF (factor VIII) was normal but was abnormal in more severe examples of these diseases. This finding reconciles previously conflicting reports. Factor V utilisation was abnormal in moderately severe cases of SF deficiency, hemophilia A and hemophilia B but normal in mild cases of SF deficiency and hemophilia B. A mild case of hemophilia A was not studied. These findings would be expected from the modern concept of blood coagulation. However, the findings with respect to AHF are equally well explained if AHF is destroyed by some intermediate product of blood coagulation, such as thrombin, appearing at the time of the appearance of fibrin.The concentration of SF was found to remain constant during the clotting of both normal blood and blood deficient in factor VILThe concentration of factor VII during the coagulation of normal blood remained constant until the appearance of fibrin. The concentration then increased, but this finding was not consistently obtained. No abnormality in the fate of factor VII during the clotting of blood deficient in SF was found.


1970 ◽  
Vol 23 (03) ◽  
pp. 593-600
Author(s):  
P Pudlák ◽  
I Farská ◽  
V Brabec ◽  
V Pospíšilová

Summary1. The following coagulation changes were found in rats with experimental hypersplenism: a mild prolongation of the recalcification time, shortened times in Quick’s test, a lowered activity in plasma thrombin time and shortened times in the partial thromboplastin test. Concentrations of factor II, V, VII (+X), VIII and X did not differ from those of normal control rats.2. The administration of adrenaline to hypersplenic rats induced the correction of the partial thromboplastin test, Quick’s test and plasma thrombin time to normal values. Concentrations of coagulation factors were not significantly changed. An increase was found in factor V.3. Splenectomy performed in hypersplenic rats was followed by a shortened recalcification time, a prolongation of the partial thromboplastin test and of the test with partial thromboplastin and kaolin. A prolongation was also observed in Quick’s test. Complete correction of plasma thrombin time was not observed. The concentration of factor VII increased.4. The administration of adrenaline to splenectomized rats with experimental hypersplenism did not induce any significant changes with the exception of a corrected plasma thrombin time and a decreased concentration of factor VIII.5. A different reaction of factor VIII to adrenaline in normal and hypersplenic rats is pointed out.


2000 ◽  
Vol 84 (09) ◽  
pp. 396-400 ◽  
Author(s):  
Steve Humphries ◽  
Belinda Smillie ◽  
Lily Li ◽  
Jacqueline Cooper ◽  
Samad Barzegar ◽  
...  

SummaryThe risk of venous thrombosis is increased in individuals who carry specific genetic abnormalities in blood coagulation proteins. Among Caucasians, the prothrombin G20210A and factor V Arg506Gln (FV R506Q) mutations are the most prevalent defects identified to date. We evaluated their influence on markers of coagulation activation among participants in the Second Northwick Park Heart Study, which recruited healthy men (aged 50–61 years) from nine general medical practices in England and Wales. They were free of clinical vascular disease and malignancy at the time of recruitment. Genotypes for the two mutations were analyzed using microplate array diagonal gel electrophoresis, and coagulation markers (factor XIIa; activation peptides of factor IX, factor X, and prothrombin; fibrinopeptide A) were measured by immunoassay. Factor VII coagulant activity and factor VIIa levels were determined by a functional clotting assay. Among 1548 men genotyped for both mutations, 28 (1.8%) and 52 (3.4%) were heterozygous for prothrombin G20210A and FV R506Q, respectively. The only coagulation marker that was significantly associated with the two mutations was prothrombin activation fragment F1+2 [mean ± SD, 0.88 ± 0.32 nmol/L in men with prothrombin G20210A (p = 0.002) and 0.89 ± 0.30 in men with FV R506Q (p = 0.0001) versus 0.72 ± 0.24 among non-carriers for either mutation]. This data provides conclusive evidence that heterozygosity for the prothrombin G20210A as well as the FV R506Q mutations in the general population leads to an increased rate of prothrombin activation in vivo.


1987 ◽  
Author(s):  
A Blanco ◽  
R Bonfil ◽  
O Bustoabad ◽  
M Lazzari

Increased deposition and lysis of fibrin, associated with malignant tissue, has led to look for activators of both the coagulation and fibrinolytic systems produced by tumor cells. We report the evidences of a procoagblant activity (PA) in the extracts of intratumoral necrosis from two experimental breast adenocarcinomas in murine model (BALB/c). The tumors have different metastatic capacity (MC). M3 without MC and MM3 with high MC.The addition of the extracts to: 1- Normal Plasma, 2- Deficient substrates in coagulation factors, 3- Purified, fibrinogen (I), showed: 1- Shortening of the plasma recalcification time (PRT) and APTT, without ;modification on prothrombin time (PT), 2- Reduction of the PRT on deficient substrates in factors: VIII; VII; VII and X; V; V, VII and X; without modification on II deficient substrate, 3- No PA on I. Table:C: Control, s: seconds, m: minutes. The PA was not affected by heparin. The results suggest that the PA is independent of the presence of either factor VIII or factor VII (intrinsic or extrinsic pathway respectively), as well as presence of either factor V or factor X. Any effect was observed either on factor II deficient substrate or on I, so, there was no evidence of thrombin activity The PA could be act directly on factor II, suggesting that fibrin formation could be induced by a “non-classical” activation pathway. No significant differences (p>0.5) in PA were observed between both tumoral necrosis extracts. The necrotic area in M3 (37%) is bigger than in MM3 (18%). So, much more PA could be present in MM3 and this could play a role in the MC of this tumor.


1958 ◽  
Vol 36 (1) ◽  
pp. 249-259 ◽  
Author(s):  
D. C. Triantaphyllopoulos

Sterile fibrinogen rendered non-clottable by incubation was mixed with fresh plasma and the thrombin time determined. An appreciable prolongation was observed. The incubated fibrinogen was then fractionally precipitated with ammonium sulphate. The material precipitated between 25 and 50% ammonium sulphate saturation, when added to freshly drawn but still unclotted blood, or native plasma, prevented its coagulation. This action could be reversed by an approximately fivefold dilution with distilled water and addition of calcium chloride and thrombin, thus excluding fibrinolysis as the cause of the anticoagulant effect. Determinations of the respective coagulation factors showed that no decrease occurred in prothrombin, factor VII, plasma thromboplastin component, and fibrinogen. On the other hand a statistically significant decrease in factor V was observed when calcium was present.


1969 ◽  
Vol 28 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Teodor Kuennapas ◽  
Anne-Jeanette Janson

28 lower-case letters of the Swedish alphabet were studied by the method of multidimensional similarity analysis. 57 Ss participated in the experiment. 9 factors were found. Factor I is called ‘t’ or ‘Vertical linearity,’ Factor II: ‘o’ or ‘Roundness,’ Factor III: ‘n’ or ‘Parallel vertical linearity,’ Factor IV: ‘i’ or “Vertical linearity with dot,’ Factor V: ‘p’ or ‘Roundness attached to vertical linearity,’ Factor VI: ‘k’ or ‘Vertical linearity with crossness,’ Factor VII: ‘a’ or ‘Roundness attached to a hook,’ Factor VIII: V or ‘Angularity open upward’ and Factor IX: ‘z’ or ‘Zigzaggedness.’ ‘Vertical linearity’ and ‘Roundness’ are the most important of these factors and account for a considerable portion of the similarity among many letters.


1975 ◽  
Author(s):  
R. Chakrabarti ◽  
M. Brozovic ◽  
T. W. Meade ◽  
W. R. S. North ◽  
Y. Stirling

Fibrinolytic activity, coagulation factors I, V, VII and VIII, blood cholesterol and triglyceride levels have been measured in a randomyl selected group of 650 men aged 17–64 and 350 women aged 17–59 working in an industrial population. Fibrinolytic activity (the reciprocal of the dilute blood clot lysis time in hours) decreases significantly (0.003 per annum) with advancing age in men; there is no significant change in women. Factors I and V increase significantly with age in both men and women at about the same rate (1.0% per annum for factor I and 0.6% for factor V), their mean levels in each group being very similar. Factor VIII also increases significantly with age in both sexes up to the age of about 50 years, after which levels continue to rise in men, but fall in women. Factor VII and blood cholesterol levels are lower in young women than in young men; they rise in both sexes, but significantly faster in women than in men (1.1% and 0.4%, respectively for factor VII, for example), so that in older women they are substantially higher than in older men. Triglyceride levels rise with age in both sexes, levels in men being hig er than those in women.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3655-3655
Author(s):  
Michael Joshua Levitt ◽  
Arthur A. Topilow ◽  
William Lerner ◽  
Peter Mencel ◽  
Carl Henningson ◽  
...  

Abstract Abstract 3655 Acquired inhibitors of coagulation are bleeding disorders that require prompt recognition, diagnosis, and management. Antibodies against factor VII are extremely rare with only a few cases reported in the literature. We present a case of a patient with an acquired Factor VII inhibitor. This is an 87 year old female with a past medical history of breast cancer, hypertension, and hyperlipidemia who presented to the emergency room with right flank pain and hematuria. A CT scan of the abdomen and pelvis showed bilateral hydronephrosis with no evidence of nephrolithiasis. The patient denied hematemesis or hematochezia but was noted to have hemoccult positive stools. The patient denied any anticoagulant use. Admission laboratories revealed a coagulopathy with a normal partial thromboplastin time (PTT) of 28 seconds and prolonged prothrombin time (PT) of greater than 50 seconds and INR of 19.59. The patient received vitamin K without improvement in coagulation parameters. A mixing study revealed a markedly prolonged PT that did not correct with 1:1 (18.9 seconds) and 4:1 (27.3 seconds) mix normal plasma. Factor assays shows an abnormal Factor VII level of less than 1%, and normal Factor II 121%, Factor V 140%, Factor VIII 201%, Factor IX 99%, and Factor XI 126% levels. A FVII inhibitor was 1.66 Bethesda units per milliliter. Immunosuppressive treatment was initiated with prednisone 1 milligram per kilogram daily and cyclophosphamide 200 milligrams daily. Factor VII levels normalized without evidence of inhibitor. The patient clinically improved and immunosuppressive medications were gradually tapered off. This case emphasizes the importance of prompt recognition in a patient with a rare acquired inhibitor of coagulation. Treatment with immunosuppressive therapy consisting of corticosteroids and cyclophosphamide resulted in normalization of factor VII levels and resolution of bleeding symptoms and should be considered as first-line management for such patients. Disclosures: Philipp: Baxter: Research Funding; Wyeth: Research Funding; Octapharma: Research Funding.


1959 ◽  
Vol 197 (4) ◽  
pp. 791-794 ◽  
Author(s):  
Armand J. Quick ◽  
Clara V. Hussey ◽  
John Harris ◽  
Kenneth Peters

On infusing a dilute solution of thrombin intravenously into a dog at a constant and carefully regulated rate, no massive thrombosis occurs and no evidence of a thrombo-embolic state is obtained. An occult type of intravascular clotting is produced which is characterized by a progressive decrease of the level of fibrinogen, thrombocytopenia, a prolonged prothrombin time and a poor consumption of prothrombin. Labile factor (factor V) and thromboplastinogen (factor VIII) are strikingly diminished. Prothrombin is moderately decreased while stable factor (factor VII) and PTC (factor IX) are not significantly affected. It is postulated that the adsorption of thrombin to the fibrin fibrils which are filtered off in the capillary network and destroyed, constitutes the principal means for preventing dangerous accumulation of thrombin in the blood.


1968 ◽  
Vol 19 (01/02) ◽  
pp. 129-135 ◽  
Author(s):  
L Leandoer ◽  
S.-E Bergentz ◽  
Inga Marie Nilsson

SummaryThoracic duct lymph of the dog was compared with blood regarding the concentration of various coagulation factors, coagulation properties, and components of the fibrinolytic system.The recalcification time for lymph was almost twice as long as for blood. The quotients between the concentration of the coagulation factors in the lymph and blood varied considerably. For fibrinogen the lymph/blood concentration ratio was 1/3, for factor V 1/4, for factor VIII 1/4, for factor IX 2/3 and for P & P 1/2.The fibrinolytic activity in the lymph was lower than in the blood and no split products were found in the lymph. The lymph/blood concentration ratio was 1/2 for plasminogen and 2/3 for the urokinase inhibitor activity.


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