Chicken prothrombin, thrombin, and fibrinogen

1961 ◽  
Vol 200 (5) ◽  
pp. 1013-1017 ◽  
Author(s):  
C. H. Bigland ◽  
D. C. Triantaphyllopoulos

Avian blood coagulation studies revealed the mean one-stage prothrombin time of plasma from 100 chickens, 10 weeks of age, as determined with chicken brain thromboplastin, to be 11.4 seconds, compared with 10–300 seconds found by other workers; the mean prothrombin content was 137% of human prothrombin levels, as determined by the one-stage prothrombin-time technique, but only 53% by the adsorption and elution technique used. Fibrinogen determinations on the same plasma revealed a mean of 346 mg/ 100 ml of plasma, compared with 250–400 for humans. Chicken thrombin was prepared which gave a mean thrombin time on the same, but buffered, plasma of 12 seconds. Coagulation of chicken plasma with chicken thrombin was found to be highly sensitive to variations in pH, being 12 seconds at pH 7.1, but lengthening to over 60 seconds at pH 7.7. Greatly increased clotting times of chicken plasma with bovine thrombin and with rabbit thromboplastin indicated evidence of species specificity.

1993 ◽  
Vol 20 (3) ◽  
pp. 371 ◽  
Author(s):  
CT Eason ◽  
SE Jolly

The anticoagulant and toxic effect of the rodenticide pindone were compared in the rabbit and the Australian brushtail possum (Trichosurus vulpecula). Six possums and six rabbits were dosed orally with 25mg kg-1 pindone, and another five possums were dosed with 100mg kg-1 pindone. Blood samples were taken before dosing and 6 days after dosing. In rabbits, the mean haematocrit was reduced from 0.41 to 0.14, the one-stage prothrombin time increased from 7.1 to more than 120 s, and activated partial prothrombin time increased from 26.1 to more than 180 s. These parameters were unchanged in the possums that received 25mg kg-1. In possums that received 100mg kg-1 the one-stage prothrombin time increased from 41.9 to 80.0 s and the activated partial prothrombin time increased from 30.2 to 103.9 s. The haematocrit was unchanged. Half the rabbits died with extensive haemorrhaging within 6 days, but there was no haemorrhaging or mortality in the possums in either dose group.


1974 ◽  
Vol 31 (02) ◽  
pp. 309-318
Author(s):  
Phyllis S Roberts ◽  
Raphael M Ottenbrite ◽  
Patricia B Fleming ◽  
James Wigand

Summary1. Choline chloride, 0.1 M (in 0.25 M Tris. HCl buffer, pH 7.4 or 8.0, 37°), doubles the rate of hydrolysis of TAME by bovine thrombokinase but has no effect on the hydrolysis of this ester by either human or bovine thrombin. Only when 1.0 M or more choline chloride is present is the hydrolysis of BAME by thrombokinase or thrombin weakly inhibited. Evidence is presented that shows that these effects are due to the quaternary amine group.2. Tetramethyl ammonium bromide or chloride has about the same effects on the hydrolysis of esters by these enzymes as does choline chloride but tetra-ethyl, -n.propyl and -n.butyl ammonium bromides (0.1 M) are stronger accelerators of the thrombokinase-TAME reaction and they also accelerate, but to a lesser degree, the thrombin-TAME reaction. In addition, they inhibit the hydrolysis of BAME by both enzymes. Their effects on these reactions, however, do not follow any regular order. The tetraethyl compound is the strongest accelerator of the thrombokinase-TAME reaction but the tetra-ethyl and -butyl compounds are the strongest accelerators of the thrombin-TAME reaction. The ethyl and propyl compounds are the best (although weak) inhibitors of the thrombokinase-BAME and the propyl compound of the thrombin-BAME reactions.3. Tetra-methyl, -ethyl, -n.propyl and -n.butyl ammonium bromides (0.01 M) inhibit the clotting of fibrinogen by thrombin (bovine and human proteins) at pH 7.4, imidazole or pH 6.1, phosphate buffers and they also inhibit, but to a lesser degree, a modified one-stage prothrombin test. In all cases the inhibition increases regularly as the size of the alkyl group increases from methyl to butyl. Only the ethyl com pound (0.025 M but not 0.01 M), however, significantly inhibits the polymerization of bovine fibrin monomers. It was concluded that inhibition of the fibrinogen-thrombin and the one-stage tests by the quaternary amines is not due to any effect of the com pounds on the polymerization process but probably due to inhibition of thrombin’s action on fibrinogen by the quaternary amines.


1969 ◽  
Vol 21 (03) ◽  
pp. 573-579 ◽  
Author(s):  
P Fantl

SummaryTreatment of human and dog oxalated plasma with 0.2 to 1.0 × 10−1 M 2.3-dithiopropanol (BAL) or dithiothreitol (DTT) at 2–4° C for 30 min results in the reduction of the vitamin-K dependent clotting factors II, VII, IX and X to the respective-SH derivatives. The reaction is pH dependent. Under aerobic conditions the delayed one stage prothrombin time can be partly reversed. Under anaerobic conditions a gradual prolongation of the one stage prothrombin time occurs without reversal.In very diluted plasma treated with the dithiols, prothrombin can be converted into thrombin if serum as source of active factors VII and X is added. In contrast SH factors VII, IX and X are inactive in the specific tests. Reoxidation to active factors II, VII, IX and X takes place during adsorption and elution of the SH derivatives. The experiments have indicated that not only factor II but also factors VII, IX and X have active-S-S-centres.


1967 ◽  
Vol 18 (01/02) ◽  
pp. 198-210 ◽  
Author(s):  
Ronald S Reno ◽  
Walter H Seegers

SummaryA two-stage assay procedure was developed for the determination of the autoprothrombin C titre which can be developed from prothrombin or autoprothrombin III containing solutions. The proenzyme is activated by Russell’s viper venom and the autoprothrombin C activity that appears is measured by its ability to shorten the partial thromboplastin time of bovine plasma.Using the assay, the autoprothrombin C titre was determined in the plasma of several species, as well as the percentage of it remaining in the serum from blood clotted in glass test tubes. Much autoprothrombin III remains in human serum. With sufficient thromboplastin it was completely utilized. Plasma from selected patients with coagulation disorders was assayed and only Stuart plasma was abnormal. In so-called factor VII, IX, and P.T.A. deficiency the autoprothrombin C titre and thrombin titre that could be developed was normal. In one case (prethrombin irregularity) practically no thrombin titre developed but the amount of autoprothrombin C which generated was in the normal range.Dogs were treated with Dicumarol and the autoprothrombin C titre that could be developed from their plasmas decreased until only traces could be detected. This coincided with a lowering of the thrombin titre that could be developed and a prolongation of the one-stage prothrombin time. While the Dicumarol was acting, the dogs were given an infusion of purified bovine prothrombin and the levels of autoprothrombin C, thrombin and one-stage prothrombin time were followed for several hours. The tests became normal immediately after the infusion and then went back to preinfusion levels over a period of 24 hrs.In other dogs the effect of Dicumarol was reversed by giving vitamin K1 intravenously. The effect of the vitamin was noticed as early as 20 min after administration.In response to vitamin K the most pronounced increase was with that portion of the prothrombin molecule which yields thrombin. The proportion of that protein with respect to the precursor of autoprothrombin C increased during the first hour and then started to go down and after 3 hrs was equal to the proportion normally found in plasma.


1984 ◽  
Vol 12 (01n04) ◽  
pp. 116-123 ◽  
Author(s):  
Jih-Pyang Wang ◽  
Mei-Feng Hsu ◽  
Che-Ming Teng

Bleeding time in rats was markedly prolonged after the adminstration of the water extract of Hsien-Ho-T'sao. This antihemostatic effect was more marked in the group of i.p. injection of the drug than in the group of p.o. administration for 2 to 7 consecutive days. Blood coagulation studies showed that plasma prothrombin time, activated partial thromboplastin time and stypven time were prolonged, while thrombin time adnd fibrinogen level were not changed. The thromboelastographic recording showed that reation time was prolonged and maximal elasticity of clot was decreased. In addition, ADP- and collagen- induced aggregations of platelet-rich plasma was suppressed. In conclusion, the prolongation of the bleeding time might be due to both anticoagulant and antiplatelet action of the drug.


1961 ◽  
Vol 265 (26) ◽  
pp. 1286-1289 ◽  
Author(s):  
Armand J. Quick ◽  
Clara V. Hussey
Keyword(s):  

PEDIATRICS ◽  
1961 ◽  
Vol 27 (2) ◽  
pp. 204-213
Author(s):  
Helen I. Glueck ◽  
James M. Sutherland

A case of factor-VII deficiency of a congenital nature in a Negro male child has been reported. As far as can be determined, this is the first case reported in this race. The defect was detected at 6 hours of age. Prothrombin, as contrasted to factor VII, after initially low levels normally found in infants, rose to adult levels. The patient's one-stage prothrombin time has ranged between 25 to 35 second (normal 11 to 12 seconds). In spite of this, he has never shown any manifestations of hemorrhage. The patient's family was studied and the findings indicate that the patient's defect represented a homozygous state and that both parents with a less severe deficiency were heterozygous for the trait. The defect is an autosomal disorder directly inherited. It is clinically apparent and easily detected only in the homozygous state. The heterozygous state is characterized by a very slight prolongation of the one-stage prothrombin time, the difference from the control value being so minimal as to be overlooked. In one subject studied, an aunt of the propositus, the quantitative defect (42% of normal) could not be regularly detected by the usual methods. Only by using the plasma of the propositus as the test plasma, was the defect in her plasma detected, thus explaining the transmission of the trait to her offspring. These findings explain the difficulties previously encountered in understanding the inheritance of the disorder.


BMJ ◽  
1955 ◽  
Vol 1 (4919) ◽  
pp. 934-937 ◽  
Author(s):  
A. J. Quick ◽  
C. V. Hussey
Keyword(s):  

1987 ◽  
Vol 17 (6) ◽  
pp. 313-320
Author(s):  
Knut Korsbrekke ◽  
Ingebrigt Talstad

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