Two-stage Procedure For the Quantitative Determination of Prothrombin Concentration*

Ware, Arnold G.; Seegers, Walter H.

doi:10.1093/ajcp/19.5_ts.471

Cited by 380 publications

(77 citation statements)

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“…Plasma prothrombin was assayed by the two-stage technique of Ware and Seegers (11), slightly modified (2). Results were corrected for the volume of anticoagulant used in the blood collection.…”

Section: Coagulation Methodsmentioning

confidence: 99%

“…During prothrombin activation experiments (see below) thrombin concentrations were determined by adding 0.1 ml of a suitable dilution of test material to a tube containing 0.1 ml of fibrinogen solution and 0.3 ml of buffered acaciacalcium solution, so that, except for the absence of tissue extract and accessory factors, conditions were the same as in the clotting stage of the prothrombin two-stage assay (11,2).…”

Section: Coagulation Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Congenital dysprothrombinemia: an inherited structural disorder of human prothrombin

Shapiro¹,

Martinez²,

Holburn³

1969

J. Clin. Invest.

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Section: Coagulation Methodsmentioning

confidence: 99%

Section: Coagulation Methodsmentioning

confidence: 99%

Congenital dysprothrombinemia: an inherited structural disorder of human prothrombin

Shapiro¹,

Martinez²,

Holburn³

1969

J. Clin. Invest.

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“…For instance, thrombin formed during clotting is determined in the two stage prothrombin time by its ability to clot exogenous fibrinogen (Ware and Seegers 1949). The prothrombinase formed in the first stage of the thromboplastin generation test is determined in the second stage by its ability to clot substrate plasma (Brown 1984).…”

mentioning

confidence: 99%

A simple method for the determination of plasma extrinsic coagulant activity.

Hussein

Medoukh

1986

Tohoku J. Exp. Med.

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A spectrophotometric study of plasma coagulation is presented with a method for the determination of plasma coagulant activity, via the extrinsic pathway. Dilute citrated plasma was coagulated by recalcification after the addition of a very small amount of thromboplastin. The maximum increase in absorbance per min during coagulation was used as a measure of coagulant activity. The method was applied to normal platelet-rich plasma samples, and the effect of changing the concentration of plasma, thromboplastin, fibrinogen, and heparin was studied.plasma coagulant activity ; extrinsic pathway ; thromboplastin ; fibrinogen ; heparin Tests commonly used for the determination of plasma coagulant activity depend mainly on measuring the reaction velocity, or measuring the yield of coagulation activity. The determination of the clotting time, as a measure of reaction velocity is based on the relationship between the clotting time and the coagulant activity, which is a complex relationship due to the sequential nature of the coagulation reactions (Bloom and Thomas 1981). A plot of the clotting time against coagulant activity yields a hyperbola on rectangular coordinates, where small differences in clotting time represent major differences in activity, when the clotting times are short, and represent minor differences in activity, when the clotting times are long. A standard curve must also be used with each test to convert the clotting times to units or percentages of maximum activity (Williams et al. 1977).The determination of the product of coagulation activity usually adds one more stage to the test. For instance, thrombin formed during clotting is determined in the two stage prothrombin time by its ability to clot exogenous fibrinogen (Ware and Seegers 1949). The prothrombinase formed in the first stage of the thromboplastin generation test is determined in the second stage by its ability to clot substrate plasma (Brown 1984). Recently, thrombin generated during coagulation was determined by measuring the activity of thrombin eluted from the clot. This amount was found to be proportional to the total amount

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“…For the specific determination of prothrombin, the two-stage method described bv Ware and Seegers was used (24). This depends on the entire conversion of prothrombin to thrombin, which is then measured by the clotting of a fibrinogen solqtion previously standardized against known amounts of thrombin.…”

mentioning

confidence: 99%

The effect of chlorpromazine on haemostasis

Dobkin¹,

Fisher²,

Wyant³

1957

Can. Anaes. Soc. J.

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RECENT STtrDmS INDICATE that the lethal effect of experimental, traumatic and chronic haemorrhagic shock is decreased or prevented by pre-treatment with chlorpromazine (1,2). In animals this treatment also attenuates the deleterious influence of bacterial invasion, and when bacterial contamination does occur, congestion and haemorrhage in the bowel does not develop (8). In a clinical study of patients undergoing surgical treatment for pulmonary tuberculosis, it was found also that pre-treatment with chlorpromazine possibly prevented or minimized the decompensatory uptake of blood following severe or prolonged haemorrhage and improved the postoperative course of these patients (4).This protective action of chlorpromazine has been partially explained on physiological, pharmacological and psychological grounds. Physiologically, the major known effect of the drug is to decrease peripheral vascular resistance. This causes hypotension and reduces the head of pressure in the peripheral circulation (5, 6). Zweifach and associates believe that the protection afforded by chlorpromazine is due to the block of neurogenic peripheral vascular control and a hyper-reactive response by the arterioles and venulc~ to vaso-active materials in the circulation during sh'ess (7). This hyper-reactivity sustains regional blood flow in the presence of a decreased circulating blood volume more effectively than sympathetic over-compensation in response to stress as seen in the unprotected or unblocked peripheral circulation. This effect is noted both in the visceral and in the peripheral (sldn) circulation. The hyper-reactivity of arterioles and venules is considered a favourable sign, indicating that tJhe deleterious pooling of blood in the splanchnic area, as seen in irreversible shock, has been eliminated and that a sustained circulation of the skin and peripheral vascular bed is present in spite of depletion of the blood volume.Pharmacologically, there is a potent anti-adrena~u effect, a protective action on the heart against epinephrine-induced arrhythmias of chloroform, cyclopropane and trichlorethylene; a slight anti-histaminic effect, an anti-acetytcholine (parasympatholytic) effect; and a potent anti-5-hych'oxytryptamine effect. There is also a moderate local anaesthetic effect and a "pharmacological leucotomy" which extends from the level of the cortex to the brain 'stem and to the cervical ganglia (8, 9, i0, 11, 12, 18).Psychologically, chlorpromazine suppresses primary epinephrine-precipitable subcortical warning or tension anxiety. It exerts only an indirect influence on the secondary cortical manifestations, consisting of the traumatic state of the ego, ir~ inverse proportion to the degree to which important ego functions have been

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Two-stage Procedure For the Quantitative Determination of Prothrombin Concentration*

Cited by 380 publications

References 0 publications

Congenital dysprothrombinemia: an inherited structural disorder of human prothrombin

Congenital dysprothrombinemia: an inherited structural disorder of human prothrombin

A simple method for the determination of plasma extrinsic coagulant activity.

The effect of chlorpromazine on haemostasis

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