Studies on the Initiation of Blood Coagulation. Ii. An Anticoagulant Inhibiting the Activation of a Plasma Thromboplastic Factor 1

Conley, C. Lockard; Ratnoff, Oscar D.; Ellicott, Charles E.; Hartmann, Robert C.

doi:10.1172/jci102356

Cited by 21 publications

(5 citation statements)

References 12 publications

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“…The fraction's lack of thromboplastic activity was also demonstrated by a study of the plasma of a patient with a circulating anticoagulant whose case was described in an earlier report (21 ). This patient's plasma clotted in a normal time upon the addition of highly diluted human brain thromboplastin.…”

Section: Resultsmentioning

confidence: 69%

A Familial Hemorrhagic Trait Associated With a Deficiency of a Clot-Promoting Fraction of Plasma 1

Ratnoff¹,

Colopy²

1955

J. Clin. Invest.

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435

187

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Section: Resultsmentioning

confidence: 69%

A Familial Hemorrhagic Trait Associated With a Deficiency of a Clot-Promoting Fraction of Plasma 1

Ratnoff¹,

Colopy²

1955

J. Clin. Invest.

Self Cite

435

187

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“…This substance, which acts as a potent anticoagulant, appears to inhibit only the activation of plasma thromboplastin and has no effect on other stages of blood coagulation. A study of the properties of this anticoagulant has provided further support for the existence of a plasma thromboplastin (21).…”

Section: Discussionmentioning

confidence: 88%

Studies on the Initiation of Blood Coagulation. Iii. The Clotting Properties of Canine Platelet-Free Plasma 1

Hartmann¹,

Conley²,

Poole³

1952

J. Clin. Invest.

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The changes which take place in shed blood and thereby initiate its coagulation remain a source of considerable speculation. It is still common belief that platelets are necessary for the initiation of blood coagulation although a number of investigators have presented evidence to the contrary (1-8). While platelets appear to be essential for efficient clotting, there is good evidence that coagulation can occur in their absence. Investigations in this laboratory revealed that human platelet-free plasma, prepared without anticoagulant, regularly clotted in glass tubes at 370C (7). However, aliquots of the same plasma clotted much more slowly or not at all in silicone-treated tubes. It was demonstrated that the rate of clotting of platelet-free plasma was directly related to the area of the glass surface to which the plasma was exposed. These studies were interpreted as providing evidence for the existence of a "plasma thromboplastin" which is activated on contact with glass surfaces and can bring about clotting in the absence of platelets (7,8).On the other hand Patton and his associates obtained different results with canine plasma using similar techniques (9). In their experiments canine plasma was freed of formed elements by high-speed centrifugation. This plasma when stored at room temperature was observed to clot imperfectly or not at all. Fibrin formation occurred with equal frequency in glass and siliconetreated tubes. These authors interpreted their results as providing no evidence for the view that plasma contains a soluble factor which can initiate clotting independent of platelet action.

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“…Where biochemical characterization has been carried out, the anticoagulant in previous cases has been a globulin and in many instances has been localized to they globulin fraction. The view has been repeatedly expressed that the anticoagulant in these cases is of the nature of an antibody, and positive precipitin reactions have been reported by several authors in the haemophilic group Frommeyer et al, 1950;Hougie and Fearnley, 1954;Verstraete and Vandenbroucke, 1956) and in the idiopathic group (Hougie, 1953;Verstraete and Vandenbroucke, 1956); other authors have reported negative precipitin reactions in cases from all four groups (Conley, Ratnoff, Ellicott, and Hartmann, 1950;Hardisty, 1954;Biggs and Bidwell, 1959;Breckenridge and Ratnoff, 1962). The association of circulating anticoagulants of this type with the various disorders of the immunological mechanisms in the third group has been invoked as further support for the theory that these anticoagulants represent an immune phenomenon (Collins and Ferriman, 1952;Spaet and Kinsell, 1954;Nussey and Dawson, 1957;Favre-Gilly et al, 1958).…”

Section: Discussionmentioning

confidence: 93%

A circulating anticoagulant inhibiting antihaemophilic globulin

Pinkerton¹,

Dagg²,

Taylor³

1965

Journal of Clinical Pathology

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Studies on the Initiation of Blood Coagulation. Ii. An Anticoagulant Inhibiting the Activation of a Plasma Thromboplastic Factor 1

Cited by 21 publications

References 12 publications

A Familial Hemorrhagic Trait Associated With a Deficiency of a Clot-Promoting Fraction of Plasma 1

A Familial Hemorrhagic Trait Associated With a Deficiency of a Clot-Promoting Fraction of Plasma 1

Studies on the Initiation of Blood Coagulation. Iii. The Clotting Properties of Canine Platelet-Free Plasma 1

A circulating anticoagulant inhibiting antihaemophilic globulin

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