Studies on Platelet Factor‐3 Availability

Spaet, Theodore H.; Cintron, José

doi:10.1111/j.1365-2141.1965.tb06587.x

Cited by 220 publications

(92 citation statements)

References 15 publications

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“…Such an assay is sensitive to a deficiency of Factor X which would interfere with the interpretation of studies on newborn infants (21)(22)(23), patients with liver diseases (24,25), and individuals receiving warfarin (26). This sensitivity may contribute to the considerable variability in the results obtained by Spaet and Cintron in normal subjects, which resulted in difficulty in interpreting results on uremic patients (3).…”

Section: Discussionmentioning

confidence: 99%

“…Spaet and Cintron reported an assay of PF3 employing Stypven (3). Such an assay is sensitive to a deficiency of Factor X which would interfere with the interpretation of studies on newborn infants (21)(22)(23), patients with liver diseases (24,25), and individuals receiving warfarin (26).…”

Section: Discussionmentioning

confidence: 99%

“…It is possible to control the test system so that it is sensitive only to the increase in platelet coagulant activity (1)(2)(3). Studies of the platelet coagulant activity which has been termed platelet factor 3 availability (PF3-A) have revealed abnormalities in a variety of congenital and acquired conditions (2)(3)(4)(5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

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Platelet factor 3 in normal subjects and patients with renal failure

Rabiner¹,

Hrodek²

1968

J. Clin. Invest.

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Two tests were used to differentiate abnormalities in release of platelet factor 3 (PF3) from quantitative deficiencies of this factor in normal subjects and in patients with renal failure. The first test was an assay which determined availability of PF3 (PF3-A time) and involved the use of a mixture of patient's plateletrich plasma (PRP) and normal platelet-poor plasma (PPP) in a fixed ratio (1: 8). The second test was similar but used "frozen and thawed" platelets to obtain a quantitative estimate of PF3 (PF3-F time). An abnormal PF3-A time was found in approximately three-quarters of 55 patients with renal insufficiency; 43 of these had chronic and 12 had acute renal failure. This abnormality was present both in patients with and without hemorrhagic manifestations, although it was slightly more common in bleeders. The PF3-F test was abnormal in approximately one-third of the bleeding patients and one-quarter of the nonbleeders. The PF3-A time returned to normal or was significantly shortened 24-48 hr after peritoneal or hemodialysis. Studies on patients who were not dialyzed showed no statistically significant correlations between the PF3-A time and either the serum urea nitrogen, creatinine, calcium, or phosphorus. Furthermore, the PF3-A time was not affected by guanidinosuccinic or guanidinoacetic acids. We therefore conclude that the demonstrable platelet abnormality in patients with uremia is produced by an unknown dialyzable material.Dr. Hrodek's present address is 2nd Pediatric

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Platelet factor 3 in normal subjects and patients with renal failure

Rabiner¹,

Hrodek²

1968

J. Clin. Invest.

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“…Platelet coagulant activity (platelet factor 3) was tested as follows (16). The clotting mixtures consisted of 0.1 ml platelet-rich plasma, 0.1 ml saline, and 0.1 ml addition incubated for 20 min at 37°.…”

Section: Methodsmentioning

confidence: 99%

Aggregation of platelets by collagen

Wilner¹,

Nossel²,

Leroy³

1968

J. Clin. Invest.

172

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A B S T R A C T In studying some of the properties of collagen responsible for the ability to aggregate platelets it was found that thermal treatment at pH 2.5 of acid-soluble human collagen resulted in a sharp reduction in relative viscosity and platelet aggregating activity at about 350C. The reduction in viscosity is known to be associated with structural transition from triple helical to random coil form and it is postulated that the native structure of collagen is essential for its platelet aggregation effect. Blockage of the free amino groups by deamination, N-acetylation, or treatment with dinitrofluorobenzene resulted in over 90%o reduction in platelet aggregating activity. Addition of cationic proteins to collagen, removal of the negatively charged telopeptides by treatment with pepsin, or acetylation of the free carboxyl groups did not significantly affect the platelet aggregating activity of collagen. On the basis of these findings it is suggested that the free amino groups and specifically the epsilon amino groups of lysine are critical for the platelet aggregating activity of collagen whereas the carboxyl groups are of relatively little importance.

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“…As aggregating inducers, we used ADP (Sigma Chemical Co., St. Louis, MO, USA), collagen (Hormon-Chemie, FRG), epinephrine (Daiichi Chemical Co., Tokyo), arachidonic acid (Nakarai Chemical Co., Tokyo), thrombin (Mochida Chemical Co., Tokyo), bovine fibrinogen (Sigma Chemical Co.), A-23187 (Sigma Chemical Co.) and ristocetin (Nippon Chemico, Tokyo). Platelet factor 3 (PF3 was determined by the kaolin-clotting method (Hardisty and Hutton 1965) and by the kaolin-Russel's viper venom method (Spaet and Cintron 1965). Clot retraction time of whole blood was determined according to Macfarlane's method (Macfarlane 1939).…”

Section: Methodsmentioning

confidence: 99%