A radioimmunoassay technique for the rapid measurement of human fibrinopeptide A

Hofmann, V.; Straub, P W

doi:10.1016/0049-3848(77)90036-6

Cited by 73 publications

(14 citation statements)

References 9 publications

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“…Fibrinogen, partial thromboplastin time (FTT), thrombin time, and reptilase time were determined in citrated blood with standard methods. Fibrinopeptlde A was measured immunologically 14 ; the normal range for standard collection by single needle was 0.5 to 2.0 ng/ml. Heparin activity was determined with a commercial anti-Ma system by using a chromogenic substrate (Chromozym-Th, Boehringer GmbH, Mannheim, FRG).…”

Section: Blood Valuesmentioning

confidence: 99%

Dose- and shear rate-dependent effects of heparin on thrombogenesis induced by rabbit aorta subendothelium exposed to flowing human blood.

et al. 1990

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The effect of heparin on thrombogenesis Induced by the subendothelium of rabbit aorta was Investigated In 24 healthy volunteers after Intravenous Injection of different doses (0, 1000, 2500, and 5000 IU). By using an ex vivo perfuslon chamber system, the Interaction between flowing blood and exposed subendothelium was measured at low (50 s" 1 ), Intermediate (650 s" 1 ), and high (2600 s" 1 ) wall shear rates. The low shear rate simulated blood flow in venous, the Intermediate shear rate In arterial, and the high shear rate In small or stenosed arterial vessels. Deposition of fibrin, platelets, and platelet thrombi on vascular subendothelium (SE) was quantified by morphometrlcal and Immunological techniques. Fibrin deposition prevailed at low shear rates and was only minimal at high shear rates (30±1% vs. 1±0.4% coverage of SE with fibrin, means±SEM, p<0.001). In contrast, the Interaction of platelets with SE was more Intense at high compared to low shear rates, as Indicated by higher platelet adhesion (54±5% vs. 4 ± 1 % coverage of SE with platelets, p<0.001) and platelet thrombus volumes (4.8±1.3 vs. 0.5±0.1 pm 3 /fim?, p<0.001). Fibrin deposition on SE was Inhibited by heparin In a dose-dependent manner and was abolished after high doses. In addition, high doses of heparin reduced the height and volume of platelet thrombi at low and Intermediate wall shear rates, but no effect was found at the high shear rate. Our data show that heparin Inhibits the formation of both fibrin and platelet thrombi on vascular subendothelium. The lack of effect of heparin on platelet thrombus formation at high shear rates Indicates that thrombln modulates the growth rate and/or stability of platelet thrombi at low and Intermediate shear rates, whereas additional factors may control platelet thrombus growth and stability at high shear conditions. (Arteriosclerosis 10:607-615,

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Section: Blood Valuesmentioning

confidence: 99%

Dose- and shear rate-dependent effects of heparin on thrombogenesis induced by rabbit aorta subendothelium exposed to flowing human blood.

et al. 1990

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“…UK); fragment X (XDP) by the Ortholatex slide test (Ortho Diagnostic Systems. Beerse, Belgium); P-thromboglobulin (P-TG) by RIA (Amersham International, Amersham, UK); platelet factor 4 (PF4) by RIA (Abbott Laboratories, Chica go, 111., USA); fibrinopeptide A (FpA) by RIA according to Hof mann and Straub [10] (fibrinopeptide A I 125, Mallinckrodt, St. Louis, Mo.. USA). Heparin plasma levels were assessed by colorimetric method (Ortho Diagnostic Systems, Beerse, Belgium) 30 and 180 min after the drug administration.…”

Section: Methodsmentioning

confidence: 99%

“…Neoplastic cells can in fact (a) cause platelet aggregation through the shedding of plasma mem brane vesicles [1]; (b) activate locally factor X through the leak of X-dependent VH-independent cysteine protease [2,3]; (c) potentiate the ability of factor VII to start the extrinsic pathway of blood coagulation [4]; (d) activate factor XII through the contact of the blood with the immature, recently formed neoplas tic endothelium [5]; (e) exhibit fibrinolytic activity through the release of a urokinase type plasminogen activator and/or plasmin-like substances [6][7][8]. In the colon these substances are present in much larger amounts in the neoplastic than in normal mucosa [9]: in large bowel cancer they seem to play an important role in enhancing the metastatic spreading [10].…”

Section: Introductionmentioning

confidence: 99%

Pre- and Postsurgery Activation of Blood Coagulation in Gastric and Large Bowel Cancers: Diagnostic, Therapeutic and Prognostic Hints

Abbasciano¹,

Guerra²,

Reali³

et al. 1990

Oncology

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In 12 patients with gastric cancer and in 14 with large bowel neoplasia, classified according to the TNM system, some major blood indices of hemostasis, platelet activation and fibrinolysis were assessed before and for 1 month after surgery, to show whether possible variations of such indices may provide useful clues to follow-up, treatment effectiveness and prognosis. The following conclusions may be drawn: (1) the assay of platelets, fibrinogen, AT III, fibrin(ogen) degradation products, fragment X, platelet factor 4 has provided useful clues in neither group of patients; (2) preoperative high β-thromboglobulin (β-TG) is a reliable index of tumor presence in both gastric and large bowel cancer; (3) postoperative high β-TG and fibrinopeptide A (FpA) are reliable indices of (a) tumor persistence in both gastric and large bowel cancer; (b) lymph node involvement in gastric much more than in large bowel cancer; (c) metastatic spreading from gastric cancer; (4) the FpA levels are proportional to the tumor mass in gastric cancer. The finding of lower plasma heparin levels in neoplastic patients, when compared with controls (20 patients having undergone abdominal surgery for extraneoplastic affections) suggests higher than conventional doses (5,000 units every 8 h s.c.) of the drug should be given to neoplastic patients in order to prevent thromboembolic bouts and possibly reduce metastatic spreading.

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“…anti-FPA antiserum and desaminotyrosyl-FPA were purchased from 1MCO, Stockholm, Sweden. Desaminotyrosyl-FPA was iodinated by the chloramine-T method of Hofmann and Straub [2]. FPA values were expressed as nanograms per millili ter.…”

Section: Methodsmentioning

confidence: 99%

Coagulation and Platelet Activation after Retinal Vein Occlusions

Mari

Santori

Bertoni

et al. 1982

Pathophysiol Haemos Thromb

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The role played by coagulation and platelet activation in the pathogenesis of retinal vein occlusions (RVO) has been evaluated by measuring beta-thromboglobulin (B-TG), circulating platelet aggregates (CPA), thromboxane B₂ (T×B₂) and fibrinopeptide A (FPA) in 25 patients less than 40 years old, investigated after the acute phase of RVO. FPA and B-TG were significantly higher than in healthy subjects; CPA and T×B₂ were not different. These abnormalities, found in patients free from apparent generalized vascular disease, suggest that a thrombophilic state characterized by coagulation and platelet activation is present in a high proportion of young patients with RVO.

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A radioimmunoassay technique for the rapid measurement of human fibrinopeptide A

Cited by 73 publications

References 9 publications

Dose- and shear rate-dependent effects of heparin on thrombogenesis induced by rabbit aorta subendothelium exposed to flowing human blood.

Dose- and shear rate-dependent effects of heparin on thrombogenesis induced by rabbit aorta subendothelium exposed to flowing human blood.

Pre- and Postsurgery Activation of Blood Coagulation in Gastric and Large Bowel Cancers: Diagnostic, Therapeutic and Prognostic Hints

Coagulation and Platelet Activation after Retinal Vein Occlusions

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