The Release of Thrombin from Fibrin by Fibrinolysin

Bloom, A. L.

doi:10.1111/j.1365-2141.1962.tb06505.x

Cited by 24 publications

(6 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These increases, therefore, are likely due to intravascular thrombin activity generated as a results of fibrinolytic therapy because these assays had little crossreactivity with degradation products. Active thrombin is retained within thrombi and can be released by thrombolysis (41)(42)(43), and evidence indicates that thrombolytic therapy may generate new thrombin (44,45). As Test D showed no reactivity with degradation products of fibrin, the 7.6-fold elevation in soluble fibrin levels provides the clearest indication of the increased thrombin activity during therapy.…”

Section: Discussionmentioning

confidence: 99%

Reactivity of Soluble Fibrin Assays with Plasmic Degradation Products of Fibrin and in Patients Receiving Fibrinolytic Therapy

McCarron

Marder²,

Francis³

1999

Thromb Haemost

View full text Add to dashboard Cite

SummaryThe ability to identify the products of thrombin and plasmin action on fibrinogen is important in patients with thrombotic and fibrinolytic disorders. New assays have been developed for “soluble fibrin” which represents soluble derivatives other than fibrinopeptides formed from fibrinogen by thrombin. These assays are either immunological, using antibodies for fibrin-specific neoepitopes, or functional and based on the cofactor activity of soluble fibrin in the tissue plasminogen activator (t-PA)-mediated conversion of plasminogen to plasmin. As plasmic derivations of fibrin share structural features with soluble fibrin, they may be reactive with assays for soluble fibrin. Therefore, we prepared plasmic digests of fibrin and determined the degree of reactivity with four soluble fibrin assays. Three assays used Mabs directed toward the fibrin-specific neoepitopes at α17-23 (A), γ312-324 (B) and α17-78 (D). A fourth (C) was based on t-PA co-factor activity. Tests A and C demonstrated marked crossreactivity with fibrin degradation products, and digests containing the largest derivatives showed greatest reactivity. Plasmic derivatives of crosslinked fibrin had greater reactivity than those of non-crosslinked fibrin. Tests B and D demonstrated minimal reactivity with plasmic derivatives of crosslinked or of non-crosslinked fibrin. Samples from patients with lower limb peripheral arterial occlusion were assayed for soluble fibrin, D-dimer and fibrinogen at presentation and eight hours after thrombolytic therapy. Variable results were seen at presentation with elevations in 13, 1, 0 and 4 of 19 patients using Tests A, B, C and D, respectively. After fibrinolytic therapy, marked increases in soluble fibrin levels were observed up to 600-fold above normal. A strong correlation between baseline levels was observed with Test B and Test D, which showed the least cross-reactivity with plasmic derivations. After thrombolytic therapy there were either weak or no correlations among the different assays. The results demonstrate that assays for soluble fibrin may react with plasmic derivatives of fibrin and this must be considered in interpreting clinical results.

show abstract

Section: Discussionmentioning

confidence: 99%

Reactivity of Soluble Fibrin Assays with Plasmic Degradation Products of Fibrin and in Patients Receiving Fibrinolytic Therapy

McCarron

Marder²,

Francis³

1999

Thromb Haemost

View full text Add to dashboard Cite

show abstract

“…Для СД характерно также нарушение плазменного звена гемостаза и гемостатических функций сосудистого эндотелия. Многие исследователи отмечают, в частности, повышение со держания в плазме крови фактора Виллебранда в комплексе с фактором VIII, который синтезируется эндотелием [12]. Инте ресным представляется исследование [67], в котором показа но, что уровень фактора Виллебранда был повышен у больных СД с поражением почек, а также у больных, ДН у которых развилась в течение 3 лет после обследования.…”

Section: нарушения гемостазаunclassified

Diabetic nephropathy: Pathogenesis and treatment

Vorontsov¹,

Шестакова²

1996

Probl Endokrinol (Mosk)

View full text Add to dashboard Cite

Currently, diabetic nephropathy (DN) is the leading cause of disability and mortality in patients with diabetes mellitus (DM). Developing in 4045% of patients, both insulin-dependent IDDM (type I) and non-insulin-dependent IDDM (type II) diabetes, this formidable complication leads to the development of chronic renal failure, and ultimately to the death of patients from uremia. The first kidney damage in diabetes was described by R. Kimmelstiel and C. Wilson in 1936. It is clinically characterized by the following manifestations: increasing proteinuria (with unchanged urinary sediment), hypertension, the formation of nephrotic syndrome (in about 30% of patients) and a progressive decrease in filtration kidney function. The insidiousness of this complication of diabetes lies in the fact that it develops gradually and remains unnoticed for a long time, since at the initial stages the patient does not cause discomfort. And in the later stages, when the presence of DN is no longer in doubt, preventing its further progression is extremely difficult, and often impossible. For many years in our country, the classification of DNs was used by V. R. Klyachko, according to which prenephrotic, nephrotic, and nephrosclerotic stages were distinguished. According to this classification, DN is diagnosed only from the moment when the patient develops proteinuria, registered by conventional laboratory methods, which indicates the severity and irreversibility of pathological changes in the kidneys. The modern classification, distinguishing stages at which clinical manifestations are still absent, and only functional disorders are detected, was proposed by S. Mogensen in 1983 (see table). In accordance with this classification, the first 3 stages are not detected by conventional clinical methods (preclinical stage of DN). The most informative marker of the early stages of DN is the determination of microalbuminuria (MAU), which means the excretion of albumin with urine in an amount of 30 to 300 mg / day. Identification of UIA in a patient with type I diabetes means that the probability of developing a clinical picture of DN in his next 10 years is 80%.

show abstract

“…Determination of fibrinolytic activity of whole blood with special reference to the effects of exercise and fat feeding (Billimoria, Drysdale, James, and Maclagen, 1959). The release of thrombin from fibrin by fibrinolysis (Bloom, 1962). Some physico-chemical properties of human fibrinogen (Caspary and Kekwick, 1957).…”

Section: Appendixmentioning

confidence: 99%

The fibrinolytic mechanism in haemostasis: A review

Stafford¹

1964

Journal of Clinical Pathology

View full text Add to dashboard Cite

The Release of Thrombin from Fibrin by Fibrinolysin

Cited by 24 publications

References 9 publications

Reactivity of Soluble Fibrin Assays with Plasmic Degradation Products of Fibrin and in Patients Receiving Fibrinolytic Therapy

Reactivity of Soluble Fibrin Assays with Plasmic Degradation Products of Fibrin and in Patients Receiving Fibrinolytic Therapy

Diabetic nephropathy: Pathogenesis and treatment

The fibrinolytic mechanism in haemostasis: A review

Contact Info

Product

Resources

About