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Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 5 uppsatser.

Thesis (Ph. D.)--University of Washington, 1998. / Vita. Includes bibliographical references (leaves [263]-275).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1982. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 210-218).

17β-Estradiol (E2) and progesterone (P4) have various important functions but the effect of these endogenous hormone concentrations on fibrin network formation has not been established. It is essential to understand natural hormone mechanisms since these hormones are still present in circulation while hormonal contraceptives, which are associated with increased risk of venous thromboembolism, are used. In this study the formation of a fibrin network is analysed when different physiological concentrations of E2 and P4 is added to platelet poor plasma. Blood coagulation is critical for haemostasis but when the formation of a stable clot is influenced in such a way that hypercoagulation takes its course, it can have detrimental effects as it increases the risk of venous thrombosis. During blood coagulation fibrinogen is converted into fibrin in the presence of thrombin. The formation of a dense fibrin clot structure is quite an intense process and packaged in very specific ways. Both E2 and P4 has the ability to shift the haemostatic balance to a hypercoagulable state and therefore viscoelastic studies, morphological analysis as well as turbidimetry were used in this study to observe the possible changes in the fibrin network formation. Viscoelastic studies included thromboelastography (TEG) which gave insight to the properties of clot formation. Morphological studies included scanning electron microscopy (SEM) and atomic force microscopy (AFM) which delivered an investigation in fibrin network morphology, fibrin fiber diameter and surface roughness. Turbidimetry included further analysis of plasma fibrin clot formation and clot lysis time (CLT). Results showed that E2 and P4 showed hypercoagulable viscoelastic properties with decreased fibrin diameter and surface roughness while increased occurrence of dense matted deposits (DMDs) were evident. Turbidimetry showed decreased CLT for E2, but not P4. These results suggest in the presence of endogenous estrogen and progesterone, which is associated with hypercoagulability, the additional burden of synthetic hormones may result in a prothrombotic and hypercoagulable state in females with an inflammatory predisposition. It appears that both E2 and P4, which are known for their anti- and pro-inflammatory action, may influence fibrin network formation on a molecular level. These results are of clinical importance when considering hormones as either a pathological agent or therapeutic intervention. / Dissertation (MSc)--University of Pretoria, 2016. / Physiology / MSc / Unrestricted

The adsorption of fibrinogen from human plasma onto various surfaces was investigated under differing conditions of plasma composition. Previous studies by Vroman have indicated that fibrinogen is only transiently adsorbed from normal human blood plasma, possibly due to displacement by high molecular weight kininogen (HMWK). It is possible that this "Vroman Effect" is a manifestation of the activation of the intrinsic clotting pathway responsible, in part, for thrombus formation on artificial surfaces. The effect was studied using dilutions of human plasma from 0.01% to 20.0% of normal concentration trace-labelled with a small amount of ¹²⁵I labelled fibrinogen. Adsorption of fibrinogen to various materials, including glass and several potentially useful biomaterials was measured. Fibrinogen is initially adsorbed apparently under diffusion limitation and later displaced at a rate which depends on the type of material being tested. There does not appear to be a direct relationship between material properties (contact angle, biocompatibility) and the "Vroman Effect". Studies comparing the effect for a series of clotting factor deficient plasmas seem to indicate that plasminogen and HWNK are the main displacing agents on glass. Factors XI and XII, prekallikrein and other components do not appear to be involved. An attempt to mathematically model the effect was hampered by the lack of adequate models to describe even one-component protein adsorption. An isotherm equation was developed based on a theoretical model of protein exchange and spreading on the surface. The resulting parameter estimates based on data for different surfaces were well conditioned and may provide a good in vitro basis for comparing materials. It is hoped that the theoretical model will also be compatible with dynamic adsorption and ultimately a multicomponent system such as plasma (and the Vroman Effect). This work may lead to a better understanding of blood-material interactions and may provide the basis for a simple in vitro test for the characterization of potential biomaterials. / Thesis / Master of Engineering (ME)

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