Diagnosis of deep-vein thrombosis.
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Biomedical subjects
Publications and source records attributed to J Jespersen.
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In a prospective study of deep vein thrombosis (DVT), detected by the Tc-plasmin test, in 34 patients with acute myocardial infarction sequential determinations were made in plasma by immunologic methods of histidine-rich glycoprotein (HRG) and total plasminogen and the concentrations of free plasminogen calculated. Mean plasma HRG concentrations were consistently higher in the group of patients, in which Tc-plasmin scanning had revealed the existence of DVT. The effect of HRG caused the level of free plasminogen to be only 50-60% of the level of total plasminogen. Fluctuations of HRG caused only minor changes in free plasminogen concentrations. Our data suggest that HRG acts as a weak, negative acute phase reactant.
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The dynamic haemostatic balance between blood coagulation and fibrinolysis and its influence on the development of disseminated intravascular coagulation are described. The effects of heparin and antithrombin-III are illustrated by clinical cases.
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Determinations of alpha 2-antiplasmin and alpha 2-macroglobulin were made in plasma samples collected during one normal or hormone induced cycle in 15 normal women and 11 women using oral contraceptives containing 30 micrograms ethinyl oestradiol and 150 micrograms levo-norgestrel. The immediate plasmin inhibition test for determination of alpha 2-antiplasmin was modified for application on a centrifugal analyser using the chromogenic peptide substrate Chromozym PL. alpha 2-Macroglobulin concentration was determined by radial-immunodiffusion. There were no differences between the two groups in the mean concentrations of alpha 2-antiplasmin and alpha 2-macroglobulin, but during the cycle a slight, and statistically significant fall occurred in the alpha 2-antiplasmin concentration in both groups, while the fluctuations of alpha 2-macroglobulin were small and insignificant. Distinctly individual levels of both inhibitors were found to exist. The variations in these during the periods of the cycle fluctuated within a much narrower range than the variation of the total average. The results stress the importance of determining the fluctuations in individual levels in longitudinal studies. These findings exclude variations in the concentrations of these inhibitors as possible sources of a change in the antithrombotic potential caused by oral contraceptives.
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Biopsies of the gastric mucosa were collected from two patients with Ménétrièr's disease before, during, and after treatment with cimetidine and studied for fibrinolytic activity. The fibrinolytic activity in the homogenates or in the potassium thiocyanate soluble fractions increased markedly during the treatment. Immunological characterization of the activity indicated that its major component was an endothelium-derived type of plasminogen activator, and that the increase in activity was caused solely by an increase in the concentration of this component. This suggests an increase in the vascularity of the mucosal layers during treatment thus reflecting a repair process.
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The reproducibility, precision and required conditions of the fibrin plate method for determination of fibrinolytic agents are described in detail. Under optimal conditions the assay is a sensitive and precise method for the quantitative determination of fibrinolytic agents. Thus, with a tissue plasminogen activator preparation its sensitivity is approximately 0.02 CTA urokinase units/ml, and dilutions yielded a curve with a slope (double-logarithmic) with a day-to-day mean of 0.53 with a coefficient of variation of 5.1%.