[The function of fibrin in wound healing].
Physiology of wound healing especially in its first phase is the basis for understanding application of fibrin sealant. The several components have been reported.
Biomedical subjects
Publications and source records attributed to G Oehler.
Physiology of wound healing especially in its first phase is the basis for understanding application of fibrin sealant. The several components have been reported.
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The radiological and clinical findings of 12 patients with ectopic gastric mucosa in the duodenal bulb are presented. This is a defined disease with characteristic radiological features: multiple small nodular defects of the contrast medium of 1-3 mm diameter. Histology shows complete heterotopia. Pathogenesis and clinical significance are discussed with reference to the literature on this subject.
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Hypercoagulability and disseminated intravascular coagulation (DIC) are characterized by the presence of circulating fibrin monomer complexes in plasma. In 342 patients with possible DIC fibrin monomers, fibrinogen, Reptilase Time, antithrombin III and other coagulation parameters were determined at frequent intervals. Testing of soluble fibrin monomer complexes was performed using a sensitive and reliable hemagglutation assay with red cells sensitized by fibrin monomers (FM-Test) and the ethanol gelation test (EGT). Method comparison regarding the influence of fibrinogen levels and fibrin degradation products shows that high fibrinogen levels lead to false-positive results with EGT. The same effect is observed for fibrin degradation products and EGT whereas no influence of fibrinogen level and fibrin degradation products on the FM-Test occurs. It is well-known that during DIC AT III level decreases caused by proteolytic activity. In this study it could be shown that fibrin monomer increases parallel to the decrease of AT III. The same effect does not occur due to fibrin degradation products.
The antithrombin III (AT III) activity and the AT III concentration were investigated in 62 consecutive patients with acute myocardial infarction (AMI). To identify the reactant pattern of AT III in postaggressive situations, we also determined labile and acute phase proteins. Firstly, 29 patients were nourished orally and then 33 patients were fed by i.v. hyperalimentation (additional caloric intake of approximately 1,000 cal). AT III activities and concentrations as well as prealbumin and retinol-binding protein decreased concomittantly and significantly whereas haptoglobin, C-reactive protein and fibrinogen increased significantly after AMI. The changes cannot be interpreted as being alterations of the haematocrit. The alterations of AT III correlated significantly with the changes of labile proteins but not with the acute phase reactant proteins. The AT III decrease in the postinfarctional phase may promote a prethrombotic state. In In addition it can be concluded from our results that AT III reacts as (nutritive-dependent) labile protein, which is lowered in postaggressive situation and does not increase as an acute phase reactant. This is in accordance with results from recent animal experiments.
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Following single doses of heparin and with continuous heparin infusion the activity of lipase in the serum increases temporarily and can attain pathological values also in healthy persons. Even when the heparin infusion is continued, the lipase values return after at the most 24 hours to the initial value before application of heparin. For a diagnosis of diseases of the pancreas the interpretation of lipase values in serum must consider how long the patient has been treated with heparin.
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