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H Vinazzer

Publications and source records attributed to H Vinazzer.

At least 19 recordsLinked to original sources
PubMed1979

[Heparin assay in plasma. Comparison of different methods (author's transl)].

Four different heparin assay methods were compared. Only procedures which can be routinely carried out in clinical laboratories were taken into consideration. A range of heparin concentrations was chosen for these tests which is likely to be expected in low dose heparin prophylaxis. The lowest sensitivity was found when the thrombin clotting time was applied, and slightly better results were obtained by the aPTT method. Addition of purified antithrombin III to the reaction mixtures improved the sensitivity of both methods. When factor Xa was used in a clotting test, the results were comparable to the aPTT method. The sensitivity was however, about 10 times higher when the remaining factor Xa was directly measured in a photometric assay system with a chromogenic substrate. The advantages and disadvantages of the different methods and the usefulness of heparin assays for clinical purposes are discussed.

Antithrombin III↗
PubMed1979

[Clinical-experimental studies on the inhibition of thrombocyte function with acetylsalicylic acid and with indobufen].

The mode of action of two inhibitors of platelet function is reported. At low doses both substances inhibit platelet aggregation, at higher doses they inhibit the availability of platelet factor 3 and liberation of platelet factor 4. Acetylsalicylic acid, however, possesses a long-lasting effect produced by irreversible acetylation of platelet membrane. This was demonstrated in a series of clinico-experimental studies in which 14C-labelled ASA was used. Indobufen was found to cause transitory changes of platelet function. It is easily washed out from platelets and binds loosely to cytosol proteins of platelets, as shown in studies with 14-C-labelled indobufen. In contrast to ASA, it exerts an effect on platelets lasting for a few hours only.

Aspirin↗
PubMed1978

[Effect of heparin and ASA on changes of haemostasis induced by venous occlusion (author's transl)].

The influence of venous occlusion on plasmatic coagulation, on platelets, and on fibrinolysis was examined. After occlusion, activated factors XI and X could be demonstrated. Simultaneously, platelet aggregation induced by both collagen and epinephrine was increased. Fibrinolysis was found to be moderately enhanced. In patients taking acetylsalicylic acid (ASA), platelet functions were not altered by occlusion but the activation of plasmatic clotting factors was not influenced. Low dose heparin inhibited plasmatic activation but had no influence on the increase of platelet activities. By simultaneous administration of both substances, an additive effect was observed resulting in inhibition of plasmatic and platelet activation due to venous occlusion.

Adult↗
PubMed1978

Uptake by blood components and by subcellular platelet fractions of 1-14C-acetylsalicylic acid.

1-14C-Acetylsalicylic acid was used to study the distribution and the kinetics of the acetyl group in blood components. Tests were carried out in 4 patients in vivo and on four blood samples in vitro. At various intervals after tagging, whole blood, plasma, platelets and platelet fractions were examined. In vitro, relative activity was found to be higher in platelets than in all other blood components. When platelet fractions were examined, the highest specific activity was found in membranes. In vivo, rapid disappearance of activity from circulation was observed. The decrease of activity was slower in platelets than in whole blood and in plasma. The highest specific acitivty was again found in platelet membranes. The half-life of the 14C tag was measured in all components. It was found to be longest in platelet membranes where it corresponded to the half-life of platelets in circulation. From the results obtained, the conclusion was drawn that irreversible acetylation of the platelet membrane must be considered to be one of the main causes of platelet dysfunction induced by acetylsalicylic acid.

Aspirin↗
PubMed1978

A simplified assay method for platelet factor 4 in plasma and in platelets with a chromogenic substrate.

A simple assay method for platelet factor 4 is described. When factor Xa was added to a system containing antithrombin III in excess and heparin in low concentration, the amount of factor Xa immediately inactivated was found to be a function of the concentration of heparin. When an antiheparin such as platelet factor 4 was added, an increase of the residual activity of factor Xa was observed. The magnitude of this increase was shown to be correlated to the amount of heparin inactivation in the system. Platelet factor 4 could be assayed when the concentrations of antithrombin III, heparin, and factor Xa were maintained at a constant level and in excess. As an indicator of the reaction, factor Xa was measured with the chromogenic substrate benzoyl-Ile-Gou-Gly-Arg-p-nitroanilide (S-2222).

Blood Coagulation Factors↗
PubMed1977

Photometric assay of platelet factor 4 with a chromogenic substrate.

A photometric assay procedure for platelet factor 4 is described. The synthetic oligopeptide benzoyl-Ile-Glu-Gly-Arg-p-nitroanilide (S-2222) is used as a substrate. By the action of factor Xa, p-nitroaniline (pNA) is split form the peptide bond. The amount of pNA liberated from S-2222 per minute is in direct relation to the activity of factor Xa. This reaction permits a photometric assay. Addition of heparin to an activation system consisting of plasma, thromboplastin and calcium chloride inhibits development of Xa activity. Since platelet factor 4 neutralizes heparin, its activity can be measured in such a system when all other components are kept at a constant level. Experimental details of the reactions involved and clinical results of the assay in comparison to a clotting method are described.

Anilides↗
PubMed1977

On the interaction between the anti-inflammatory substance proquazone (RU 43-715) and phenprocoumone.

In a double blind study on 20 anticoagulated patients, the influence of the anti-inflammatory drug 1-isopropyl-4-phenyl-7-methyl-2 (1H) quinazolone on the degree of hypocoagulability was examined. In comparison to a placebo group, there was no statistical difference in the Quick precentage, in coagulation factors II, VII, and X, and in platelet aggregation induced by collagen and by epinephrine respectively. In addition, no increased bleeding tendency could be observed during the study.

4-Hydroxycoumarins↗
PubMed1977

[Autotransfusion].

Explore the source record for details and available documents.

Blood Preservation↗
PubMed1976

Dose-dependent influence of acetylsalicyclic acid on platelet functions and plasmatic coagulation factors.

Lysine salt of acetylsalicylic acid (ASA) was given to ten patients by intravenous infusion. Blood samples taken at intervals during the infusion permitted the examination of the influence of the dose of ASA on platelet functions. Aggregation was significantly reduced when 50 mg ASA had entered circulation, while a diminution of PF3 and PF4 availability could only be demonstrated when the dose had reached 500 and 200 mg, respectively. In order to exclude a longer latency time for the diminution of PF3 and pf4 availability, a second series of ten patients received intravenous injections of 100 and 300 mg ASA, respectively. From these patients, blood was taken 1 h after the injection. The decrease of PF3 and PF4 availability in these cases was comparable to the results of the first group. In a third series of patients, a daily intravenous dose of 2,000 mg ASA was given. In these cases, a moderate decrease of factors II, VII, IX and X was observed. Since the appearance of a PIVKA effect could also be demonstrated, vitamin K antagonism was assumed when a high dose of AS

Adult↗