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Biomedical subjects

H Vinazzer

Publications and source records attributed to H Vinazzer.

At least 37 records · Page 2Linked to original sources
PubMed1988

Basics and practice in evaluating plasminogen.

There exist different ways of assays of plasminogen which give information about different properties of this proenzyme. The concentration of plasminogen can be determined by its antigenicity. Since the normal concentration of plasminogen in plasma is between 15 and 25 mg/dl the test can be carried out by simple methods such as radial immunodiffusion on Partigen plates. The possibility of errors is small and there is no need of special apparatus. The disadvantages are the lapse of 24 h until the result is available and the fact that the knowledge of the concentration does not give any information about the activity. The activity can be measured by different coagulation tests. A typical assay would involve activation of plasminogen to plasmin, addition of plasminogen-free thrombin and measuring of the lysis time. The result is however, dependent on more than one variable. Plasmin is rapidly inhibited by alpha-2-antiplasmin (APL) and there is also a dependence of the lysis time on the amount of clottable fibrinogen in the test system. Better results can be obtained by the use of diluted test plasma and addition of a constant amount of plasminogen-free fibrinogen. A different way would be the use of the euglobulin fraction instead of plasma. This has however, the possible disadvantage of incomplete precipitation of plasminogen. Instead of coagulation tests the activity can also be determined when diluted activated plasma is placed on plasminogen-free fibrin plates and the amount of lysis in the plate is recorded. All assays of this group also depend on the method of activation of plasminogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Tests↗
PubMed1988

New diagnostic possibilities for the detection of thrombophilic states.

A series of coagulation tests is described by which an increased thrombotic tendency is likely to be detected. These tests were carried out in 268 patients with venous thromboembolic disease and in 583 patients with arterial thrombotic manifestations. In venous thromboembolism alterations which point to hypercoagulability were found in 50% of all cases. Most frequent findings were a diminished availability of t-PA followed by low levels of Protein C, AT III and of Heparin cofactor II. In arterial thrombotic disease alterations of the clotting system were found in 77% of the patients. There was a high frequency of increased spontaneous platelet aggregation, of a diminished t-PA availability and of a combination of both alterations. Other abnormal results were rare with the exception of a diminished Heparin cofactor II which was found in 3% of the patients. The consequences which arise for prophylaxis and therapy when the defect is known are discussed.

Adult↗
PubMed1987

Heparin cofactor II: a simple assay method and results of its clinical application.

A simple assay method of heparin cofactor II (HC II) activity is described. The procedure is based on the following principle: Antithrombin III (AT III) in plasma is inactivated by addition of an IgG fraction of goat serum after immunization of the animals against human AT III. Complete inactivation of AT III could be shown by absence of an anti Xa-effect of heparinized plasma treated with this antibody. Thrombin was only partially inhibited after inactivation of AT III. The characteristics of this inhibition were typical for the action of HC II. This method was applied for an assay of HC II activity. After optimizing of the method practical application in clinical routine screening was carried out. A diminution of HC II was observed in liver cirrhosis and in DIC but not in AT III deficiency. In 15 out of 269 cases of recurrent DVT there were HC II activities below 70% of normal. In 4 out of these patients activities of HC II were repeatedly between 44% and 52%. In arterial obstructive disease there was an HC II activity of less than 60% in 18 out of 583 patients and in 11 of them the HC II levels were repeatedly between 45% and 54%.

Antithrombin III↗
PubMed1987

[Modification of eicosanoid synthesis by calcium dobesilate].

Calcium dobesilate is a vasoactive drug with well-known effects on endothelial integrity, vascular wall permeability and blood viscosity. A clinical study demonstrated that serum thromboxane formation is significantly decreased by calcium dobesilate in patients suffering from peripheral vascular disease. Hence an in vitro study has been undertaken to determine the influence of calcium dobesilate on eicosanoid formation both by platelets and the arterial wall. Radio-thin-layer chromatography (RTLC) of human platelets does not show any influence of the drug on eicosanoid conversion in a dose range from 10 to 1000 micrograms/ml. By contrast, the vascular conversion of eicosanoids shows a dose-dependent trend towards a decrease in cyclooxygenase products. However, using the same doses, no effect is observed on vascular PGI2 formation in vitro, as assessed by means of the platelet aggregation bioassay and thus no inhibitory effect on cyclooxygenase of the arterial wall can be deduced. These laboratory findings provide no explanation for the clinical efficacy of calcium dobesilate and the diminution in serum thromboxane. A different mode of metabolic conversion of endogenous and exogenous arachidonic acid is suggested as explanation for these contradictory results.

Arachidonic Acid↗
PubMed1987

[New methods of thrombolysis].

Different possibilities of clinical thrombolysis are described. The classical therapy with streptokinase has the disadvantages of antigenicity and of a considerable influence on the clotting system. For this reason new methods of thrombolysis were examined. Urokinase, plasmin and t-PA are physiological substances and have, therefore, no antigenicity. However, plasmin also has a considerable influence on the clotting system whilst coagulation is only moderately influenced by urokinase. This necessitates additional administration of heparin when the dose of urokinase is low. t-PA is adsorbed onto the fibrin clot in the same manner as plasminogen. Thereby both substances acquire a considerably higher affinity for each other. In addition, inactivation by physiological inhibitors is considerably diminished after adsorption. This causes an almost exclusive lysis of the clot without alterations of systemic coagulation. Clinical results after application of the newer thrombolytic drugs are presented.

Coronary Disease↗
PubMed1987

Protein C: comparison of different assays in normal and abnormal plasma samples.

Two assay methods for Protein C (PC) are described. Both tests are based on the activation of PC by a fraction of the venom of the Copperhead snake. Activated PC can be measured either by cleaving of a chromogenic substrate or by an APTT test. Both tests were compared with ELISA tests for PC. In 27 healthy persons the results were around 100% by all test systems when compared with normal pooled plasma. In 13 patients under stable anticoagulant therapy the average results were 54% for the ELISA and 52% for the chromogenic substrate test whilst the corresponding figures were 22% for the APTT test and 25% for the Quick test. In 4 cases of liver cirrhosis PC was diminished and there was no difference between the three tests. In two patients with congenital PC deficiency all results were close to 50% and in three patients the ELISA and the substrate tests were normal but the APTT test showed results of 44, 28 and 54% respectively. These results give rise to the conclusion that the snake venom activator is also capable of activation of decarboxylated PC molecules which can thereby split a chromogenic substrate but remain inactive in an APTT test.

Biological Assay↗
PubMed1987

Platelet function and prostaglandins in patients with peripheral vascular disease treated with calcium dobesilate.

In a double-blind placebo controlled study, 25 male patients (age range: 48-67 years) suffering from peripheral vascular disease were treated daily for 4 weeks with either 2 g of calcium dobesilate (n = 13) or placebo (n = 12). Different platelet and prostaglandin parameters were examined before and at the end of therapy. The number of circulating endothelial cells decreased significantly (4.9 +/- 2.9 to 2.0 +/- 1.9; p less than 0.0004). In addition, a decrease in serum TXB2 was noted (p less than 0.0001), but no significant change in plasma TXB2. The fibrinogen half-life was shortened (p less than 0.0001) and the platelet half-life was prolonged (p less than 0.04). The level of beta TG was decreased (p less than 0.006), but PF4 was unchanged. No alteration in the conversion of exogenous 14C-arachidonic acid by platelets to eicosanoids was observed. These observations indicate that calcium dobesilate is able to exert a favourable effect on some parameters of platelet function and prostaglandin synthesis which are important in the regulation of the hemostatic process. It is suggested that these pharmacological actions might explain, at least in part, the beneficial clinical effect of the drug.

Aged↗
PubMed1987

Clinical use of antithrombin III concentrates.

The biochemical and biological properties of antithrombin III (AT III) and the clinical consequences of a deficiency of this inhibitor are described. Therapy with concentrates of purified AT III has been carried out for about 10 years and the present experience is reviewed. In a relatively small number of patients with congenital AT III deficiency it is necessary, under certain condition to substitute AT III. A considerably more frequent use of AT III concentrates has been made in acquired AT III deficiency, especially in shock and diffuse intravascular coagulation (DIC). This therapy was shown to be promising since the duration of DIC could be considerably shortened and the frequency of fatal events could be significantly diminished. No undesirable side effects of substitution with virus-sterilized AT III concentrates have been hitherto observed.

Antithrombin III↗
PubMed1986

A new low molecular weight heparin fragment (PK 10169): in vitro and in vivo studies.

The depolymerized heparin fragment PK 10169 was compared with unfractioned mucosal sodium heparin. The inhibition of factors Xa and IXa by heparin and by PK 10169 was comparable on a weight base, whilst the inhibition of thrombin by PK 10169 was at least 5 times weaker than by heparin. Subcutaneous injection of PK 10169 was not followed by an increase of the thrombin time. The activated partial thromboplastin time was considerably less prolonged after PK 10169 than after heparin. Platelet count and platelet functions were not influenced by PK 10169. In vitro, the euglobulin lysis time (ELT) was shortened after addition of heparin to plasma but not after addition of PK 10169. After injection however, there was an equal shortening of the ELT by both substances. The half-life in circulation of PK 10169 was longer than the half-life of heparin. The advantages of PK 10169 over heparin are therefore the weaker influence on overall coagulation, the missing influence on platelet functions and the longer half-life in circulation.

Blood Coagulation↗
PubMed1986

[Clinical studies on the fibrinolytic action of pentosan polysulfate].

The influence on fibrinolysis of the heparin-like substance Polyanion SP 54 is described. In vitro tests showed an increase of fibrinolysis by activation of the endogenous pathway via factor XII and prekallikrein. In vivo an increase of the availability of tissue plasminogen activator was assumed in addition. When different ways of administration of Polyanion SP 54 were tested an enhancement of fibrinolysis was also found after oral application of the substance. In a long term test the stimulation of fibrinolysis after oral therapy did not diminish within 12 months. A trial on patients with cerebral ischemic attacks and diminished fibrinolysis is not yet concluded but permits the assumption of a considerable diminution of ischemic attacks during therapeutic use of Polyanion SP 54.

Administration, Oral↗
PubMed1986

[Laboratory control of fibrinolytic therapy].

The mode of action of the different thrombolytic substances which are presently available is described. Alterations of the clotting mechanism which are to be expected during thrombolytic therapy as well as possible side effects of the fibrinolytic drugs are listed. Laboratory tests necessary for the control of thrombolytic therapy as well as the different test methods and their normal ranges are mentioned in detail.

Blood Coagulation Tests↗
PubMed1985

A new low molecular weight heparin fragment (PK 10169): in vitro and in vivo studies.

The depolymerized heparin fragment PK 10169 was compared with conventional mucosal sodium heparin. The inhibition of factors Xa and IXa by heparin and by PK 10169 was similar on a weight base whilst the inhibition of thrombin by PK 10169 was at least 5 times weaker than by heparin. Subcutaneous injection of PK 10169 was not followed by prolongation of the thrombin time. The APTT was considerably less prolonged after PK than after heparin. Platelet reaction was increased by heparin but was not influenced by PK 10169. In vitro the euglobulin lysis time (ELT) was shortened after addition of heparin to plasma but not after addition of PK 10169. After injection, however, there was an equal shortening of the ELT by both substances. Advantages of PK 10169 over heparin are therefore a weaker anticoagulant effect and the missing influence on platelet functions.

Anticoagulants↗
PubMed1985

Substitution of antithrombin III in shock and DIC: a randomized study.

In 51 shock patients with DIC Antithrombin III (AT III) substitution, heparin or a combination of both substances respectively was administered. In the two groups which had been given AT III substitution the concentration of AT III rose considerably higher than the activity. There was a drop of the platelet count in both groups which had received heparin. C1 esterase inhibitor was diminished in the beginning but spontaneously increased in all groups. This increase was slowest in the group without substitution of AT III. The blood loss in cases of traumatic shock was considerably higher in the group which had received both substances. The consumption of AT III concentrates was slightly higher in the combined therapy group than in the AT III group. The duration of symptoms of DIC was considerably shorter in the two substituted groups than in the heparin group. It is concluded that additional administration of heparin does not improve the effect of AT III substitution in patients with DIC and that side effects such as thrombocytopenia and an increased blood loss are likely to develop when both substances are given simultaneously.

Antithrombin III↗
PubMed1984

[Comparison of the antilipemic effect of bezafibrate with that of piperazine-sultosilate (A 585). A crossed double-blind study].

In 20 patients suffering from primary hyperlipoproteinaemia the action of sultosilic acid piperazine salt (A-585) was compared with bezafribrate. In a double-blind cross-over study parameters of the lipoprotein metabolism, as well as of fibrinolysis and of platelet function were examined. Both drugs significantly diminished total cholesterol, triglycerides, beta- and pre-beta cholesterol whilst alpha-cholesterol increased. Moreover, both drugs caused a significant shortening of the euglobulin lysis time and a diminution of platelet adhesiveness. In patients under oral anticoagulants the thrombotest levels were not influenced by A-585, but were depressed by bezafibrate. A slightly elevated gamma-GT normalized during bezafibrate therapy but was not influenced by A-585.

Adult↗
PubMed1984

[Diagnosis of hypercoagulability].

Disturbances of the mechanism of coagulation are relatively frequent causes of thromboembolic disease, especially a diminution in activity of antithrombin III, a decrease in fibrinolytic potential and an increase in platelet functions. These activities were assayed in 512 patients who were in remission after thromboembolic events. Alterations of the clotting system reflecting hypercoagulability were detected in 40% of the patients investigated after venous thrombosis and in 61% to 89% of the patients after arterial thromboembolic events.

Antithrombin III Deficiency↗