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Biomedical subjects

L Róka

Publications and source records attributed to L Róka.

At least 19 recordsLinked to original sources
PubMed1991

Evaluation of an amidolytic test for comparative calibration of HMW- and LMW-heparins.

Amidolytic chromogenic substrate assays are frequently used to determine the anticoagulant activities of various commercial heparins. With the help of a combined assay method heparin characterization is made possible using the TAT/XAT quotient under consideration of the simultaneous inhibition of the two serine proteases thrombin and factor Xa by antithrombin III. The test is primarily designed for qualitative characterization where a numerical value can be assigned to every heparin. However, quantitative aspects may also be evaluated.

Amides↗
PubMed1989

Enzyme catalytic concentrations in human plasma after a marathon.

Blood was obtained from 11 males participating in the Berlin marathon 1986, directly before and after the marathon, and on the three following days. Several observations were made: a) catalytic concentrations (activity) of creatine kinase (CK), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (AP) increased directly after the marathon or on the three following days; b) Cholinesterase (CHE), amylase (AML) and gamma glutamyltransferase (GGT) decreased directly after the marathon; c) the time course of AP and LDH isoenzyme activity after the race indicated an elimination from plasma to lower values than those originally observed before the run.

Alanine Transaminase↗
PubMed1984

Fructose 1,6-bisphosphatase in the diagnosis of chronic hepatitis. I. Activity measurements of fructose 1,6-bisphosphatase in human serum.

In this communication, we propose a method for the determination in human serum of fructose 1,6-bisphosphatase based on parallel measurements of enzyme activities in presence of 1-p-bromotetramisole oxalate and adenosine 5'-monophosphate. The employment of these specific inhibitors renders the discrimination between specific and non-specific activities feasible. A regression analysis identifies fructose 1,6-bisphosphatase (EC 3.1.3.11) as the origin of the specific and alkaline phosphatase (EC 3.1.3.1) as the source of the non-specific fructose 1,6-bisphosphate dephosphorylating activities. This procedure lends itself to the diagnosis using serum samples of 'piecemeal' necrosis in liver disease.

Adenosine Monophosphate↗
PubMed1984

Fructose 1,6-bisphosphatase in the diagnosis of chronic hepatitis. II. Classification of chronic hepatitis based on fructose 1,6-bisphosphatase and other laboratory data.

The histomorphology of typical liver cell necroses are here correlated with heterotope distributions of enzymes in liver parenchyma. A variety of findings indicate a congruence between gluconeogenetic areas of the liver and the typical pattern of 'piecemeal' necrosis. We therefore propose a diagnostic index based on fructose 1,6-bisphosphatase activity and the data from the clinical laboratory. This index makes it possible to distinguish between chronic persistent and chronic aggressive hepatitis.

Acute Disease↗
PubMed1984

Detection of organic hydroperoxides in rabbit lung lavage fluid, but not in lung tissue homogenate, using GSH peroxidase and GSH reductase.

A specific method for the detection of organic hydroperoxides in lung lavage fluid (lung surfactant system) and lung tissue homogenate is described. After the inactivation of endogenous GSH peroxidase and GSH reductase and preincubation with catalase, organic hydroperoxides are consumed by addition of GSH and GSH peroxidase. The increase of GSSG, compared to a blank without addition of GSH peroxidase, is measured in a second enzymatic step with GSH reductase. The recoveries of t-butyl hydroperoxide and of peroxidized, free fatty acids added to lavage fluid or to lung homogenate are higher than 85% in each case. The detection limits of this assay for organic hydroperoxides are 0.9 nmol/mg surfactant phospholipid (molar ratio of 0.00066) and 40 nmol/g wet lung weight. The assay detects organic hydroperoxides in the surfactant system of normal rabbit lungs, but not in lung tissue homogenate.

Animals↗
PubMed1984

Creatine kinase isoenzyme MB determination on the ACA: dependence on serum matrix and other effectors.

Creatine kinase isoenzyme MB catalytic activities in human serum, determined by ACA ion exchange chromatography and immunoinhibition, differ significantly, the correlation coefficient being 0.88. The reasons for this variation are interference of antibodies with the creatine kinase B subunit in the immunoinhibition assay, nonreproducible elution of creatine kinase isoenzyme MB from the ion exchange resin in the ACA pack, due to varying protein concentrations in the serum samples and increasing elution of creatine kinase isoenzyme MM from the ion exchange column caused by a preceding partial inactivation of creatine kinase isoenzyme MM. Pretreatment of serum samples with a solution containing magnesium sulphate, maleate and 2-oxoglutarate (solution A) prior to determination of creatine kinase isoenzyme MB catalytic activities on the ACA significantly improves the sensitivity and specificity of the method; the correlation coefficient for the values from the ACA and immunoinhibition then becomes 0.92. Dilution of serum samples with bovine serum albumin solution is now practicable.

Aspartate Aminotransferases↗
PubMed1984

[Effect of heparin on platelet aggregation in vitro].

Heparin added to citrated platelet rich plasma influences shape change and aggregation of platelets in different ways. In the presence of heparin neither ADP nor collagen induces shape change, while shape change after thrombin or arachidonic acid remains unaltered. Heparin potentiates the first aggregation step induced by ADP and epinephrine but inhibits aggregation induced by thrombin and ristocetin. The second phase of aggregation and the release reaction are not directly influenced by heparin no matter which aggregation agent is used.

Adenosine Diphosphate↗
PubMed1982

Increased pulmonary vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lungs.

Liberation and metabolism of arachidonic acid may be the common final pathway of different stimuli on the pulmonary vascular bed. In a model of isolated, ventilated rabbit lungs, perfused with Krebs Henseleit albumin buffer in a recirculating system, changes of pulmonary vascular resistance and of vascular permeability are monitored continuously. The addition of free arachidonic acid or of the Ca-ionophore A 23187 to the perfusion fluid consistently evokes a biphasic increase in vascular resistance as well as an initially reversible increase in vascular permeability, followed by pulmonary edema. Both phases of increased vascular resistance are completely suppressed by inhibition of the cyclooxygenase, decreased to a large degree by inhibitors of thromboxane synthetase, and markedly augmented by short preincubation of arachidonic acid with ram seminal vesicular microsomes and by sulfhydryl reagents. The increased pulmonary vascular permeability is augmented by inhibition of cyclooxygenase and reduced by simultaneous lipoxygenase inhibition. Antagonists of histamine, serotonin and sympathic or parasympathic activity do not have any influence. PG F2alpha., TxB2, PG E2 and PG I2 alter the pulmonary vascular resistance, but do not increase vascular permeability. In conclusion, increased availability of free arachidonic acid evokes a rise in pulmonary vascular resistance, which can be ascribed to cyclooxygenase products, especially to thromboxane, and causes a rise in vascular permeability which can be ascribed to lipoxygenase products. The findings may be related to acute pulmonary lesions with increase in vascular resistance and with vascular leakage.

Animals↗
PubMed1982

Influence of tocopherol, its chromane compound, phytyl chains and superoxide dismutase on increased vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lung.

In the model of isolated, ventilated rabbit lungs, perfused with isoionic and isooncotic fluid, the addition of arachidonic acid to the perfusion fluid or the liberation of arachidonic acid by the Ca-ionophore A 23187 result in an increase in pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products, the latter to lipoxygenase products of arachidonic acid. The effect of alpha-tocopherol, its chromane compound, alpha-tocopherolquinone, phytol, 2-methyl-1,4-naphthoquinone, 2-methyl-3-phytyl-1,4-naphthoquinone and of superoxide dismutase (SOD) on the increase in pulmonary vascular resistance and permeability was investigated. A membrane effect of the phytyl side chain and an antioxidative effect of the chromane compound can be distinguished: phytol increase the arachidonate-induced rise of pulmonary vascular resistance and permeability, whereas the chromane compound decreases both to a large degree. Methyl-phytyl-naphthoquinone and methyl-naphthoquinone gave equivalent results. SOD decreases the enhanced vascular resistance and the vascular leakage. The possibility of antioxidative therapy in acute pulmonary lesions with vascular leakage and increased vascular resistance is discussed.

Animals↗
PubMed1981

[Increase of pulmonary vascular resistance and permeability due to the metabolism of free arachidonic acid (author's transl)].

Release and metabolism of arachidonic acid are supposed to form the common final pathway of different stimuli on the pulmonary vascular endothelium. In a model of isolated, ventilated and perfused rabbit lungs we investigated the influence of increased availability of free arachidonic acid on pulmonary vascular resistance and permeability. Addition of arachidonic acid to the perfusion fluid or release of arachidonic acid by Ca-ionophore A 23187 regularly produces a characteristic biphasic increase of the pulmonary vascular resistance as well as a continuous increase in permeability, followed by pulmonary edema. Inhibition of cyclooxygenase by indomethacin prevents the augmentation of vascular resistance, the increase of vascular permeability however is enhanced. thus the raise in pulmonary vascular resistance can be ascribed to cyclooxygenase products, the increased pulmonary vascular permeability to lipoxygenase products of arachidonic acid.

Animals↗
PubMed1981

[The antioxidative chromane structure of alpha-tocopherol protects against the consequences of arachidonic acid release in the pulmonary vascular bed (author's transl)].

In the model of isolated, ventilated and perfused rabbit lungs release of arachidonic acid results in an increase of pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products, the latter to lipoxygenase products of arachidonic acid. The effect of alpha-tocopherol on the increase of pulmonary vascular resistance and permeability either after the addition of arachidonic acid to the perfusion fluid or after stimulation of arachidonic acid liberation by Ca-ionophore A 23187 was investigated. It is possible to distinguish a membrane effect of the phytol side chain of alpha-tocopherol and an antioxidative effect of its chromane structure: Phytol augments the increase of pulmonary vascular resistance and permeability, whereas the chromane-structure decreases both to a large degree. The possibility of antioxidative therapy in disturbances of pulmonary vascular permeability is discussed.

Animals↗