PubMed Health⌕ Search

Biomedical subjects

W Lösche

Publications and source records attributed to W Lösche.

69 records · Page 4Linked to original sources
PubMed1984

Effect of acetylsalicylic acid on glutathione consumption and hexose monophosphate shunt during arachidonic acid induced stimulation of human blood platelets.

Aggregation of human blood platelets by exogenous arachidonic acid is accompanied by a powerful increase in the net flux through the hexose monophosphate shunt and a decrease of the level of reduced glutathione. When platelet cyclooxygenase is inhibited by acetylsalicylic acid diminution by about 60% of arachidonic acid induced flux through the hexose monophosphate shunt as well as lower initial decrease of the glutathione level are found. Investigations with other glutathione oxidizing agents as diamide or tertiary butyl hydroperoxide reveal that acetylsalicylic acid influences neither the activities of glutathione providing enzymes nor that of glutathione peroxidase which catalyzes glutathione consuming reactions in the arachidonic acid metabolism. Together with literature data the results point to a consumption of reduced coenzymes in both cyclooxygenase and lipoxygenase pathways in platelets.

Arachidonic Acid↗
PubMed1983

Effect of compounds causing reversible perturbation of the cellular thiol-disulfide status on the aggregation of human blood platelets.

Diamide, cumene hydroperoxide, t-butyl hydroperoxide and divicine are compounds which cause a reversible oxidation of cellular SH groups. They influence the aggregation of human platelets in a common manner when added to platelet rich plasma, simultaneously with different types of aggregation inducer: (1) The initial phase of aggregation becomes accelerated. This is accompanied by a more sensitive response to the inducer. (2) The aggregation becomes reversible. The accelerated initial phase of aggregation is followed by a switchover to deaggregation. Addition of diamide to platelet suspensions results in an immediate and fast diminution of the platelet GSH level. Extent and duration of the GSH fall depend on the diamide concentration used. The time courses found for the platelet GSH level suggest a causal connection with the altered aggregation response. Therefore, the conclusion is drawn that perturbation of the cellular thiol-disulfide status influences a fundamental and common part of the platelet activation sequence.

Arachidonic Acid↗
PubMed1983

Differences in morphology and protein pattern of human blood platelets during irreversible and diamide mediated reversible aggregation.

Morphological alterations of platelets during reversible aggregation mediated by diamide are compared with those observed during irreversible aggregation. Diamide prevents cell fusion and the formation of loop-like structures which probably arise from fusing plasma membranes. Differences in the protein pattern of platelets after reversible and irreversible aggregation suggest a specific involvement of SH-proteins in irreversible platelet aggregation. The diamide mediated alterations of platelet aggregation behaviour are transitory, i.e. reversibly aggregated platelets respond normally to a new addition of aggregation inducers without and with diamide, respectively.

Arachidonic Acid↗
PubMed1981

Effect of arachidonic acid on the hexose monophosphate shunt and related coenzymes in human blood platelets.

The aggregation of human platelets after addition of arachidonic acid (AA) is accompanied by a 30 fold increase in the net flux through the hexose monophosphate shunt (HMPS). The levels of reduced glutathione (GSH) and NADPH as well as the NADPH/NADPH+NADP quotient show a temporary fall which is restricted to the interval between AA addition and beginning of aggregation suggesting a lag phase between the onset of enhanced coenzyme consumption and that of increased coenzyme regeneration. together with literature data the results point to a possible regulatory function of reduced coenzymes and the HMPS in the process of platelet activation.

Arachidonic Acid↗
PubMed1981

Red cell response to A23187 and valinomycine in Duchenne muscular dystrophy.

Treatment of red cells from Duchenne muscular dystrophy (DMD) patients with A23187 induced identical responses with those in controls in terms of Ca++ flux, shrinkage, ATP depletion, hypotonic lysis protection, and glycolysis stimulation. The level of RC-free calcium seemed not to be altered in DMD. Valinomycine-induced shrinkage was enhanced significantly in DMD red blood cells.

Anti-Bacterial Agents↗
PubMed1981

Glucose-6-phosphate dehydrogenase deficiency in human platelets and its effect on platelet aggregation.

Platelets from patients with known red blood cell G-6-PD deficiency were investigated to find out whether this genetic defect is associated with changes in platelet aggregation. The enzyme defect in platelets could be verified by a decreased G-6-PD activity which was as low as 15% compared to control subjects. The decreased enzyme activity was reflected by lowered levels of NADPH and GSH and by a diminished maximum capacity of the hexose monophosphate shunt. Aggregation measurements in platelet-rich plasma from deficient patients revealed an enhanced dose response to ADP which was higher by about one order of magnitude compared to controls. The same effect was observed in a smaller degree in arachidonic acid induced aggregation.

Blood Platelets↗
PubMed1980

Anticoagulant-free prepared blood platelets and the effect of calcium on their aggregation behaviour.

Human blood platelets were prepared by gel filtration of native blood and subsequent centrifugation in a Ficoll density gradient avoiding any anticoagulant during the preparation. In ADP, ionophore A 23 187 and thrombin induced aggregation an increase in extracellular Ca++ enhanced the velocity of aggregation. From a defined Ca++ concentration threshold on there was a shift from monophasic to biphasic aggregation.

Adenosine Diphosphate↗
PubMed1979

[Preparation of human platelets without the use of anticoagulants and study of the effect of Catt on aggregation].

A method for the preparation of human blood platelets is presented which substitutes the use of anticoagulants by a gelfiltration for the removal of plasma calcium from native blood. In a second step the platelets are separated from the gel filtered blood by a centrifugation on a Ficoll density gradient. The anticoagulant-free platelets reveal an intact morphological feature and a normal aggregation behaviour in response to different aggregation inducers. It was found that in ADP-induced aggregation monophasic aggregation is shifted to a biphasic one by increasing concentrations of extracellular calcium.

Blood Platelets↗