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C A Demopoulos

Publications and source records attributed to C A Demopoulos.

At least 37 records · Page 2Linked to original sources
PubMed1994

Platelet-activating factor acetylhydrolase (PAF-AH) in human kidney.

1. PAF-AH activity in human kidney (cortex and medulla) has been demonstrated and shares the following properties. 2. Does not require the presence of Ca2+ and appears to be different from phospholipase A2. 3. The pH optimum shows a peak at 7-7.4. 4. It is stable for 4 days at -30 degrees C. 5. It is mainly distributed in the microsomal fraction. 6. The apparent Km values of the enzymes of cortex and medulla are 0.553 and 0.207 microM, respectively and distinct from serum PAF-AH (1.439 microM). 7. The apparent molecular weight values are 60,000 and 25,000 for medulla and cortex, respectively and distinct from serum PAF-AH (94,000).

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1993

Inhibition by cardiolipins of platelet-activating factor-induced rabbit platelet activation.

Evidence is presented that cardiolipin, a naturally occurring phospholipid, inhibits the aggregatory effect of platelet-activating factor (paf) on rabbit platelets in vitro. Bovine heart cardiolipin was shown to inhibit the aggregation of washed rabbit platelets induced by 1 x 10(-10) M and 2 x 10(-10) M paf with IC50 values (doses for half-maximal inhibition) of 8.4 +/- 0.8 x 10(-7) M and 2.6 +/- 0.6 x 10(-6) M, respectively. Phosphonocardiolipin was also able to inhibit platelet aggregation induced by 1 x 10(-10) M paf with an IC50 value of 3 +/- 1 x 10(-7) M. Both compounds, in concentrations up to 1 x 10(-5) M, were unable to aggregate washed rabbit platelets and failed to inhibit the aggregation induced by 0.9 and 1.8 microM adenosine diphosphate or 0.2-1.0 microM arachidonic acid. By contrast, the acetylated derivative of cardiolipin exerted an aggregatory effect on aspirin-treated rabbit platelets in the presence of creatine phosphate/creatine phosphokinase. This aggregation was inhibited by the specific paf antagonists BN 52021 and WEB 2086. Also, platelets treated with acetyl-cardiolipin were insensitive to the aggregatory effect of paf. Phosphatidic acid, phosphatidylglycerol, bis(dipalmitoylglycero)phosphate and their phosphono analogues were totally inactive. Similar data were obtained when platelet-rich plasma was used instead of washed rabbit platelets. Our results support the hypothesis that the effect of cardiolipin is mediated through specific paf receptors that act on the rabbit platelet membrane.

Animals↗
PubMed1992

Study of the glycogenolytic action of platelet activating factor in Tetrahymena pyriformis.

1. A novel action of AGEPC on non-inflammatory cells was revealed, namely the ability to stimulate glycogenolysis in Tetrahymena pyriformis cells. 2. The glycogenolytic effect of AGEPC seems to be dependent on Ca2+ transport and regulation, thus the effects are completely inhibited by Verapamil and partially by EGTA. 3. The influence of Propranolol, Labetalol, Atenolol and Theophylline in the glycogenolytic effect of AGEPC are also studied. 4. Our findings suggest that the AGEPC promoted glycogenolysis in Tetrahymena through a mechanism distinct from that of catecholamines.

Animals↗
PubMed1988

Abnormal platelet response to PAF and ADP in beta-thalassaemia.

1. AGEPC (2 microM) caused a noticeable increment in platelet aggregation, in increasing order, in 9 heterozygous beta-thalassaemic subjects, 18 homozygous beta-thalassaemics and 12 splenectomized homozygous beta-thalassaemics. 2. Recombination experiments with "patient" platelets and "normal" plasma or the reverse, as well as hydrolysis of labelled AGEPC from "normal" and "patient" serum, suggested that the observed abnormalities were due to platelets rather than to the plasma PAF hydrolase. 3. A normal splenectomized subject showed also hyperaggregability and PAF serum levels in a splenectomized patient were found twice as high in a non-splenectomized patient. 4. ADP (5 microM) caused decreased or normal platelet aggregation in the homozygous patients, approximately normal in the heterozygous subjects and increased in the splenectomized patients.

Adenosine Diphosphate↗
PubMed1988

Study of digoxin as inhibitor of the in vivo effects of acetyl glyceryl ether phosphorylcholine (AGEPC) in mice.

Acetyl glyceryl ether phosphorylcholine (AGEPC) and the cardiac glycoside digoxin were administered intravenously through the tail vein into ether-anesthetized SWR mice (two months old). The administered doses were 0.18 nmol AGEPC/g b.w. (a lethal one) and 75 or 125 ng digoxin/b.w. Digoxin ameliorates the effects of the lethal dose of AGEPC showing maximum activity when given 5 or 10 min after AGEPC administration to female and male animals respectively. Digoxin shows also a protective action towards the effects of AGEPC and maximum activity appears when it is given 10 min before AGEPC administration. In agreement with the picture of increased survival in digoxin pretreated animals, are our findings on life prolongation of mice which finally die from AGEPC, the amelioration of the expected fall in blood platelet counts after AGEPC administration as well as the improved performance of the animals in a series of physical tests.

Animals↗
PubMed1987

Electrocardiographic alterations induced by AGEPC in Wistar rats in relation to its hypotensive and hematologic effects.

AGEPC administration into Wistar rats caused no remarkable thrombocytopenia, slight decrease of the percent count of PMNs in whole blood accompanied by anequal leukocytopenia and a transient increase in hematocrit, due to fluid extraversion. Apart from the dramatic fall in blood pressure caused by AGEPC, relatively sinus bradycardia was recorded at doses over 6 micrograms/kg b.w. S-T segment elevation, mainly evident in II, III and AVF leads, was also recorded within the first minutes after AGEPC administration, at doses over 1 microgram/kg b.w. At lethal doses, various degrees of A-V block resulting in complete A-V block with idioventricular rhythm, or injury pattern resulting in ventricular fibrillation or ventricular flutter, were recorded. At sublethal doses no arrhythic manifestations were recorded, while S-T segment elevation upward inversion became gradually normal.

Animals↗
PubMed1986

Effects of AGEPC on the intracellular levels of ions in Tetrahymena pyriformis.

1-0-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine(Platelet Activating Factor) is a very potent stimulator of Ca2+ influx into the cells of Tetrahymena pyriformis; increases the levels of bound and free intracellular Ca2+ and this effect is time- and dose-dependent. Also AGEPC enhances the Na+ influx into the cells, while has no effect on the intracellular levels of K+ and on the packed cell volume. The effects of AGEPC on intracellular Ca2+ and Na+ are completely inhibited by verapamil which also inhibits the Ca2+ influx observed in the control, but has not any effect on the Na+ uptake observed in the control. These results provide evidence that the effect of AGEPC on Na+ influx, depends on its effect on free intracellular Ca2+. The non acetylated derivative of AGEPC, lyso-GEPC has no effect on all the studied parameters.

Calcium↗
PubMed1986

Biological activity of lipids of pine pollen on platelet aggregation in correlation with the platelet activating factor.

Pollen lipids of a pine species were separated by thin layer chromatography systems. The purified neutral and polar lipid classes were examined for their possible platelet aggregation activity and for their effect on Platelet Activating Factor activity. The lipid fraction comigrating on thin layer chromatography with glycerylether standards was shown to have a remarkable inhibition of Platelet Activating Factor activity on washed rabbit platelets in a concentration of 4.5.10(-6) M. At a ten fold higher concentration these lipids also induced platelet aggregation.

Animals↗
PubMed1981

Intravascular pathobiology of acetyl glyceryl ether phosphorylcholine (AGEPC), a synthetic platelet-activating factor (PAF). I. Intravenous infusion in guinea pigs.

Intravenous infusion of 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (AGEPC), a synthetic platelet-activating factor (PAF), induced fatal anaphylactoid reaction in guinea pigs, or reversible thrombocytopenia and leucopenia. These reactions showed a maximal depression of circulating platelet and leucocyte numbers within 30 s after AGEPC infusion. Fatal reaction occurred at doses higher than 0.81 micrograms AGEPC/kg, while lower doses of AGEPC caused a reversible thrombocytopenia and leucopenia. The levels of circulating platelets and leucocytes at lower - non-fatal - doses of AGEPC, returned to pre-infusion levels within 60 min. These studies document that intravenous administration of AGEPC, into guinea pigs, initiates identical intravascular infusion of AGEPC into the rabbit and baboon, and supports the notion that the biological activity of AGEPC can cross species barriers.

Anaphylaxis↗
PubMed1980

Identification of platelet activating factor isolated from rabbit basophils as acetyl glyceryl ether phosphorylcholine.

Platelet activating factor obtained from antigen-stimulated rabbit buffy coat leukocytes containing 10% IgE-sensitized basophils was shown by gas-liquid chromatographic and mass spectrometric analysis of products after acetolysis and by base and acid hydrolysis to be acetyl-alkylglyceryl phosphorylcholine. The alkyl side chains were composed of octadecyl (greater than 90%) and hexadecyl (less than 10%) residues.

Animals↗