Diminished production of thromboxane B2 and prostaglandin E by stimulated polymorphonuclear leukocytes from insulin-treated diabetic subjects

Diabetes ◽  
1983 ◽  
Vol 32 (7) ◽  
pp. 622-626 ◽  
Author(s):  
R. Qvist ◽  
R. G. Larkins
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Thromboxane B2 ◽  
Prostaglandin E

scholarly journals Thromboxane generation by human peripheral blood polymorphonuclear leukocytes.

1978 ◽  
Vol 148 (3) ◽  
pp. 787-792 ◽  
Author(s):  
I M Goldstein ◽  
C L Malmsten ◽  
H Kindahl ◽  
H B Kaplan ◽  
O Rådmark ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Gas Chromatography ◽  
Arachidonic Acid ◽  
Thin Layer ◽  
Peripheral Blood ◽  
Polymorphonuclear Leukocytes ◽  
Cytochalasin B ◽  
Human Peripheral Blood ◽  
Thromboxane B2 ◽  
Cyclooxygenase Inhibitor

Human peripheral blood polymorphonuclear leukocytes were stimulated to generate thromboxane B2 in a time- and concentration-dependent fashion upon exposure to serum-treated zymosan particles. Conversion by stimulated PMN of [14C] arachidonic acid to [14C]thromboxane B2 was confirmed by thin-layer radiochromatography, radio-gas chromatography, and mass spectrometry. Generation of thromboxane B2 was independent of platelet contamination and could be inhibited by the cyclooxygenase inhibitor, indomethacin. Cells rendered incapable of ingesting particles by treatment with cytochalasin B generated comparable amounts of thromboxane B2. These results suggest that human peripheral blood polymorphonuclear leukocytes synthesize thromboxanes in response to surface stimulation independently of phagocytosis.

Decreased systemic formation of prostaglandin E and prostacyclin, and unchanged thromboxane formation, in alcoholics during withdrawal as estimated from metabolites in urine

1987 ◽  
Vol 73 (3) ◽  
pp. 277-283 ◽  
Author(s):  
Ulrich Förstermann ◽  
Thomas J. Feuerstein
Keyword(s):  
Hydrolysis Product ◽  
Thromboxane A2 ◽  
Normal Subjects ◽  
Thromboxane B2 ◽  
Urinary Metabolite ◽  
Prostaglandin E ◽  
Dioic Acid ◽  
Control Subjects ◽  
Major Urinary Metabolite ◽  
Prostaglandins E1 And E2

1. The rates of secretion into the circulation of prostaglandin E, prostacyclin, and thromboxane A2 were estimated in male alcoholics on the third day of withdrawal and in control subjects by measuring appropriate metabolites in urine. 2. Urinary levels of tetranor-5,11-diketo-7α-hydroxyprostane-1,16-dioic acid (the major urinary metabolite of prostaglandins E1 and E2), of 2,3-dinor-6-ketoprostaglandin F1α (the major urinary metabolite of prostacyclin) and of 6-keto-prostaglandin F1α (the stable hydrolysis product of prostacyclin) were significantly different from the normal subjects in the alcoholic group. In contrast, 2,3-dinor-thromboxane B2 (the major urinary metabolite of thromboxane A2) and thromboxane B2 (the stable hydrolysis product of thromboxane A2) were not significantly different between the groups. 3. These data suggest that the ratio of the vasodilator prostanoids prostaglandin E and prostacyclin and the vasoconstrictor prostanoid thromboxane A2 is lower than in normal subjects, in alcoholics during withdrawal. This may be one causal factor for the higher incidence of hypertension observed in withdrawing alcoholics compared with control subjects.

Cell-Bound C3b Stimulates Human Monocyte Release of Prostaglandin E and Thromboxane B2

1987 ◽  
Vol 41 (4) ◽  
pp. 363-366 ◽  
Author(s):  
David E. Fulford ◽  
R. Bruce Rutherford
Keyword(s):  
Human Monocyte ◽  
Thromboxane B2 ◽  
Prostaglandin E

PROSTAGLANDIN E, THROMBOXANE B2 AND 6-OXO-PROSTAGLANDIN F1α IN AMNIOTIC FLUID AND MATERNAL PLASMA OF RHESUS MONKEYS (MACACA MULATTA) DURING THE LATTER THIRD OF GESTATION

1979 ◽  
Vol 81 (3) ◽  
pp. 345-349 ◽  
Author(s):  
J. S. ROBINSON ◽  
R. NATALE ◽  
L. CLOVER ◽  
M. D. MITCHELL
Keyword(s):  
Rhesus Monkey ◽  
Amniotic Fluid ◽  
Macaca Mulatta ◽  
Rhesus Monkeys ◽  
Maternal Plasma ◽  
Thromboxane B2 ◽  
Prostaglandin E ◽  
Peripheral Plasma ◽  
Prostaglandin F ◽  
Serial Samples

The concentrations of prostaglandin E (PGE), thromboxane B2 (TXB2) and 6-oxo-prostaglandin F1α (6-oxo-PGF1α) were measured by radioimmunoassay in serial samples of amniotic fluid and maternal peripheral plasma in the latter third of pregnancy in rhesus monkeys (Macaca mulatta). The samples were collected under ketamine-induced anaesthesia. The concentration of PGE was undetectable in amniotic fluid until a few days before delivery when a large increase was observed in three of the five animals. There were small increases of TXB2 and 6-oxo-PGF1α in amniotic fluid before delivery. In maternal plasma the concentrations of PGE, TXB2 and 6-oxo-PGF1α were generally higher and more variable than in amniotic fluid and did not increase with advancing gestation. It is suggested that increased production of primary prostaglandins occurs before, and is involved in, the onset of parturition in the rhesus monkey.

Platelet activation by polymorphonuclear leukocytes exposed to chemotactic agents

1990 ◽  
Vol 258 (3) ◽  
pp. H870-H879 ◽  
Author(s):  
A. Del Maschio ◽  
V. Evangelista ◽  
G. Rajtar ◽  
Z. M. Chen ◽  
C. Cerletti ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Polymorphonuclear Leukocytes ◽  
Platelet Activating Factor ◽  
Cell Interaction ◽  
Leukotriene B4 ◽  
Simultaneous Recording ◽  
Human Platelets ◽  
Thromboxane B2 ◽  
Induce Platelet Aggregation ◽  
Platelet Thromboxane

Human platelets were loaded with aequorin, a Ca2(+)-sensitive photoprotein, and tested in the platelet-ionized calcium aggregometer for simultaneous recording of platelet aggregation and intraplatelet Ca2+ levels both in the presence and in the absence of autologous polymorphonuclear leukocytes. Cells were exposed to one of three chemotactic stimuli: platelet-activating factor (PAF), N-formyl-methionyl-leucyl-phenylalanine (FMLP), or leukotriene B4 (LTB4). Platelets alone aggregated and showed intracellular Ca2+ movement only when exposed to PAF. Amplification of both platelet aggregation and intraplatelet Ca2+ movement was induced by PAF in the presence of leukocytes. Aggregation and intraplatelet Ca2+ mobilization were also observed in the presence of leukocytes activated by either FMLP or LTB4. Both parameters increased with the concentration of the stimuli and/or the number of leukocytes. Platelet thromboxane B2 production was also significantly increased in the presence of leukocytes. Addition of platelets at different times after leukocyte activation resulted in progressively reduced cytoplasmic Ca2+ increase. Cell-free supernatants prepared from FMLP-stimulated leukocytes were able to induce platelet aggregation, thromboxane B2 generation, and Ca2+ mobilization, although at a reduced degree as compared with intact leukocyte addition. The activity of leukocyte supernatants was stable at 37 degrees C for up to 30 min and was suppressed by trypsin inhibitor. Our study indicates that stimulated leukocytes release a soluble enzymatic activity able to activate platelets; cell-to-cell interaction may also play a role in this phenomenon. Platelet-leukocyte interaction could have physiopathological relevance and constitutes a new model for studying old and new platelet inhibitory drugs.

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