Inhibitory effect of stobadine on FMLP-induced chemiluminescence in human whole blood and isolated polymorphonuclear leukocytes

Luminescence ◽  
2007 ◽  
Vol 22 (2) ◽  
pp. 67-71 ◽  
Author(s):  
Katarína Drábiková ◽  
Viera Jančinová ◽  
Radomír Nosál ◽  
Jana Pečivová ◽  
Tatiana Mačičková ◽  
...  
Keyword(s):  
Whole Blood ◽  
Polymorphonuclear Leukocytes ◽  
Inhibitory Effect ◽  
Human Whole Blood

Chloroquine inhibits proinflammatory cytokine release into human whole blood

1998 ◽  
Vol 274 (4) ◽  
pp. R1058-R1064 ◽  
Author(s):  
Ina Karres ◽  
Jean-Pierre Kremer ◽  
Ingrid Dietl ◽  
Ursula Steckholzer ◽  
Marianne Jochum ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Whole Blood ◽  
Inhibitory Effect ◽  
Potential Effect ◽  
Therapeutic Benefit ◽  
Human Whole Blood ◽  
Weak Bases ◽  
Factor Α ◽  
Dose Dependent ◽  
Necrosis Factor

Excessive synthesis and release of proinflammatory cytokines during endotoxemia causes severe pathophysiological derangements and organ failure. Because the lysosomotropic agent chloroquine has been effective in the treatment of diseases associated with increased secretion of proinflammatory cytokines such as malaria or rheumatoid arthritis, this study evaluates the potential effect of chloroquine on endotoxin-induced cytokinemia using human whole blood from healthy volunteers. Chloroquine revealed a dose-dependent inhibitory effect on endotoxin-induced secretion of tumor necrosis factor-α, interleukin-1β, and interleukin-6 that was associated with reduced cytokine mRNA expression. Moreover, ammonia and methylamine, which react as weak bases like chloroquine, reduced synthesis and secretion of proinflammatory cytokines. These data indicate a potent anti-inflammatory effect of chloroquine on endotoxin-induced synthesis of proinflammatory cytokines that may be due to its weak base effect. Thus chloroquine may be of therapeutic benefit not only during chronic inflammation but also in diseases that are related to bacteria-induced inflammation.

Polymorphonuclear leukocyte-derived O2-reactive species activate primed platelets in human whole blood

1993 ◽  
Vol 264 (5) ◽  
pp. H1582-H1587 ◽  
Author(s):  
D. Pratico ◽  
L. Iuliano ◽  
C. Alessandri ◽  
C. Camastra ◽  
F. Violi
Keyword(s):  
Arachidonic Acid ◽  
Whole Blood ◽  
Polymorphonuclear Leukocytes ◽  
Human Platelets ◽  
Reactive Species ◽  
Oxidase Inhibitor ◽  
Cellular Interaction ◽  
Platelet Response ◽  
Human Whole Blood ◽  
H2o2 System

The activation of human platelets by polymorphonuclear leukocytes (PMN) was investigated in human whole blood challenged with "priming" concentrations of arachidonic acid or collagen in the presence or absence of N-formyl-Met-Leu-Phe (FMLP), a selective activator of PMN. With the use of arachidonic acid or collagen alone at priming concentrations or FMLP alone, no platelet response was observed. In contrast, FMLP in combination with arachidonic acid or collagen caused irreversible platelet aggregation with thromboxane A2 production. Platelet response to FMLP-activated PMN was enhanced by superoxide dismutase and blocked by catalase or the NADPH oxidase inhibitor diphenyliodonium, suggesting a role for the O2-.-H2O2 system in this cellular interaction. This was corroborated by experiments with exogenously added H2O2, which mimicked FMLP effects in the activation of primed platelets in whole blood. The present investigation indicates that platelets primed with minute amounts of arachidonic acid or collagen can be activated, in human whole blood, by oxygen-reactive species released by PMN.

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

Mechanism of the Antiplatelet Action of Dipyridamole in Whole Blood: Modulation of Adenosine Concentration and Activity

1986 ◽  
Vol 55 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Paolo Gresele ◽  
Jef Arnout ◽  
Hans Deckmyn ◽  
Jos Vermylen
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Receptor ◽  
Whole Blood ◽  
Blood Cells ◽  
Inhibitory Action ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Adenosine Concentration ◽  
Pharmacological Studies

SummaryDipyridamole inhibits platelet aggregation in whole blood at lower concentrations than in plasma. The blood cells responsible for increased effectiveness in blood are the erythrocytes. Using the impedance aggregometer we have carried out a series of pharmacological studies in vitro to elucidate the mechanism of action of dipyridamole in whole blood. Adenosine deaminase, an enzyme breaking down adenosine, reverses the inhibitory action of dipyridamole. Two different adenosine receptor antagonists, 5’-deoxy-5’-methylthioadenosine and theophylline, also partially neutralize the activity of dipyridamole in blood. Enprofylline, a phosphodiesterase inhibitor with almost no adenosine receptor antagonistic properties, potentiates the inhibition of platelet aggregation by dipyridamole. An inhibitory effect similar to that of dipyridamole can be obtained combining a pure adenosine uptake inhibitor (RE 102 BS) with a pure phosphodiesterase inhibitor (MX-MB 82 or enprofylline). Mixing the blood during preincubation with dipyridamole increases the degree of inhibition. Lowering the haematocrit slightly reduces the effectiveness.Although we did not carry out direct measurements of adenosine levels, the results of our pharmacological studies clearly show that dipyridamole inhibits platelet aggregation in whole blood by blocking the reuptake of adenosine formed from precursors released by red blood cells following microtrauma. Its slight phosphodiesterase inhibitory action potentiates the effects of adenosine on platelets.

scholarly journals Monocyte CD163 and CD36 Expression in Human Whole Blood and Isolated Mononuclear Cell Samples: Influence of Different Anticoagulants

2006 ◽  
Vol 13 (6) ◽  
pp. 704-707 ◽  
Author(s):  
Marcin Moniuszko ◽  
Krzysztof Kowal ◽  
Malgorzata Rusak ◽  
Miroslawa Pietruczuk ◽  
Milena Dabrowska ◽  
...  
Keyword(s):  
Density Gradient ◽  
Mononuclear Cell ◽  
Whole Blood ◽  
Cell Isolation ◽  
Scavenger Receptors ◽  
Published Data ◽  
Healthy Individuals ◽  
Human Whole Blood ◽  
Cd36 Expression

ABSTRACT We investigated whether the choice of anticoagulant or the application of density gradient mononuclear cell isolation may account for conflicting published data regarding the levels of the scavenger receptors' expression in healthy individuals. We demonstrate that the detection of CD163, but not CD36, differs dramatically among the methods.

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