scholarly journals Virgin olive oil polyphenol hydroxytyrosol acetate inhibits in vitro platelet aggregation in human whole blood: comparison with hydroxytyrosol and acetylsalicylic acid

2008 ◽  
Vol 101 (8) ◽  
pp. 1157-1164 ◽  
Author(s):  
José Antonio González Correa ◽  
Juan Antonio López-Villodres ◽  
Rocío Asensi ◽  
José Luis Espartero ◽  
Guillermo Rodríguez-Gutiérez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Olive Oil ◽  
Whole Blood ◽  
Virgin Olive Oil ◽  
Nitric Oxide Production ◽  
Human Whole Blood ◽  
Platelet Thromboxane

Hydroxytyrosol acetate (HT-AC) is a polyphenol present in virgin olive oil (VOO) at a proportion similar to hydroxytyrosol (HT) (160–479 μmol/kg oil). The present study was designed to measure the in vitro platelet antiaggregating activity of HT-AC in human whole blood, and compare this effect with that of HT and acetylsalicylic acid (ASA). The experiments were designed according to the standard procedure to investigate the activity of ASA. HT-AC and HT inhibited platelet aggregation induced by ADP, collagen or arachidonic acid in both whole blood and platelet-rich plasma (PRP). ASA and HT-AC had a greater effect in whole blood than in PRP when ADP or collagen was used as inducer. ASA and HT-AC had a greater effect in PRP+leucocytes than in PRP alone. All three compounds inhibited platelet thromboxane B2 and leucocyte 6-keto-prostaglandin F1α (6-keto-PF1α) production. The thromboxane/6-keto-PGF1α inhibition ratio (as an indirect index of the prostanoid equilibrium) was 10·8 (se 1) for HT-AC, 1·0 (se 0·1) for HT and 3·3 (se 0·2) for ASA. All three compounds stimulated nitric oxide production, although HT was a weaker effect. In our experiments only concentrations higher than 500 μm (HT) or 1 mm (HT-AC and ASA) inhibited 3-nitrotyrosine production. All three compounds inhibited the production of TNFα by leucocytes, with no significant differences between them. In quantitative terms HT-AC showed a greater antiplatelet aggregating activity than HT and a similar activity to that of ASA. This effect involved a decrease in platelet thromboxane synthesis and an increase in leucocyte nitric oxide production.

Endotoxin-Induced Platelet Activation in Human Whole Blood In Vitro

1988 ◽  
Vol 59 (03) ◽  
pp. 378-382 ◽  
Author(s):  
Gyorgy Csako ◽  
Eva A Suba ◽  
Ronald J Elin
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Atp Release ◽  
Human Platelets ◽  
Lag Phase ◽  
Human Whole Blood ◽  
Dose Dependent

SummaryThe effect of purified bacterial endotoxin was studied on human platelets in vitro. In adding up to 1 μg/mL of a highly purified endotoxin, we found neither aggregation nor ATP release in heparinized or citrated human platelet-rich plasma. On the other hand, endotoxin at concentrations as low as a few ng/mL (as may be found in septic patients) caused platelet aggregation in both heparinized and citrated human whole blood, as monitored by change in impedance, free platelet count, and size. Unlike collagen, the platelet aggregation with endotoxin occurred after a long lag phase, developed slowly, and was rarely coupled with measurable release of ATP. The platelet aggregating effect of endotoxin was dose-dependent and modified by exposure of the endotoxin to ionizing radiation. Thus, the activation of human platelets by “solubilized” endotoxin in plasma requires the presence of other blood cells. We propose that the platelet effect is mediated by monocytes and/or neutrophils stimulated by endotoxin.

The Antiplatelet Effects of a New Nitroderivative of Acetylsalicylic Acid - An In Vitro Study of Inhibition on the Early Phase of Platelet Activation and on TXA2 Production

1996 ◽  
Vol 76 (05) ◽  
pp. 791-798 ◽  
Author(s):  
Clara Lechi ◽  
Giuseppe Andrioli ◽  
Stefania Gaino ◽  
Rosamaria Tommasoli ◽  
Valeria Zuliani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Platelet Activation ◽  
Cyclic Gmp ◽  
Thromboxane A2 ◽  
Antiplatelet Activity ◽  
Ncx 4016

SummaryWe studied in vitro the antiplatelet activity of a new nitroderivative chemically related to acetylsalicylic acid: 2 acetoxybenzoate 2-[l-nitroxy-methyl]-phenyl ester (NCX 4016), in order to identify any effects due to the release of nitric oxide and the blockade of cyclooxygenaseThe effects of scalar doses of NCX 4016 on the early phase of platelet activation, platelet aggregation and thromboxane A2 production were investigated. We observed inhibitory effects of NCX 4016 on platelet adhesion (IC50 = 7.3 × 10−5 M), platelet cytosolic calcium concentration, assayed by fluorescent probe Fura 2, and the expression of glycoprotein IMIIa (CD41 / αIIbβ3) (IC50 = 3.4 × 10−5 M) and P-selec-tin (CD62 / GMP-140) (IC50 = 4.9 × 10−5 M) measured by flow cytometry. NCX 4016 also prevented thrombin-induced platelet aggregation (IC50 = 3.9 × 10−5 M). None of these parameters were affected by acetylsalicylic acid. These inhibitory activities of NCX 4016 were abolished by oxyhaemoglobin and methylene blue. Intracellular cyclic GMP observed during thrombin-induced aggregation was increased by incubation with NCX 4016. These results appear to be attributable to the release of nitric oxide, which activates soluble platelet guanylyl-cyclase and promotes intracellular cyclic GMP increase. NCX 4016 almost completely inhibited platelet thromboxane A2 production and arachidonic acid-induced platelet aggregation. This also occurred in the presence of oxyhaemoglobin and methylene blue, indicating that its antiplatelet activity can be attributed not only to nitric oxide release but also to cyclo-oxygenase inhibition.

Acidosis in Human Whole Blood Does Not Necessarily Impair the Coagulation and the Effect of RFVIIa.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3930-3930
Author(s):  
Dorthe Viuff ◽  
Marianne Kjalke ◽  
Vivian Lind ◽  
Egon Persson ◽  
Mirella Ezban
Keyword(s):  
Flow Cytometry ◽  
Platelet Aggregation ◽  
Whole Blood ◽  
Annexin A5 ◽  
In Vivo Models ◽  
Human Whole Blood ◽  
Major Interest ◽  
R Value

Abstract Introduction: Acidosis is associated with high mortality in trauma patients. Therefore there is a major interest in generating acidosis models in vitro and in vivo to determine the effect of acidosis on coagulation and to develop treatments. The aim of this study was to examine the effect of acidosis induction in human whole blood using HCl versus Hepes and to analyze the subsequent effect of rFVIIa (NovoSeven®). Materials and Methods: Native human whole blood was obtained from healthy volunteers (n=6) and pH was adjusted to 6.8 using 1 M HCl or 1 M Hepes (pH 6.8). Coagulation was triggered with kaolin or tissue factor (TF, Innovin, final dilution 1:42500) and measured by thrombelastography (TEG, Haemoscope®). Furthermore, the effect of rFVIIa (25nM ∼ 90 mcg/kg) was measured. The TEG parameters R (sec), angle (deg) and maximum amplitude (MA, mm) were recorded and presented as mean±SD. A shorter R and greater angle and MA values are indicative of a more robust clot formation. Statistical analysis was performed by a two-way ANOVA-model. Platelet function was analyzed by platelet aggregation using Multiplate (Dynabyte Medical). Exposure of P-selectin, negatively charged phospholipids (annexin A5 binding) and induction of the active conformation of the fibrinogen receptor GPIIb/IIIa (PAC-1 binding) on platelets after TRAP-stimulation of whole blood was analyzed using a FACS Canto flow cytometer (BD). Results: TEG, platelet aggregation and flow cytometry indicated that lowering the pH to 6.8 by HCl affected the blood significantly different than when pH was lowered by addition of Hepes. HCl-treated blood triggered with either kaolin or TF showed a significantly decreased R value (378±45 or 661±130 vs 539±98 or 888±353 in untreated controls), significantly decreased MA (52±6 or 51±9 vs 66±8 or 62±13) and decreased angle (50±7 or 36±10 vs control 57±10 or 44±19, not significant). Hepes-treated blood triggered with kaolin showed no difference in R (458±52), angle (64±4) and MA (58±9) compared to untreated controls, whereas blood triggered with TF showed significantly shortened R-value (461±91) and enhanced angle (63±5) compared to untreated controls. Hepes treatment had no effect on MA (64±12). rFVIIa significantly shortened R irrespective of the acidosis inducer or clot trigger(HCl/kaolin 283±34, HCl/TF 307±52; Hepes/kaolin 363±32, Hepes/TF 313±46). Although the other TEG parameters were also improved, the effect was only significant when blood was treated with HCl and clotting initiated with TF (angle 48±11, MA 56±10). HCl-induced acidosis abolished platelet aggregation, whereas Hepes-induced acidosis did not alter platelet aggregation compared to normal blood. Flow cytometry showed that platelets from HCl-treated blood were pre-activated as evidence by expression of P-selectin on 70% of the platelets, annexin A5 binding to 14% of the platelets and PAC-1 binding to 62% of the platelets before stimulation. TRAP-stimulation increased P-selectin expression, and PAC1 and Annexin A5 binding to platelets in HCl-treated blood. In contrast, Hepes-treatment did not pre-activate the platelets and the increase in P-selectin expression, and annexin A5 and PAC-1 binding after TRAP-stimulation was as seen for control blood. Conclusion: The method used to lower pH in human blood strongly influences the functionality of the platelets and coagulation factors independent of the final pH. It is therefore important in experimental in vitro and in vivo models to be aware of these dramatically different effects in order to draw correct conclusions.

Antioxidant and Anti-atherogenic Activities of Olive Oil Phenolics

2005 ◽  
Vol 75 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Rufus Turner ◽  
Nicolas Etienne ◽  
Maria Garcia Alonso ◽  
Sonia de Pascual-Teresa ◽  
Anne Marie Minihane ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Cell Culture ◽  
Cell Adhesion ◽  
Platelet Aggregation ◽  
Olive Oil ◽  
Adhesion Molecule ◽  
Nitric Oxide Production ◽  
Cytotoxic Effects ◽  
Oxide Production

The aim of the current study was to investigate the antioxidant and cellular activity of the olive oil phenolics oleuropein, tyrosol, hydroxytyrosol, and homovanillic alcohol (which is also a major metabolite of hydroxytyrosol). Well-characterized chemical and biochemical assays were used to assess the antioxidant potential of the compounds. Further experiments investigated their influence in cell culture on cytotoxic effects of hydrogen peroxide and oxidized low-density lipoprotein (LDL), nitric oxide production by activated macrophages, and secretion of chemoattractant and cell adhesion molecules by the endothelium. Inhibitory influences on in vitro platelet aggregation were also measured. The antioxidant assays indicated that homovanillic alcohol was a significantly more potent antioxidant than the other phenolics, both in chemical assays and in prolonging the lag phase of LDL oxidation. Cell culture experiments suggested that the olive oil phenolics induce a significant reduction in the secretion of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 (and a trend towards a reduced secretion of monocyte chemoattractant protein-1), and protect against cytotoxic effects of hydrogen peroxide and oxidized LDL. However, no influence on nitric oxide production or platelet aggregation was evident. The data show that olive oil phenolics have biochemical and cellular actions, which, if also apparent in vivo, could exert cardioprotective effects.

Propofol Inhibits In Vitro Platelet Aggregation in Human Whole Blood

1997 ◽  
Vol 84 (4) ◽  
pp. 919-921 ◽  
Author(s):  
J. P. De La Cruz ◽  
J. A. Carmona ◽  
M. V. Paez ◽  
E. Blanco ◽  
F. Sanchez De La Cuesta
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Human Whole Blood
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