scholarly journals Comparison between the efficacy of prostacyclin analogue (beraprost) with low-dose aspirin and aspirin alone to platelet aggregation and serum prostanoids (thromboxane B2 and 6-ketoPGF1.ALPHA.).

Nosotchu ◽  
1995 ◽  
Vol 17 (4) ◽  
pp. 356-361
Author(s):  
Manabu Kudo ◽  
Tadatoshi Komiya ◽  
Takao Urabe ◽  
Nami Morikawa ◽  
Yoshikuni Mizuno
Keyword(s):  
Platelet Aggregation ◽  
Low Dose ◽  
Thromboxane B2 ◽  
Prostacyclin Analogue ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Effect of Diltiazem and Low-Dose Aspirin on Platelet Aggregation and ATP Release Induced by Paired Agonists

1993 ◽  
Vol 70 (02) ◽  
pp. 332-335 ◽  
Author(s):  
Marjorie L Zucker ◽  
Susan E Budd ◽  
Lawrence E Dollar ◽  
Steven B Chernoff ◽  
Raul Altman
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Low Dose ◽  
Atp Release ◽  
Thromboxane B2 ◽  
Platelet Response ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Significant Difference

SummaryThe authors studied the effects of diltiazem, administered alone and together with low-dose aspirin, on the platelet response to paired agonists. After a baseline period, 25 healthy volunteers were given oral diltiazem for 1 week (120, 240, or 360 mg/day), and then crossed over randomly between 1 week on diltiazem plus aspirin (81 mg/day), and 1 week on aspirin (81 mg/day) alone. Platelet function was tested on 2 consecutive days in each period. Synergistic platelet aggregation and ATP release were obtained at baseline using a subthreshold concentration of arachidonic acid combined with platelet activating factor, ADP, or epinephrine. Diltiazem resulted in a significant decrease from baseline in platelet aggregation and ATP release using the arachidonic acid-epinephrine combination (35% and 40% decrease, respectively, p <0.01) and a significant decrease in aggregation using the arachidonic acid-ADP combination (22% decrease, p <0.01). The effects were neither dose-related, nor accompanied by any significant change in serum thromboxane B2 levels or bleeding times. There was no significant difference between the effects of aspirin alone and aspirin plus diltiazem on the synergistic platelet aggregation and ATP release induced by the paired agonists, or on thromboxane B2 levels or bleeding times. Diltiazem administered in vivo partially inhibits the synergistic platelet aggregation and ATP release induced by paired agonists; however, in contrast to a previous in vitro study it does not potentiate the platelet-inhibitory effect of aspirin.

Maternal serum thromboxane B2 concentrations do not predict improved outcomes in high-risk pregnancies in a low-dose aspirin trial

1998 ◽  
Vol 179 (5) ◽  
pp. 1193-1199 ◽  
Author(s):  
John Hauth ◽  
Baha Sibai ◽  
Steve Caritis ◽  
Peter VanDorsten ◽  
Marshall Lindheimer ◽  
...  
Keyword(s):  
High Risk ◽  
Low Dose ◽  
Maternal Serum ◽  
Thromboxane B2 ◽  
Dose Aspirin ◽  
Improved Outcomes ◽  
Low Dose Aspirin ◽  
Serum Thromboxane

Effects of low-dose aspirin on in vitro platelet aggregation in the early minutes after ingestion in normal subjects

1994 ◽  
Vol 74 (7) ◽  
pp. 720-723 ◽  
Author(s):  
Salim F. Dabaghi ◽  
Suraj G. Kamat ◽  
John Payne ◽  
Gary F. Marks ◽  
Robert Roberts ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Low Dose ◽  
Normal Subjects ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Abstract 5067: Responsiveness to Low Dose Aspirin Influences Levels of Inflammatory Biomarkers

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rehan Qayyum ◽  
Nauder Faraday ◽  
Lisa R Yanek ◽  
Dhananjay Vaidya ◽  
Lewis C Becker ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Low Dose ◽  
Thromboxane B2 ◽  
Inflammatory Biomarkers ◽  
Premature Coronary Artery Disease ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Healthy Family ◽  
Hs Crp

Platelets participate in cellular and humoral immunity; however the effect of low dose aspirin (ASA) therapy on platelet-mediated inflammation is unknown. Healthy family members (N=1934) of patients with premature coronary artery disease (CAD) participated in a 14-day trial of ASA 81 mg/day. Urinary 11-dehydro thromboxane B2 (uTxM), which reflects in vivo platelet activation, was measured at baseline and after ASA. Subjects were dichotomized by post-ASA uTxM levels into ASA responsive (lower quartile) and ASA resistant (upper quartile) groups based on previous studies showing an association between the upper quartile and incident CAD events. Levels of the inflammatory biomarkers, plasma hs-CRP and IL-6, were measured at both time points and compared between the two quartile extremes using multivariable-adjusted models. The study sample had 967 participants (females, 59%; blacks, 43%, age, 43.9±13 years). At baseline, plasma hs-CRP levels were similar between the upper and the lower uTxM quartiles, but IL-6 levels were significantly higher in the upper quartile (Table ). After ASA therapy, hs-CRP and IL-6 decreased in the lowest quartile, but increased in the upper (resistant) quartile, and the between-quartile difference (post-adjusted for pre) became significant for both inflammatory markers. Compared to ASA responsive subjects, those who are ASA “resistant” have higher levels of plasma inflammatory markers after ASA therapy and demonstrate lesser reductions in inflammatory markers from baseline. These extreme quartile differences in hs-CRP and IL-6 may reflect differences in ASA’s ability to suppress platelet-mediated inflammation, and may contribute to the increased CAD risk observed in aspirin resistant persons. Table. Comparison of hs-CRP and IL-6 in the Extreme Quartiles of 11-dehydro thromboxane B2 (uTxM)

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