TY - JOUR
T1 - Effect of a single dose aspirin on platelets in humans with multiple risk factors for coronary artery disease
AU - Malinin, Alex I.
AU - Atar, Dan
AU - Callahan, Kevin P.
AU - McKenzie, Marcus E.
AU - Serebruany, Victor L.
PY - 2003/2/21
Y1 - 2003/2/21
N2 - We sought to assess how one tablet of non-enteric coated aspirin (325 mg) affects human platelets in subjects with risk factors for coronary artery disease. Data from 63 individuals with multiple cardiac risk factors were analyzed. Platelets were assessed twice at baseline (pre-aspirin), and after 3-4 h (post-aspirin). We employed 5 μM epinephrine-induced conventional aggregometry, closure time with epinephrine/collagen cartridge by PFA-100® (Dade-Behring), and aspirin response units (ARU) stimulated by propyl gallat with Ultegra® (Accumetrics, San Diego, CA, USA) for measuring platelet function. In addition, the expression of platelet receptors was determined by using the following monoclonal antibodies: anti-CD31, CD41, CD42b, CD51/CD61, CD62p, CD63, CD107a, and CD151. Platelet-leukocyte formation was detected utilizing dual antibodies for a pan-platelet marker CD151, and CD14, a monocyte/macrophage marker. PAC-1 was used to measure fibrinogen-platelet binding. One pill of aspirin significantly decreased platelet-rich plasma (PRP) aggregation (74.18±16.75% vs. 24.92±8.64%; p2=0.73-0.86) between platelet analyzer readings and aggregation was observed. One tablet of aspirin moderately inhibited expression of most surface platelet receptors measured, and such inhibition reached significance (p
AB - We sought to assess how one tablet of non-enteric coated aspirin (325 mg) affects human platelets in subjects with risk factors for coronary artery disease. Data from 63 individuals with multiple cardiac risk factors were analyzed. Platelets were assessed twice at baseline (pre-aspirin), and after 3-4 h (post-aspirin). We employed 5 μM epinephrine-induced conventional aggregometry, closure time with epinephrine/collagen cartridge by PFA-100® (Dade-Behring), and aspirin response units (ARU) stimulated by propyl gallat with Ultegra® (Accumetrics, San Diego, CA, USA) for measuring platelet function. In addition, the expression of platelet receptors was determined by using the following monoclonal antibodies: anti-CD31, CD41, CD42b, CD51/CD61, CD62p, CD63, CD107a, and CD151. Platelet-leukocyte formation was detected utilizing dual antibodies for a pan-platelet marker CD151, and CD14, a monocyte/macrophage marker. PAC-1 was used to measure fibrinogen-platelet binding. One pill of aspirin significantly decreased platelet-rich plasma (PRP) aggregation (74.18±16.75% vs. 24.92±8.64%; p2=0.73-0.86) between platelet analyzer readings and aggregation was observed. One tablet of aspirin moderately inhibited expression of most surface platelet receptors measured, and such inhibition reached significance (p
KW - Aspirin
KW - Coronary artery disease
KW - Platelet
KW - Receptor
UR - http://www.scopus.com/inward/record.url?scp=12244255075&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=12244255075&partnerID=8YFLogxK
U2 - 10.1016/S0014-2999(02)02956-4
DO - 10.1016/S0014-2999(02)02956-4
M3 - Article
C2 - 12591106
AN - SCOPUS:12244255075
SN - 0014-2999
VL - 462
SP - 139
EP - 143
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 1-3
ER -