Platelet hyperaggregability, blood prostacyclin and dipyridamole.
This study demonstrates the presence of PGI2 in blood and its influence on platelet retention tests, possibly by the intermediate of a releasing system in the columns, which is followed by a proximate recuperation on the erythrocyte sites after the passage. The presence of prostacyclin on the erythrocyte sites seems to depend upon the red cell deformability in relation to the good condition of their erythrocyte ATP reserve. The load of the erythrocyte sites increases with the daily dose of dipyridamole. The maximum load of the sites appears to be reached with a daily dose of dipyridamole 450 mg. Approximately 10% of the atherosclerosis patients who have been treated by dipyridamole keep their platelet hyperaggregability and their abnormally lowered prostacyclin level.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000097:blood*; D001665:Binding Sites / Q000187:drug effects; D004176:Dipyridamole / Q000008:administration & dosage / Q000494:pharmacology*; D004334:Drug Administration Schedule; D011464:Epoprostenol / Q000097:blood*; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*
D015121:6-Ketoprostaglandin F1 alpha; D004176:Dipyridamole; D011464:Epoprostenol