ABSTRACT
This experiment suggests the following points: 1. Erythrocytes in control patients and in atherosclerosis patients seem to have a variable grade of affinity for adenosine and for plasma glucose. This variable grade seems to fix the level of the adenosine triphosphate (ATP) reserves and induces the erythrocytes' deformability. 2. The drop in the level of ATP reserves that induces the poor deformability of the erythrocytes in atherosclerosis patients would appear to be caused by two consecutive shortages: first a shortage that seems to be related to a deficiency of erythrocyte adenosine as the ATP shortage disappears with dipyridamole treatment and then a shortage induced by the lack of erythrocyte glucose and suppressed by the addition of ticlopidine to the dipyridamole treatment.
Subject(s)
Adenosine Triphosphate/blood , Blood Glucose/blood , Erythrocytes/metabolism , Adenosine/blood , Adenosine/deficiency , Arteriosclerosis/blood , Dipyridamole/administration & dosage , Dipyridamole/pharmacology , Drug Therapy, Combination , Humans , Ticlopidine/administration & dosageABSTRACT
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.