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Effects of intravenous epoprostenol on platelets and the cardiovascular system are not potentiated by dipyridamole
Author(s) -
Pickles Hilary,
Fish Alison,
Hassan S,
Burke Christine,
Warrington S,
O'Grady J
Publication year - 1983
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1983.27
Subject(s) - dipyridamole , medicine , prostacyclin , blood pressure , heart rate , platelet , anesthesia , placebo , cardiology , hemodynamics , alternative medicine , pathology
Normal subjects received infusions of epoprostenol (prostacyclin, PGI 2 ) at doses of 2, 4, 6, and 8 ng/kg/min on each of two occasions after pretreatment with dipyridamole (400 mg/day for 3 days) or placebo. Baseline headache and bleeding time were increased and preejection period (PEP) shortened after dipyridamole. The baseline heart rate was increased on dipyridamole by an amount that correlated to the blood dipyridamole level. PGI 2 infusion increased heart rate, systolic blood pressure (BP), pulse pressure, left ventricular ejection time index, and degree of flushing and severity of headache, and reduced diastolic BP, PEP, and T wave height. There was no apparent interaction between PGI 2 and dipyridamole on these variables. PGI 2 inhibited adenosine diphosphate‐induced platelet aggregation and increased bleeding time. We conclude that, despite the synergism between dipyridamole and PGI 2 that might be predicted and has been demonstrated in some animal experiments, no such interaction is apparent in normal humans after standard doses. Clinical Pharmacology and Therapeutics (1983) 33, 178–182; doi: 10.1038/clpt.1983.27