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The Effect of Clinical Prostacyclin Infusions in Advanced Arterial Disease on Platelet Function and Plasma 6‐keto PGF 1α Levels
Author(s) -
Machin S. J.,
Chamone D. A. F.,
Defreyn G.,
Vermylen J.
Publication year - 1981
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1981.tb02809.x
Subject(s) - prostacyclin , platelet , radioimmunoassay , medicine , alpha (finance) , endocrinology , platelet aggregation , anesthesia , chemistry , surgery , construct validity , patient satisfaction
S ummary . We have infused synthetic prostacyclin (PGI 2 ) continuously for approximately 72 h at the maximum tolerated dose (ranging from 5 to 60 ng/kg/min) into nine patients with advanced arterial disease. Prior to the infusion seven out of nine patients had spontaneous platelet aggregation and five out of six patients tested had an abnormal circulating platelet aggregate ratio. During the infusion only one patient still had spontaneous aggregation and all the abnormal circulating platelet aggregate ratios returned to the normal range. However, none of the patients showed any suppression of ADP induced aggregation. The level of exogenous PGI 2 required in vitro prior to the infusion to completely inhibit ADP induced aggregation was 5–10 ng/ml in three of the four patients tested. Ten healthy adults showed complete inhibition with 1 ng/ml of PGI 2 . It appears that the platelets of some patients with arterial disease are more resistant to the anti‐aggregating properties of PGI 2 .