The Effect of Clinical Prostacyclin Infusions in Advanced Arterial Disease on Platelet Function and Plasma 6-keto PGF1αLevels

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Abstract
Synthetic prostacyclin (PGI2) was infused continuously for .apprx. 72 h at the maximum tolerated dose (5-60 ng/kg per min) into 9 patients with advanced arterial disease. Prior to the infusion 7 of 9 patients had spontaneous platelet aggregation and 5 of 6 patients tested had an abnormal circulating platelet aggregate ratio. During the infusion, 1 patient had spontaneous aggregation and all abnormal circulating platelet aggregate ratios returned to the normal range. No patient showed any suppression of ADP induced aggregation. The level of exogenous PGI2 required in vitro prior to the infusion to completely inhibit ADP induced aggregation was 5-10 ng/ml in 3 of 4 patients tested. Ten healthy adults showed complete inhibition with 1 ng/ml of PGI2. The platelets of some patients with arterial disease apparently are more resistant to the anti-aggregating properties of PGI2. Plasma 6-keto PG[prostaglandin]F1.alpha. levels, measured by radioimmunoassay, were within the normal range (100-381 pg/ml) in all but 1 patient prior to the infusion. During the infusion plasma, 6-keto PGF1.alpha. levels rose proportionally to the infusion dose. After stopping the infusion 6-keto, PGF1.alpha. levels declined according to an exponential process with a half-life of 18-29 min, prolonged to 47 min in 1 patient who was anuric. The linear increase in 6-keto PGF1.alpha. levels suggests this as a useful indicator of increased circulating PGI2.