Why the study?
Does intravenous prostacyclin sodium inhibit platelet aggregation and affect cyclic AMP levels in healthy volunteers?
Does intravenous prostacyclin sodium inhibit platelet aggregation and affect cyclic AMP levels in healthy volunteers?
Intravenous prostacyclin sodium produces measurable platelet inhibition at infusion rates tolerated by healthy volunteers, though it has a narrow safety margin.
Produces measurable platelet inhibition at tolerated doses in volunteers; leaves open clinical translation to cardiovascular patients.
Clinical tolerance, inhibition of platelet aggregation and intracellular platelet adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels were evaluated in normal volunteers given i.v. infusions of prostacyclin sodium at rates up to 15 ng/kg/min. Short-term infusions (30 and 60 minutes) were tolerated at rates up to 10.0 ng/kg/min; higher rates produced headaches, anxiety, nausea and vomiting. Six-hour and 24-hour infusions were tolerated at rates up to only 4.0 ng/kg/min. Twenty-four hour infusions at 4 ng/kg/min produced a consistent 4-7 microM shift to the right in the platelet ADP dose-response curve; this platelet inhibitory activity did not diminish during the infusion. Prostacyclin sodium infusion elevated intracellular cyclic AMP levels, the increases corresponding to the onset of measurable inhibition of ADP-induced aggregation, although the magnitude of the increase did not necessarily reflect the degree of inhibition. Increased template bleeding times were seen with a greater than 10-microM shift in the ADP dose-response curve. We conclude that although prostacyclin sodium has a narrow safety margin, the drug does produce platelet inhibition at infusion rates generally tolerated by healthy volunteers.
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Data et al. (1981) studied this question.
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