animals: donor animals and/or receiver animals were treated daily for 1 week with 13,14-dihydro-PGE1 (DIHYDROPROSTAGLANDIN E1), PGE1, 15-keto-PGE1, 15-keto-13,14-dihydro-PGE1, or the vehicle only, respectively. From the group of the receiver animals, a subgroup of 6 animals each was treated for the same period of time with either 13,14-dihydro-PGE1, PGE1, 15-keto-PGE1, 15-keto-13,14-dihydro-PGE1, or the vehicle. Immediately after the last administration of the respective PG or solvent, native blood from a donor rabbit was circulated [30 mL/min. under in vivo flow conditions (60 Hz)] over an arterial segment of a receiver animal.

The actions of the in vivo metabolite of PGE1, 13,14-dihydro-PGE1 (DIHYDROPROSTAGLANDIN E1/ PGE0), on platelet and neutrophil (PMN) function and vessel tone were studied in vitro. PGE0 inhibited aggregation, ATP release and thromboxane generation by human platelets (IC50 10-100 nmol/l). The compound also inhibited superoxide anion generation and lysosomal enzyme release from human PMN. PGE0 was also potent relaxants of several arterial preparations in the rabbit at comparable concentrations.