1In 13 of 15 experiments, prostaglandin E2 (PGE2) and sulprostone (a prostanoid EPI/EP3-receptor agonist) contracted isolated rings of human pulmonary artery at low concentrations () 5 and > 0.5 nM respectively). Tissue was obtained from patients undergoing surgery mainly for carcinoma of the lung. Characterization of the receptors involved was complicated by loss of sensitivity to the contractile PGE action over the experimental period. In contrast, contractile responses to KCI, phenylephrine and the specific thromboxane (TP-) receptor agonist, U-46619, did not decrease with time. 2 The relative contractile potencies for seven PGE analogues, measured during the first few hours after setting up the preparations, were as follows: sulprostone > misoprostol = gemeprost > PGE2 > GR 63799X> 17-phenyl-w-trinor PGE2 1 1 1-deoxy PGE1. This ranking indicates that an EP3-receptor is involved. 3 The contractile action of sulprostone was not blocked by the TP-receptor antagonists, EP 169 and GR 32191, and the EPI-receptor antagonist, AH 6809.4 In two experiments, PGE2 (50 nM) reduced basal tone and sulprostone was a weak contractile agent.Phenylephrine-induced tone was also inhibited by PGE2 (EC50 = 5-20 nM), 1 1-deoxy PGEI and butaprost (a selective EP2-receptor agonist); the latter prostanoids were about 2 and 4 times less potent than PGE2 respectively. Interactions with phenylephrine were different in experiments where PGE2 alone was contractile: PGE2 induced contraction superimposed on the phenylephrine response and 11-deoxy PGE, induced either further contraction or had no effect. Butaprost produced relaxation at high concentrations; this may not be an EP2 action since preparations were highly sensitive to relaxant actions of prostacyclin (IP-) receptor agonists (cicaprost and TEI-9063). 5 The study has shown that in the majority of experiments on the human isolated pulmonary artery, the contractile EP3 system outweighed the relaxant EP2 system. However, in two experiments the reverse was true. It is not clear to what extent these differences are due to disease processes affecting the tissues. The findings are discussed in relation to the adverse cardiovascular responses occasionally encountered during treatment of postpartum haemorrhage with sulprostone, and more generally to the clinical use of EP-receptor agonists in man.

External cephalic versions in the study period were performed in a double blind design by 2 experienced practitioners. Sixty-three patients were allocated to treatment with either placebo, ritodrine or hexoprenaline. The main outcome measure studied was successful completion of external cephalic version. Hexoprenaline, but not ritodrine, was statistically more likely to be associated with successful version than placebo (p = 0.04 versus p = 0.22).

The incidence of fetomaternal haemorrhage after external cephalic version was 1.8% in 167 patients. The occurrence of this complication was not found to be associated with difficult or unsuccessful version, or with any adverse perinatal outcome. We conclude that routine assessment of fetomaternal haemorrhage after external version is not necessary, except in rhesus negative women to detect the 2% in whom the routine dose of 500 iu (100 micrograms) of anti-D immunoglobulin is inadequate.