[Effect of ritodrine on prostaglandin production in vivo and in vitro].

In 11 women between the 26th and 36th week of gestation the concentration of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) was measured serially in the peripheral maternal plasma before and during treatment with ritodrine at a concentration of up to 350 mcg/min. On admission the mean plasma PGFM concentration was 268.0 +/- 43.3 pg/ml, which was significantly higher than the mean PGFM plasma level of the control group (156.0 +/- 21.8; n = 10). Treatment with ritodrine was successful in 7 women and led to a small, but statistically significant decrease in maternal plasma PGFM levels. In unsuccessful treated cases plasma PGFM levels also dropped initially, but increased again at 12 and 24 hours after initiation of therapy. The addition of ritodrine in concentrations of 10(-8) to 10(-6)M to the incubation medium led to a decrease in prostaglandin-(PG-)synthesis in vitro in the decidua and amnion. These changes were, however, only significant for PGE at a concentration of 10(-6)M in decidua and for PGE and PGF in a concentration of 10(-7)M in amnion. In the myometrium no effect of ritodrine on prostaglandin production could be observed. The measurement of PGFM production in the incubation vials indicated that ritodrine has no influence on the conversion of PGF2 alpha to its metabolite in any of these tissues. The results of the present study allow the following conclusions. 1. PGF2 alpha seems to play a role in the mechanism of premature labor. 2. In premature labor patients successful treated with ritodrine a significant decrease in circulating plasma PGFM levels is observed. In vitro ritodrine led to a small, but significant decrease in PGE and PGF synthesis in decidua and amnion which may add to the uterus-relaxing effect of ritodrine.