Does hypoxia selectively stimulate the generation of prostaglandin E1 by the isolated rat uterus?

The contractile activity of uterine horns maintained for 90 to 120 minutes under normal oxygenation (carbogen or 100% O2) became undetectable. When in this condition the gassing was stopped one or two minutes later, regular phasic contractions appeared super-imposed on a small increment of the basal resting tone. Indomethacin and aspirin well known inhibitors of prostaglandin (PG) synthesis, blocked the contractile influence of hypoxia whereas neither tranylcypromine or imidazole were able to alter the stimulatory action. PGE2, PGE1 and PGF2 alpha released into the bathing solution during 10 minutes of normoxia or 10 minutes of hypoxia, were measured. Under O2, PGE2 and PGF2 alpha production diminished significantly (P less than 0.05 and P less than 0.01, normoxia vs. hypoxia, respectively) whereas PGe1 increased (P less than 0.05). "PGI2-like material" generated was also detected and it was found that the values during hypoxia were lower than those observed in O2; however the difference was not statistically significant. Dose-response contractile activity to PGs with and without gassing was explored. It was necessary to add 100 times more PGF2 alpha to obtain the minimal response under hypoxic conditions as compared to normoxia. On the other hand the threshold response to PGE1 was 10 times lower under hypoxic conditions than in normoxia. The possible mechanism(s) that induce an increment in PGE1 generation accompanied by a simultaneous decrement of PGE2 during hypoxia is discussed in connection with a possible role of PGE1 evoking uterine contractions when the gassing of the suspending solution is stopped.