Abstract
The initial contractions of uteri in vitro from castrated, estrogen-treated rats, were markedly diminished following replacement with fresh bathing medium. Indomethacin and aspirin (10−5 to 10−4M) strongly stimulated such quiescent preparations and reduced their subsequent responsiveness to Ca++. Reintroducing the initial bathing medium (which contained prostaglandin-like material), or adding prostaglandin F2α to the fresh medium, initiated uterine contractions and restored responsiveness to calcium ion. Injections of indomethacin into castrated, estrogen-treated rats reduced initial in vitro uterine motility, abolished production of prostaglandin-like compounds, and prevented either indomethacin, aspirin, or Ca++ from stimulating uterine contractions. Uterine responsiveness to acetylcholine in vitro was significantly reduced in rats pretreated with indomethacin.
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