Rauk P N, Laifer S A
Department of Obstetrics Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine, Magee-Womens Hospital, Pennsylvania.
Obstet Gynecol. 1993 Mar;81(3):323-6.
To determine whether ritodrine-stimulated production of prostaglandin (PG) F2 alpha by pregnant uterine tissues can be blocked by the concurrent administration of ketorolac, a PG synthesis inhibitor.
We infused saline, ritodrine, ketorolac, or a combination of ritodrine and ketorolac into chronically catheterized pregnant sheep. Concentrations of PGF2 alpha in uterine venous plasma were measured by radioimmunoassay at 0, 1, 2, 3, 4, and 24 hours during the infusions.
Ritodrine significantly increased uterine venous PGF2 alpha; mean percent increases at 4 hours were 330% and 380%, and at 24 hours 370%, compared with controls. During concurrent ritodrine and ketorolac infusion, there was no increase in uterine venous PGF2 alpha at any time.
Ketorolac completely blocks ritodrine-stimulated production of PGF2 alpha in pregnant uterine tissues. We conclude that ritodrine stimulates PG production through mobilization of arachidonic acid, and this can be effectively blocked with a PG synthesis inhibitor. This finding may have important clinical applications in the treatment of preterm labor.
确定在妊娠子宫组织中，利托君刺激产生的前列腺素（PG）F2α是否能被同时给予的PG合成抑制剂酮咯酸所阻断。
我们将生理盐水、利托君、酮咯酸或利托君与酮咯酸的组合注入长期插管的妊娠绵羊体内。在输注期间的0、1、2、3、4和24小时，通过放射免疫分析法测量子宫静脉血浆中PGF2α的浓度。
利托君显著增加子宫静脉PGF2α；与对照组相比，4小时时平均增加百分比为330%和380%，24小时时为370%。在同时输注利托君和酮咯酸期间，子宫静脉PGF2α在任何时候均未增加。
酮咯酸完全阻断了利托君刺激妊娠子宫组织产生PGF2α。我们得出结论，利托君通过动员花生四烯酸刺激PG产生，而这可以被PG合成抑制剂有效阻断。这一发现可能在早产治疗中有重要的临床应用。
