That's the idea behind Plan B. "It prevents pregnancy mainly by stopping the release of an egg," says the manufacturer, Barr Pharmaceuticals Inc. However, Barr adds, the drug "may also prevent the fertilization of an egg" or prevent a fertilized egg "from attaching to the uterus."
On the mechanisms of action of short-term levonorgestrel administration in emergency contraceptionContraception 64 (2001) 227–234
Marta Durand, Ma. del Carmen Cravioto, Elizabeth G. Raymond, Ofelia Duran-Sanchez, Ma. De la Luz Cruz-Hinojosa, Andre´s Castell-Rodrıguez, Raffaela Schiavond, Fernando Larrea, Department of Reproductive Biology, Instituto Nacional de Ciencias Me´dicas y Nutricio´n Salvador Zubiran, Mexico City, Mexico Family Health International, Research Triangle Park, NC, USA Department of Cellular Biology, School of Medicine, Universidad Nacional Auto´noma de Me´xico, Mexico City, Mexico Reproductive Health Service, Instituto Nacional de Pediatrı´a, Mexico City, Mexico
Abstract
The effects of short-term administration of levonorgestrel (LNG) at different stages of the ovarian cycle on the pituitary-ovarian axis, corpus luteum function, and endometrium were investigated. Forty-five surgically sterilized women were studied during two menstrual cycles. In the second cycle, each women received two doses of 0.75 mg LNG taken 12 h apart on day 10 of the cycle (Group A), at the time of serum luteinizing hormone (LH) surge (Group B), 48 h after positive detection of urinary LH (Group C), or late follicular phase (Group D). In both cycles, transvaginal ultrasound and serum LH were performed from the detection of urinary LH until ovulation. Serum estradiol (E2) and progesterone (P4) were measured during the complete luteal phase. In addition, an endometrial biopsy was taken at day LH _ 9. Eighty percent of participants in Group A were anovulatory, the remaining (three participants) presented significant shortness of the luteal phase with notably lower luteal P4 serum concentrations. In Groups B and C, no significant differences on either cycle length or luteal P4 and E2 serum concentrations were observed between the untreated and treated cycles. Participants in Group D had normal cycle length but significantly lower luteal P4 serum concentrations. Endometrial histology was normal in all ovulatory-treated cycles. It is suggested that interference of LNG with the mechanisms initiating the LH preovulatory surge depends on the stage of follicle development. Thus, anovulation results from disrupting the normal development and/or the hormonal activity of the growing follicle only when LNG is given preovulatory. In addition, peri- and post-ovulatory administration of LNG did not impair corpus luteum function or endometrial morphology.
. . .
(From the conclusion)
Our results may offer a plausible explanation for the contraceptive effects of LNG given postcoitally prior to LH surge or the mechanism involving corpus luteum development. In addition, this study does not support an anti-implantation contraceptive effect of LNG in EC; however, additional targets, besides those described herein, should also be considered and further investigated for the contraceptive effects of LNG.