Despite having undergone unsuccessful IVF within the public health system, more than 75% lived with children 4-5.5 years later. This subgroup had a better quality of life, compared to those without children. Additional IVF treatment may result in increased quality of life.
An in vitro perfused rat ovary model was characterized with respect to ovulation rate, oocyte maturation and steroidogenesis after priming with various doses of pregnant mare's serum gonadotrophin (PMSG) (10, 20 or 30 IU PMSG s.c. in the morning of day 28). In ovaries stimulated with LH 0.1 microgram ml-1 after 1 h of perfusion the number of ovulations was significantly higher in the 20 IU PMSG group than in the to IU PMSG group (6.8 +/- 1.0 ovulations per treated ovary versus 2.4 +/- 1.2, P less than 0.01). Priming with 30 IU PMSG did not result in significantly more or fewer ovulations than did 10 or 20 IU PMSG. No ovaries in the non-stimulated control groups ovulated. Oocytes retrieved directly at ovulation were mature (GVB or PB stage). Among oocytes retrieved from pre-ovulatory follicles punctured at 0, 2, 4, 6 and 8 h after stimulation with LH 0.1 microgram ml-1 there was an increasing number of oocytes with GVB (0/10 at 0 h and 10/10 at 8 h). Stimulation with LH resulted in a rapid release of progesterone, testosterone and oestradiol into the medium, whereas non-stimulated control ovaries exhibited a slow rise of all steroids throughout the perfusion period. It is concluded that priming with 20 IU PMSG in this model results in an optimal number of ovulations and that this model provides a useful tool in studies of various kinds of modifying influences on the ovulatory process.
In isolated, perfused ovaries of rats treated with pregnant mare's serum gonadotropin (PMSG), purified preparations of ovine follicle-stimulating hormone (FSH) (oFSH-211B) and rat FSH (rFSH-I-6), 100 ng/ml, were found to induce ovulations (4.8 +/- 0.9, n = 4, and 6.4 +/- 2.0, n = 5, ovulations per ovary, respectively). Indomethacin (5 micrograms/ml) added to the perfusate inhibited this ovulatory effect and exogenous prostaglandin F2 alpha (PGF2 alpha) (1 microgram/ml), or prostaglandin E2 (PGE2) (0.5 microgram/ml), reversed the blockade. Ovine FSH and rFSH had only a weak stimulatory effect on estradiol release, and only rFSH caused a significant increase in progesterone accumulation. Indomethacin reduced the stimulatory effect of rFSH on progesterone release, and this effect was reversed by PGE2 but not by PGF2 alpha. In a 6-h incubation experiment with preovulatory rat follicles, we tested the biological activity of gonadotropins used to induce oocyte maturation. The concentration of FSH used in the perfusion experiments induced oocyte maturation in more than 88% of the oocytes studied. The data confirm earlier findings that FSH can induce ovulations and show that prostaglandins are involved in this process. The data also indicate that prostaglandins might be involved in the FSH-induced increase of progesterone levels.
Adjusted PGWB and SOC scores revealed a high quality of life in the adoption group. However, the group unsuccessful IVF-living without children had low quality of life scores. Quality of life appears to be independent of the outcome of IVF treatment as long as there are children in the family.
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