PROGESTERONE-DEPENDENT BLASTOCYST SURVIVAL DURING ALTERED THYROID ACTIVITY IN THE RAT

Summary. On the 8th day of pregnancy, ova were flushed from the uteri of ovariectomized albino rats maintained on progesterone. Hyperthy- roidism and even a dose of l-thyroxine as low as 8 \g=m\g/daycounteracted the detrimental effects ofprogesterone deficiency upon blastocyst survival during this delay period, while thyroidectomy contributed to the detrimental effect. This study clarifies the earlier reported effect of the thyroid upon delayed implantation of blastocysts by showing that (1) the effect occurs during the progesterone-dependent maintenance period rather than during the implantation process, and (2) the effect can be obtained with a dose of l-thyroxine which is within the physiological hypersecretory potential of the rat thyroid. There are conflicting reports in the literature concerning the effects of thyroid hormone upon pregnancy. Investigators have reported beneficial effects, disadvantageous effects and some have reported that it exerts no effect. Exam¬ ples of these investigations and possible reasons for the conflicting results were presented in an earlier publication (Holland, Dorsey, Harris & Johnson, 1967). The previous studies in our laboratory have employed the technique of delayed implantation of blastocysts (which involves ovariectomy of rats on Day 3 of pregnancy, administration of progesterone from Days 3 to 8, laparotomy on Day 8 to confirm delay, supplementation of the daily progesterone with oestrone beginning on Day 8 in order to induce implantation and, finally, observation of the number of implantation sites at autopsy on Day 13 of pregnancy). With this technique, it was demonstrated (Holland et al., 1967) that, in rats receiving daily injections of 48 µg L-thyroxine, this hyperthyroid condition significantly counteracts the detrimental effects of progesterone deficiency upon the number of implantation sites observed on Day 13 of pregnancy, while surgical thy- roidectomy has the opposite effect. More recently (Holland, Calhoun, Harris & Walton, 1968), the subnormal levels of uterine alkaline phosphatase which occur during progesterone deficiency were shown to be restored to normal by thyroxine and further depleted by hypothyroidism in uteri examined at a time