Improvement of early pregnancy diagnosis based on milk progesterone by the use of progestin-impregnated vaginal sponges.

Progestin-impregnated (250 mg medroxyprogesterone) vaginal sponges (PIVS) were inserted 6-7 days post-insemination and removed on the 17th day. Pregnancy was determined by milk progesterone on the 21-24 day post-insemination. It was found that in 52 cows which did not receive PIVS, the rate of false diagnosis of pregnancy was 21%. In 30 cows treated with PIVS, there were no false positives. The diagnosis of non-pregnant was completely accurate in both groups.

Early pregnancy diagnosis in the ewe, based on milk progesterone levels.

Plasma and milk progesterone concentrations in pregnant sheep (18--22 days after mating) were similar, about 3.7 ng/ml whereas values in non-pregnant sheep were less than 1 ng/ml. Lambing results indicated identical accuracy for both methods (82 and 84% in 2 flocks). The accuracy was 92--100% for ewes diagnosed non-pregnant in the breeding season, but for ewes tested in the non-breeding season the diagnosis of non-pregnancy according to milk progesterone levels was only 50% accurate.

Steroidogenesis and prostaglandin synthesis by cultured bovine blastocysts.

Bovine blastocysts were collected at Days 13, 15 and 16 and placed in TCM-199 supplemented with 5% fetal calf serum; some blastocysts were immediately frozen while the others were cultured for 48 h and then frozen. Samples (tissue + medium, 5--12/group) were thawed, homogenized and analysed by radioimmunoassays. Measurable amounts of progesterone were found in all blastocysts but values were higher (P less than 0.01) after culture. Testosterone was not found in the cultured or uncultured blastocysts at Day 13, but was detectable on Days 15 and 16 and in greater amounts (P less than 0.05) in the cultured blastocysts. PGF and PGE-2 were increased (P less than 0.05) in the cultured blastocysts in all 3 days. Oestradiol was measurable in some but not all blastocysts. It is suggested that PG synthetase and enzymes capable of synthesizing progesterone, testosterone and, possibly, oestradiol are present in these early bovine blastocysts.

Lipoic acid prevention of neural tube defects in offspring of rats with streptozocin-induced diabetes.

OBJECTIVE: Increased oxidant stress has been suggested to play a role in the pathogenesis of disturbed embryogenesis in diabetic pregnancies. The present study was conducted to determine whether administration of lipoic acid, a naturally occurring antioxidant, would reduce the incidence of diabetic embryopathy in the streptozocin-induced diabetic rat model. STUDY DESIGN: After conception, rats were randomly distributed to 5 groups. From day 1, rats were daily injected intraperitoneally with either lipoic acid, 30 mg/kg, or vehicle. At day 6, rats from groups 3, 4, and 5 were made diabetic by a single intraperitoneal injection of streptozocin. Group 4 rats were injected with lipoic acid from day 1 to day 6, after vehicle treatment until day 17. At day 17 of gestation, rats were killed. The fetuses were released from the yolk sacs and surrounding decidua and were examined for size, resorption rate, and neural tube defects. RESULTS: Pregnant diabetic rats treated with vehicle lost weight during pregnancy (-3.2 +/- 1.9 g/d), as opposed to normal pregnancy-related weight gain (3.5 +/- 0.5 g/d). Treatment with lipoic acid protected against diabetes-induced weight loss, without a measurable effect on fed-state glucose concentrations. Daily treatment with lipoic acid (pregnancy days 1 to 17) was efficient in reducing the resorption rate from 24.0% +/- 9.5% in vehicle-treated diabetic rats to 10.2% +/- 4.8% in lipoic acid-treated diabetic rats (P <.05). The rate of neural tube defects in diabetic rats treated with lipoic acid throughout the pregnancy was reduced from 26.0% +/- 7.0% to 10.2% +/- 3.2% (P <.05). In rats treated only during pregnancy days 1 to 5 (before diabetes induction), lipoic acid failed to exert its protective effects against neural tube defects, which emphasizes the importance of the presence of lipoic acid during the organogenesis period. The atherosis of placental vasculature demonstrated in the vehicle-treated diabetic rats was absent from placentas obtained from lipoic acid-treated diabetic animals. CONCLUSIONS: Our data demonstrate a protective effect of lipoic acid against diabetic embryopathy, fetal losses, and ultrastructural alteration of diabetic placentas.