Corpus luteum function in subdermal levonorgestrel implant users.

PIP: Occurrence of ovulation and corpus luteum function were determined in 16 women inserted with 6 silastic rods, each containing 34 +or- 2mg levonorgestrel, for 1 year. Records of all subjects indicated minimal menstrual disturbances. Mean +or- S.E. serum progesterone levels at days M -7 to M -4 of the menstrual cycle revealed: anovulation (7 subjects) with serum progesterone levels less than 3 ng/ml, inefficient corpus luteum (7 subjects) with progesterone levels of 3-5 ng/ml, and normal ovulation (2 subjects) with progesterone levels above 5 ng/ml. Mean serum estradiol levels determined in the 3 levonorgestrel subgroups were insignificantly different from each other as well as from mean estradiol levels determined in 24 normal ovulatory control women.^ieng

Endocrine profiles in pediatric andrology. I. Thyroid-stimulating hormone response to thyrotropin-releasing hormone in normal and protein-calorie malnourished infants.

Thryotropin-releasing hormone (TRH) was intravenously administered to eight normal control infants and ten infants with kwashiorkor. Stimulation caused by TRH was measured at various time intervals. The basal total protein mean value +/- SE was 6.9 +/- 0.3 and 4.0 +/- 0.3 g/dl for the control and kwashiorkor groups, respectively. Serum total thyroxine was 7.7 +/- 0.6 and 4.8 +/- 0.8 micrograms/dl for the control and kwashiorkor groups, respectively. Serum levels of thyroid-stimulating hormone (TSH) were 3.2, 13.5, 9.0, 7.4, and 8.0 microU/ml for the controls before stimulation and 20, 60, 90, and 120 min after stimulation, respectively. The corresponding values for the infants with kwashiorkor were 5.7, 13.9, 14.9, 15.2, and 15.3 microU/ml, respectively. The delayed TSH response to TRH stimulation in the infants with kwashiorkor was attributed to disturbance in the hypothalamic-pituitary-thyroid axis.

Clinical and hormonal studies of subfertile males with varicocele.

To evaluate the hormonal factor in subfertile males with varicocele, FSH, LH, estradiol (E2), and testosterone (T) were assayed both from cubital and spermatic veins. The hormonal profile of patients showed no significant differences from the normal control group. Blood hormonal levels of E2 and T in the testicular veins were much higher than those in the cubital veins while FSH and LH levels showed no significant difference. FSH, LH, and testosterone blood levels in cubital and spermatic veins were statistically correlated. A preoperative hormonal study would be helpful in excluding cases in which varicocele is not the underlying cause of infertility.

Thyroid function in lactating women using the Progestasert system.

PIP: This study determines the thyroid hormone levels, in serum and milk, of 46 healthy lactating women fitted with the Progestasert system immediately postpartum. The ages of the women ranged from 28 to 35 years, parity from 3 to 6. They were divided into 2 groups: 1) menstruating and lactating women, and 2) amenorrheic and lactating mothers. The 1st group was subdivided into: 1) non-IUD users (n=11); 2) Cu T 200 users (n=9); and 3) Progestasert users (n=6). The 2nd group was subdivided into: 1) Cu T 200 users (n=12), and 2) Progestasert users (n=8). Blood and milk samples were collected and analyzed for T4 (serum thyroxine) and T3 (triiodothyronine) using radioimmunoassay techniques. The T4/T3 ratio was calculated for each sample from the 2 parameters. In the menstruating group, the T4 level was lower in the Progestasert group than in either of the other 2 groups, although the difference was statistically significant (pO.05) only when compared with the non-IUD group. There were no significant changes observed between the mean values of the 3 groups for T3 or T4/T3 ratio, although there is a trend for decreased levels in T3 in the IUD users (Cu T 200 and Progestasert). In the amenorrheic group, no statistically significant differences were observed between the Cu T 200 and Progestasert users in any of the 3 thryoid parameters. The findings do not support the alleged contributing role of lactation to decreased serum T4 levels in Progetasert users as it is known that the hypothalamic releasing factor for thyrotropin also releases prolactin. It is possible that the absorbed progesterone on breast tissue enhances T4 transfer from serum to milk. Further comparative studies will determine the validity of these results in nonlactating women as well as the mechanism involved in the decreased serum level and increased thyroid hormone level in milk in users of medicated IUDs.^ieng

Plasma angiotensin II levels and water intake following beta-adrenergic stimulation, hypovolemia, cellular dehydration and water deprivation.

A comparison of the effects of extracellular and intracellular thirst stimuli on plasma levels of angiotensin II was made in rats. The administration of polyethylene glycol and isoproterenol elicited a strong drinking response and resulted in a significant increase in plasma angiotensin II. There was a significant correlation between the volume of water intake and plasma angiotensin II levels following the injection of polyethylene glycol but not following isoproterenol. Drinking was also elicited by the administration of hypertonic saline but there was no increase in plasma angiotensin II. The results suggest that endogenously released angiotensin II contributes to extracellular thirst but not to intracellular thirst.

Graded levels of hemorrhage, thirst and angiotensin II in the rat.

Hemorrhage was evaluated as a stimulus to drink in rats prepared with chronically implanted jugular cannulae and bled either 20, 30, 40 or 50 percent of their total blood volume. Hourly observations of water intake for 5 hr after hemorrhage revealed that the volume drunk was proportional to the degree of hemorrhage. Drinking induced by 20 percent hemorrhage did not differ significantly from control values, and intake was greatest and most persistent after 50 percent blood loss. The onset of maximal drinking at 1 hr after 40 percent hemorrhage was preceded by a twofold increase in plasma concentrations of angiotensin II. This is compatible with previous suggestions that angiotensin plays a role in hypovolemic thirst.