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We report here the results obtained with a new test of prolactin (PRL) release in six normal pre-pubertal boys, eleven children with short stature of non-pituitary origin and in thirteen pituitary dwarfs. The test consists of the administration of 100 mg of sulpiride i.m. and the measurement of PRL in serum samples up to 120 min after injection. Baseline PRL concentrations were not clearly different in the three groups. After sulpiride a marked increase (3--10 times over control values) in PRL was noted in all normal and short children without pituitary disease. A complete failure of response was observed in ten of the thirteen pituitary dwarfs. It is concluded that sulpiride has considerable potential in the differential diagnosis of children with stunted growth.

To determine whether alterations in serum thyroid hormone levels affect hypothalamic-pituitary-adrenal function, we measured the plasma immunoreactive (IR) ACTH and IR-cortisol responses to 1 microgram/kg BW ovine CRH (oCRH) given iv in the late afternoon and the plasma IR-ACTH, IR-cortisol, and IR-11-deoxycortisol responses to 2 g metyrapone given orally at midnight in 10 athyreotic patients during T4 treatment and 1 month after stopping T4 when they were biochemically, but not clinically, hypothyroid. Mean serum TSH increased from 0.7 +/- 0.9 (+/- SD) mU/L (normal range 0.5-4.9 mU/L) during T4 therapy to 107 +/- 82 mU/L after stopping T4. The serum total T4 level and free T4 index fell from 165 +/- 37 nmol/L and 1.9 +/- 0.4, respectively (normal range, 59-154 nmol/L and 0.9-2.5, respectively), to 19 +/- 9 and 0.2 +/- 0.1, respectively, after stopping T4. Basal plasma IR-ACTH and IR-cortisol levels at 0800 and 1630 h were similar during and after stopping T4 therapy. Peak plasma IR-ACTH and IR-cortisol levels after oCRH were significantly greater after stopping T4 (20 +/- 9.2 pmol/L and 880 +/- 260 nmol/L, respectively) than during T4 therapy (9.7 +/- 4.7 pmol/L and 720 +/- 190 nmol/L; P less than 0.01 and P less than 0.05, respectively). The mean integrated plasma IR-ACTH and IR-cortisol responses to oCRH were also significantly greater P less than 0.01 and P less than 0.05, respectively) after stopping T4 than during T4 therapy. Plasma IR-ACTH the morning after metyrapone was slightly (1.6-fold) but not significantly greater during therapy than after stopping T4 therapy (100 +/- 86 vs. 65 +/- 54 pmol/L, respectively). The plasma IR-11-deoxycortisol responses to metyrapone during and after stopping T4 therapy were similar (720 +/- 250 and 750 +/- 330 nmol/L, respectively), presumably because plasma IR-ACTH concentrations were maximally stimulating in both instances. These results indicate that thyroid hormone deficiency of short duration 1) increases corticotroph sensitivity to oCRH, 2) may diminish the plasma ACTH response to metyrapone-induced hypocortisolemia, and 3) has no apparent effect on the acute adrenal response to ACTH. These data together with those of previous studies that have shown reduced responses of the hypothalamic-pituitary-adrenal axis to metyrapone and hypoglycemia in hypothyroid patients suggest that the release of hypothalamic CRH and/or other ACTH secretagogues may be decreased in hypothyroidism.

The effects of the inability of suspension-feeding protozoa to collect bacteria over the whole range of sizes in the bacterial size distribution were examined by constructing mathematical models based on this assumption. Systems of suspension-feeding protozoa grown on both growing and nongrowing bacteria were examined in both batch and continuous culture. The models were able to predict three experimental observations common in such systems. Some additional features of the systems which should be useful in interpreting results of experiments with suspension feeding protozoa and in designing new experiments were predicted, also.

Dose-dependent gonadotropin suppression by a potent gonadotropin-releasing hormone (GnRH) antagonist, Nal1 Glu6 [( Ac-D2Nal1,D4ClPhe2,D3Pal3,Arg5,DGlu(AA)6,- DAla10]GnRH), was determined in five postmenopausal women by frequent sampling for immunoreactive luteinizing hormone (I-LH) and immunoreactive follicle stimulating hormone (I-FSH) for 72 hours after single intramuscular (IM) injections of 10, 50, 150, and 300 micrograms/kg. Bioactive (B) LH and B-FSH also were measured after the IM administration of the 50-micrograms/kg dose. Serum levels of Nal1 Glu6 were determined by a radioreceptor assay for the first 24 hours after the 50-micrograms/kg IM dose and in three women after a 10-micrograms/kg intravenous (IV) dose. While the disappearance rate of serum Nal1 Glu6 after a 10-micrograms/kg IV injection was rapid, gonadotropin suppression persisted longer than detectable serum levels. In contrast, after a 50-micrograms/kg IM injection, the decline from peak circulating levels was slower, contributing to its longer duration of action (greater than 24 hours). All IM doses tested resulted in a similar 51% to 63% decrease in I-LH, which was maximal by 8 hours. The duration of action was dose-dependent, with decreased levels lasting up to 72 hours at the 300-micrograms/kg dose. While decline of I-FSH was smaller (14% to 33%), the duration of suppression was also dose-dependent, although the nadir occurs later (8 to 9 hours after administration) and suppression lasted longer (72 hours at the 150-micrograms/kg dose). The reduction of B-LH was greater than that of I-LH and the suppression of B-FSH also was greater than that of I-FSH.(ABSTRACT TRUNCATED AT 250 WORDS)