Immunoreactive interleukin-1 in bronchoalveolar lavage fluid of high-risk patients and patients with the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is characterized by increased neutrophils and macrophages in bronchoalveolar lavage (BAL) fluid. Interleukin-1 (IL-1), an inflammatory mediator produced by macrophages, has been shown to be chemotactic for neutrophils and to stimulate lymphocyte activation and proliferation of fibroblasts. BAL was performed in patients with ARDS, patients at high risk to develop ARDS, and in normal nonsmokers. After removal of cells and surfactant-complexed lipids by centrifugation, the remaining supernatant was concentrated by ultrafiltration utilizing membranes retaining substances greater than 5000 daltons. The concentrate was assayed for immunoreactive IL-1 beta by a radioimmunoassay method. Patients with ARDS (n = 9) had an IL-1 level of 184 +/- 67 pg/ml, high-risk patients (n = 9) had 172 +/- 62 pg/ml, and normals (n = 10) had 4 +/- 1 pg/ml. There was a significant (p less than or equal to .05) increase in IL-1 in the ARDS and risk groups compared to normals. IL-1 was detected in serum from patients with ARDS (n = 19), high risk (n = 19), and normals (n = 8), but no difference was noted among the three groups. BAL cell differentials revealed that neutrophils were increased (p less than .05) in both the ARDS (59 +/- 10%) and high-risk (65 +/- 8%) groups compared to normals (2 +/- 1%). There was a correlation (r = 0.64, p less than .001) between IL-1 levels and BAL protein concentration. BAL IL-1 levels were highest in patients with the fully developed syndrome but were also elevated in patients at high risk. The absence of significant amounts of IL-1 in serum suggests that it may be produced within the lung.

Effects of large doses of estrogen on prolactin and growth hormone release.

The effects of large doses of estrogen on prolactin (PRL) release were assessed. Circulating PRL levels in response to intravenous infusion of 17 beta-estradiol (E2), at a rate of 50 mug per hour for 4 hours, were studied in 10 subjects, and a chronic administration of ethinyl estradiol (EE) at a dose of 400 mug per day, for 1 week, was evaluated in five hypogonadal subjects. There was a significant depression of serum level of PRL during the E2 infusion and a significant increase in PRL release after discontinuation of the infusion. The chronic treatment of large doses of EE induced a more rapid (within 36 hours) and a significantly greater elevation of PRL levels at the end of 1 week treatment than those found during smaller doses of EE administration, as reported previously. These data suggest that acute treatment of estrogen may have a biphasic action on the pituitary PRL section and that the augmentatory effect of estrogen on PRL secretion is dose-dependent in human beings.

Serum prolactin levels during puberty.

Serum prolactin (PRL) concentrations and total estrogen levels were determined in groups of boys and girls from ages eight through 15. There was no significant change in PRL concentration with advancing age in boys, and levels were comparable to adult men. In girls, mean serum PRL and estrogen levels were not significantly different from ages eight through 13 and were comparable to those found in boys of the same age groups. At age 14 and 15, an increase in PRL and estrogen levels was found in girls.

Augmentation of prolactin secretion by estrogen in hypogonadal women.

The effect of estrogen on prolactin (PRL) release and gonadotropin suppression was assessed in six experiments performed on four hypogonadal women. Ethinyl estradiol at a dose of 1 microgram/kg per day induced a significant elevation of serum PRL levels within the 1st wk of treatment. There was a further rise until a plateau was reached in about 3-4 wk to levels of more than 3 times the initial concentration. This was accompanied by a pattern of increased episodic fluctuation. The corresponding serum luteinizing hormone and follicle-stimulating hormone fell progressively during the study period. These data indicate that a positive feedback relationship between estrogen and PRL release exists in humans.