Biomedical subjects

H E Carlson

Publications and source records attributed to H E Carlson.

At least 55 records · Page 3Linked to original sources

PubMed1983

Prolactin stimulation by meals is related to protein content.

To study the effect of meals on PRL secretion, serum PRL was measured after the ingestion of mixed meals and specific single macronutrients by normal men and women. In men, only protein feeding significantly stimulated PRL secretion. In women, protein meals as well as a standard mixed meal and a liquid mixed meal resulted in PRL release. Fat, glucose, and a nonnutrient meal had no consistent effect on serum PRL. Serum TSH was not altered by any of the meals, and serum GH and cortisol showed few changes. We conclude that PRL stimulation by meals may be of occasional clinical significance, principally in confusing the diagnosis of hyperprolactinemic states, especially in women. Dietary protein is probably the agent responsible for PRL secretion induced by meals.

Adult↗

PubMed1983

Endocrine influences on the actions of morphine. II. Responses to pituitary hormones.

Studies have been made on the hypophysectomy-induced changes in antinociceptive and temperature responses to morphine and the effects various anterior pituitary hormones have on these altered responses under both acute and chronic conditions. Hypophysectomy altered the slope of the dose-response curve for morphine antinociception without significantly changing the ED50. It also induced an upward shift in the temperature-response curve. Treatment of hypophysectomized animals with s.c. adrenocorticotropic hormone decreased responsiveness to the antinociceptive and the hyperthermic actions of morphine. Administration of triiodothyronine increased the antinociceptive response and normalized the upward shift in the temperature response; however, these effects required approximately 3 weeks of hormone treatment. Both of these treatments normalized the altered antinociceptive dose-response curve slope. Growth hormone, luteinizing hormone and prolactin had no effects on acute morphine responses. Further experiments examined the effects of anterior pituitary hormones during chronic treatment with morphine. Adrenocorticotropic hormone, when administered 30 min before morphine, showed reproducible but statistically nonsignificant suppression of tolerance development. Growth hormone, which had no effects on acute morphine responses, was more effective than adrenocorticotropic hormone at suppressing tolerance. In studies with animals bearing growth hormone/prolactin secreting tumors, significant suppression of tolerance was seen for both responses to morphine. These results add further support to previous findings from our laboratory that the adrenal and thyroid systems are involved in modulation of acute opiate actions and also indicate that growth hormone can inhibit the development of opiate tolerance.

Analgesia↗

PubMed1982

Circadian pattern of prolactin secretion in postmenopausal women receiving estrogen with or without progestin.

The circadian rhythm of prolactin secretion was assessed in postmenopausal women before and after daily administration of ethinyl estradiol for 4 weeks given in the morning (AM) or evening (PM) or in combination with a synthetic progestin, 17-medroxyprogesterone acetate. In response to AM ethinyl estradiol, mean circulating levels of serum prolactin during sleep and awake phases of the day rose 2.5-fold compared to untreated control values. The sleep/wake ratios for serum prolactin were comparable prior to and after AM administration of ethinyl estradiol. Altered time of administration, PM ethinyl estradiol or concomitant ethinyl estradiol and progestin treatment produced similar increases in mean prolactin levels, which were not different from the level observed during AM administration of ethinyl estradiol. These findings indicate that estrogen replacement therapy, in a dosage recommended for treatment of the menopause, stimulated a sustained rise in serum prolactin over 24 hours. This enhanced release of prolactin was not influenced by the time of administration of estrogen or concomitant administration of 17-medroxyprogesterone acetate.

Circadian Rhythm↗

PubMed1982

Nicotine from cigarette smoking increases circulating levels of cortisol, growth hormone, and prolactin in male chronic smokers.

Results of this study indicate that nicotine from cigarette smoking increases circulating levels of cortisol, growth hormone, and prolactin in male chronic smokers. Previous studies have not addressed the question of whether the stimulus for smoking-related hormone release is the 'stress' of smoking or a pharmacologic action of nicotine and other tobacco substrates. Nicotine exposure is controlled in this study by allowing each subject to smoke only two 2.0 mg nicotine cigarettes during one experimental session and two 0.2 mg nicotine cigarettes in another session. Plasma levels of cortisol, growth hormone, and prolactin for the higher nicotine session were found to be significantly elevated over those for the low-nicotine session, indicating that nicotine itself plays a predominate role in smoking-induced hormone increases. All hormone levels for the 2.0 mg nicotine session had not returned to baseline 60 min after smoking.

Adult↗

PubMed1982

Establishment of functional human pituitary tumor cell cultures.

Five primary human pituitary tumor cell cultures were initiated from adenoma fragments obtained from patients with prolactin-secreting adenomas and acromegaly. Functional cell cultures were maintained and propagated in monolayer or suspension culture for up to 9 months. Optimal cell viability and growth were achieved using Ham's F10 medium enriched with 20% fetal bovine serum, although cells from a patient with acromegaly also grew in serum-free, defined, hormone-containing medium. Bromocriptine (100 ng/ml) did not alter the growth curve of replicating cells derived from a patient with acromegaly. These cells initially secreted 5.5 micrograms human growth hormone/10(6) cells, and hormone production diminished after 6 wk. Prolactin secretion by cells derived from prolactinomas (0.5 to 1.3 micrograms/10(6) cells/24 h) was stimulated by thyrotropin-releasing hormone (10 ng/ml) in two of the cultures. Both dopamine (10 ng/ml) and nickel chloride (1 mM) suppressed PRL secretion. These studies demonstrate that responsive human pituitary tumor cell cultures can be initiated and maintained.

Adenoma↗

PubMed1982

Histidyl-proline diketopiperazine suppresses prolactin secretion in human pituitary tumour cell cultures.

Because histidyl-proline diketopiperazine (HPD), a metabolite of TRH, has been shown to suppress prolactin (PRL) release by rat pituitary tumour cells, human pituitary tumour cells were exposed to this compound. Monolayer cell cultures were initiated from pituitary tissue removed by transsphenoidal surgery from two patients with prolactin-secreting microadenomas. Tumour fragments were mechanically dispersed; cells were seeded into multiwell plates and incubated in Ham's F-10 medium enriched with fetal calf serum (20%). HPD (7.5 ng/ml) suppressed PRL release by both tumour cell cultures. Theophylline reversed the inhibition of PRL release induced by HPD. The data raise the possibility that HPD may act as an endogenous prolactin-inhibiting factor in man.

Cells, Cultured↗

PubMed1982

Radioimmunoassay detection of endorphins from long-term culture of human pituitary tumour cells.

Using a sensitive and precise radioimmunoassay for human beta-endorphin, we have demonstrated the sustained secretion of opioid peptides from human pituitary tumour cells. Pituitary tumour tissue obtained from a patient with Nelson's syndrome was maintained in continuous monolayer culture and secreted both beta-lipotropin and beta-endorphin, with predominance of the latter. This is compatible with the idea that the beta-endorphin in normal human serum is secreted as such despite the predominance of beta-lipotropin compared with beta-endorphin in the anterior pituitary.

Cells, Cultured↗

PubMed1981

The role of opiates and endogenous opioid peptides in the regulation of rat TSH secretion.

The administration of morphine to rats at room temperature is reported to suppress serum thyrotropin (TSH) levels by a hypothalamic mechanism. However, it is unknown whether endogenous opioid peptides (EOP) are involved in the control of TSH secretion. The present studies show that naloxone (10 mg/kg, i.p.) an opiate-receptor antagonist, prevented the decline in rat serum TSH which occurs with heat exposure. Morphine sulfate (20 mg/kg, i.p.) treatment prevented the cold-induced elevation in serum TSH and pretreatment with haloperidol (0.3 mg/kg, i.p.) eliminated morphine's influence. Medial-basal hypothalamic thyrotropin-releasing hormone (TRH) content, measured by RIA, increased in the morphine-treated rats which were exposed to 4 degrees C. A submaximal intravenous dose of TRH (300 ng/100 g) was given to determine whether morphine suppresses serum TSH through the release of hypothalamic thyrotropic inhibitors. Morphine pretreatment did not alter TSH stimulation by TRH. Morphine alone or combined with TRH did not alter basal or stimulated TSH secretion in vitro. These studies strongly suggest that, in rats, the EOP modulate TSH secretion under conditions such as acute heat exposure which was associated with a decline in serum TSH. Under specific circumstances, the suppression of serum TSH by morphine may be dopamine-dependent.

Animals↗

PubMed1981

Elevated serum prolactin level in the Zollinger-Ellison syndrome.

To estimate the prevalence of prolactinoma in the Zollinger-Ellison syndrome (ZES), serum prolactin (PRL) levels were measured by radioimmunoassay in 36 patients with ZES. Eight patients had elevated PRL levels; however, in one patient the finding was attributed to primary hypothyroidism rather than a prolactinoma. The seven other patients were believed to have previously undiagnosed prolactinomas on the basis of elevated serum PRL levels; the presence of pituitary tumors were confirmed in four by demonstration of sella turcica erosions or enlargement. Serial determinations over three to six years showed a tendency for serum PRL levels to increase modestly in four of six patients. Thus far, two patients have undergone transsphenoidal tumor resections with good results. This study suggests that the prevalence of prolactinoma in patients with ZES is substantial (10% for those with isolated ZES and 54% for those with ZES with multiple endocrine neoplasia, type 1, syndrome), and that early diagnosis is possible with measurement of serum PRL levels. Since levels of PRL tend to increase and clinically significant pituitary tumors can develop, determinations of serial serum PRL levels are recommended for all patients with ZES.

Adenoma, Islet Cell↗

PubMed1981

Endocrine effects of acute and chronic cimetidine administration.

In normal men, acute oral administration of 300 mg cimetidine or intravenous injection of 50 mg of the drug had no effect on prolactin release. In contrast, intravenous injection of 150 or 300 mg led to substantial increments in serum prolactin. Peptic ulcer patients were randomly assigned to treatment with either cimetidine or antacid. Serial blood sampling until ulcer healing showed no significant changes in serum prolactin, testosterone, free testosterone, estradiol, LH, or FSH in either group. It is likely that the impotence and breast changes occasionally seen during cimetidine therapy are due to peripheral antagonism of androgen action rather than to alterations in circulating hormone levels.

Adult↗

PubMed1981

Effect of cimetidine on serum prolactin in normal women and patients with hyperprolactinaemia.

In normal women, intravenous injection of the H2-antihistamine, cimetidine, provoked a 3-4 fold rise in serum prolactin, without changes in serum growth hormone, thyrotrophin, or gonadotrophins. Hyperprolactinaemic patients with pituitary tumours, idiopathic hyperprolactinaemia or hypothalamic lesions demonstrated little or no rise in serum prolactin (expressed as a percentage increment) in response to cimetidine; these responses were significantly more blunted than the prolactin responses to intravenous TRH in the same subjects. Post-partum women also demonstrated blunted percentage prolactin responses to cimetidine, although responses to TRH were, in most patients, normal. Dynamic testing of prolactin secretion with cimetidine is no more useful than TRH in distinguishing tumourous from non-tumourous hyperprolactinaemia.

Adolescent↗

PubMed1981

Morphine and naloxone: effects on beta-endorphin immunoreactivity in canine plasma and secretions from rat pituitaries.

Morphine and naloxone were administered to five dogs to assess their effects on endogenous opioid release. Morphine (3 mg/20 kg) produced a significant (P less than 0.05) increase in plasma beta-endorphin immunoreactivity(beta EI) compared to saline control. The peak stimulation [19.2 +/- 4.97 baseline to 48.1 +/- 6.82 (SEM) pg/ml] occurred at +10 min and rapidly returned to preinjection levels at +60. At a dose 10 times equipotent to circulating basal beta EI, morphine (4-6 micrograms) failed to affect beta EI release. Naloxone, surprisingly, also caused a significant (P less than 0.025) release of beta EI. After naloxone, beta EI rose from a preinjection baseline of 36.4 +/- 5.82 pg/ml to a peak of 172 +/- 44.1 pg/ml at 45 min post injection. Naloxone pretreatment also obscured the effect of subsequently injected morphine (3 mg/20 kg). In three naloxone-treated dogs, gel chromatography of pooled basal and peak plasma revealed a preponderance of beta-lipotropin compared to beta-endorphin. To determine the site of stimulation of beta EI by opiates and opioids, a series of rat anterior pituitary incubations were performed. Neither morphine (10(-6) M) nor D-Ala2-methionine enkephalinamide (10(-6) M) nor naloxone (10(-6) M) had an effect significantly different from control medium on the release of beta EI from the pituitaries. In a second set of experiments we compared the effect on beta EI release of hypothalamic median eminence extract alone or with morphine. Hypothalamic median eminence extract at two concentrations produced significant release of beta EI, which was unaffected by the addition of morphine. These results suggest that stimulation of release of endogenous opioid peptides by opiates occurs at a suprapituitary level.

Animals↗

PubMed1981

The relationship of androgen to the thyrotropin and prolactin responses to thyrotropin-releasing hormone in hypogonadal and normal men.

Fluoxymesterone, an androgen not converted to estrogen, caused a significant decrease in the TSH response to TRH in 11 men with primary hypogonadism [maximum change in TSH: before treatment, 11.3 +/- microU/ml (mean +/- SE); 8.9 +/- 1.0 after 2 weeks (P less than 0.001); 8.2 +/- 1.1 after 6 weeks (P less than 0.01)]. There was a significant fall in serum T4-binding globulin (TBG) (measured directly by RIA) without a change in the free T4 or free T3 index. Fluoxymesterone had no effect on the PRL response to TRH in hypogonadal men. The results suggest that 1) androgen per se is at least partly responsible for the lower TSH response to TRH in men compared to women and 2) androgen is not a cause of the lower PRL response to TRH in men.

Adult↗

PubMed1981

Prolactin and calcitonin responses to parathyroid hormone infusion in hypoparathyroid, pseudohypoparathyroid, and normal subjects.

Since parathyroid hormone (PTH) has been reported to release PRL in normal humans, we studied the effects of exogenous PTH infusion (150 U) on the secretion of PRL, TSH, and calcitonin in 10 normal subjects, 5 with hypoparathyroidism, and 10 with pseudohypoparathyroidism, type I (PHP). PTH produced a rise in serum PRL in the normal subjects from 5.1 +/- 0.8 ng/ml (SE) to 14.9 +/- 3.0 ng/ml (P less than 0.01), while levels similarly rose from 4.0 +/- 0.2 to 8.5 +/- 0.8 ng/ml (P less than 0.01) in the patients with hypoparathyroidism. In 6 PHP patients with deficient PRL responses to TRH, the PRL response to PTH was also blunted (basal, 3.2 +/- 0.81 ng/ml; peak, 4.1 +/- 1.3 ng/ml; P greater than 0.1). Three of 4 PHP patients with normal PRL responses to TRH demonstrated a normal PRL increment in response to PTH infusion. Serum TSH and calcitonin were not changed by PTH infusion in any of the groups. These findings demonstrate that the resistance to PTH seen in PHP does not extend to the pituitary gland.

Adolescent↗

PubMed1981