Biomedical subjects

A G Frantz

Publications and source records attributed to A G Frantz.

At least 73 records · Page 4Linked to original sources

PubMed1976

Acute and chronic estrogen effects upon serum somatomedin activity, growth hormone, and prolactin in man.

Estrogen (E) reduces bioassayable GH-dependent serum somatomedin (SM) activity in acromegalics without affecting plasma growth hormone (GH) levels and inhibits the rise of SM activity normally produced by GH administration in GH-deficient subjects. We have now investigated the effect of E administration on serum SM activity and on plasma GH and prolactin (PRL) in 6 adult male subjects without pituitary pathology. Chronic E administration (ethinyl estradiol 0.5 mg/day for 7 to 70 days) reduced serum SM activity by 40 to 62% in each of 4 subjects (P less than 0.02 to less than 0.001). In 3 of the subjects, basal GH levels increased by 75 to 300% (P less than 0.05 to less than 0.001) and basal PRL levels increased by 90 to 200% (P less than 0.01 to less than 0.001). While iv administration of normal saline did not significantly affect either SM or GH, iv administration of E (bolus injection of 25 mg conjugated estrogens, USP) to 5 subjects resulted in: a) a 46 to 80% decrease in serum SM activity in all subjects, proceeding with an apparent half-life of 2 hours, becoming significant (P less than 0.05) at 2 hours (1 subject) to 3 hours (4 subjects), maximal at 6 hours, and persisting for 12 to 24 hours; b) GH elevation to 3 to 16 times baseline level (P less than 0.01) at 2 to 3 hours in 4 subjects; and c) no significant change of PRL levels in any subject. The mean GH response to iv E was maximal at a time (2 hours) when the mean SM activity had decreased only 20% and subsided well before the nadir of SM activity. The one patient without GH response to chronic or acute E administration may have been affected by absorption of triamcinolone being applied topically during the study. These results demonstrate that in males with normal pituitary function, E reduces serum SM activity, enhances basal GH and PRL secretion, and, upon iv injection, stimulates acute GH release. Although opposite chronic E effects upon GH and SM activity support a putative negative SM-GH feed-back mechanism, iv E administration apparently provokes acute GH release by a different mechanism. The half-life of serum SM activity in the human is probably much shorter than previously estimated.

Adult↗

PubMed1976

The effect of aspirin and indomethacin on the TRH response in man.

A double-blind study of the effect of two inhibitors of prostaglandin synthesis on the TRH stimulation of serum TSH and prolactin was carried out in 35 normal males. The subjects were evaluated before and after the administration of indomethacin or aspirin for one week. Both indomethacin and aspirin lowered plasma prostaglandin E and F levels significantly. Indomethacin treatment had no effect on the serum TSH or prolactin response to 100 mug TRH or the serum T3 and T4 levels. In contrast, aspirin treatment significantly decreased the serum TSH response to TRH and significantly lowered mean total serum T3 (RIA) and T4 (D). There was no effect on the prolactin response to TRH. These findings suggest that aspirin blocks TRH responsiveness by a mechanism other than the inhibition of prostaglandin synthesis, probably by its previously demonstrated effect on increasing the fraction of unbound thyroid hormone.

Adolescent↗

PubMed1976

Suppression of prolactin secretion by L-dopa in the stalk-sectioned rhesus monkey.

The effects of iv administration of L-dopa on serum prolactin were studied in both normal female rhesus monkeys and in monkeys in which the pituitary stalk had been previously sectioned. Revascularization of the pituitary gland was prevented by the insertion of a silastic barrier over the diaphragma sellae. Prolactin secretion was increased in all stalk-sectioned monkeys and, in contrast to intact animals, chlorpromazine administration was ineffective in further releasing prolactin. In both normal and stalk-sectioned monkeys, iv administration of L-dopa (3-120 mg) significantly inhibited prolactin release from the pituitary (P less than .005 normal; P less than .001 stalk section). L-dopa also suppressed the TRH-induced release of prolactin in both groups. These results indicate that L-dopa or dopamine may act directly on the anterior pituitary to inhibit prolactin secretion.

Animals↗

PubMed1976

Phencyclidine sedation as a technique for handling rhesus monkeys: effects on LH, GH, and prolactin secretion.

Rhesus monkeys, sedated with phencyclidine hydrochloride (Sernylan), were quieted for prolonged periods of time, while maintaining somatic reflexes, muscle tone, and respiration. Brief daily periods of sedation did not interfere with the menstrual cycle. Prolonged sedation, however, interfered with the experimentally estrogen-induced LH surge, but not with the inhibitory action of estrogen on LH tonic secretion. Pulsatile release of LH, GH, and prolactin persisted even under prolonged sedation. The secretion of prolactin in response to the administration of TRH was increased in animals sedated with phencyclidine.

Animals↗

PubMed1976

Prolactin, thyrotropin, and growth hormone release during stress associated with parachute jumping.

Prolactin, growth hormone, and thyrotropin (TSH) release during the stress of parachute jumping has been evaluated in 14 male subjects. Subjects were studied at several times before and immediately after their first military parachute jump. All three hormones had risen significantly 1 to 14 min after the jump, compared to mean levels measured immediately beforehand. Earlier studies of physical exercise by ourselves and others would suggest that emotional stress played a role in producing changes of this magnitude. We conclude that prolactin, TSH, and growth hormone are released in physiologically significant amounts in association with the stress of parachute jumping.

Adolescent↗

PubMed1975

Thioridazine stimulates prolactin secretion in man.

Thioridazine, unlike most other effective antipsychotic drugs, appears to be only a weak dopamine antagonist in various regions of the brain. We decided to test, indirectly, thioridazine's effects on another brain dopaminergic system, the tuberoinfundibular tract, which regulates prolactin secretion by stimulating hypothalamic secretion of prolactin-inhibiting factor. Chlorpromazine and several other phenothiazines have been shown to stimulate prolactin secretion. Five healthy men ingested 50 mg of chlorpromazine concentrate on one occasion, and 50 mg of thioridazine concentrate on another. Both drugs noticeably stimulated prolactin secretion within two hours. It is concluded that thioridazine is a potent dopamine antagonist in the tuberoinfundibular system, and it is suggested that this system's regulation of prolactin secretion may provide a useful method for studying antipsychotic drug effects in man.

Administration, Oral↗

PubMed1975

Failure of oral water loading and intravenous hypotonic saline to suppress plasma prolactin in man.

To test the effect of acute changes in plasma osmolality on plasma prolactin concentrations, the hormone was measured before and during oral water loading, hypotonic saline infusion, and hypertonic saline infusion in normal subjects. In 10 normal men there was a small but statistically significant rise in mean prolactin, from 7.6 to 12.3 ng/ml, occurring within half an hour after the ingestion of a water load of 20 ml/kg. A small but statistically insignificant rise in mean plasma prolactin was observed in 11 normal women, although there was a significant negative correlation between plasma prolactin and plasma osmolality in these subjects. No effect of the intravenous infusion of either hypotonic saline (0.45%) or hypertonic saline (5%) on mean plasma prolactin was noted in 5 normal men. These studies do not confirm a previously reported suppression of prolactin concentrations by oral water loading of hypotonic saline infusions in normal subjects. While the data suggest a negative correlation between plasma osmolality and plasma prolactin, at least after water loading, they do not support a physiological role for prolactin in the short-term regulation of plasma osmolality in humans.

Administration, Oral↗

PubMed1975

Failure of propranolol to alter thyroid iodine release, thyroxine turnover, or the TSH and PRL responses to thyrotropin-releasing hormone in patients with thyrotoxicosis.

A dual isotope method allowing simultaneous analysis of both endogenous thyroidal release and peripheral thyroxine disposal was employed in four patients with thyrotoxicosis before and during propranolol therapy (160 mg/day) to determine whether beta adrenergic blockade with this agent affected the secretion or metabolism of thyroid hormone. Since catecholamines may be involved in the regulation of both thyrotropin (TSH) and prolactin (PRL) release from the pituitary, the effect of propranolol on the TSH and PRL responses to thyrotropin-releasing hormone (TRH) was also examined. In the dosage employed in these patients, propranolol had no demonstrable effect on either thyroid hormone secretion, the peripheral disposal of T4, or the TSH and prl responses to TRH.

Humans↗

PubMed1975

Effect of an oral water load on serum TSH in normal subjects, and on TSH and prolactin response to thyrotropin-releasing hormone (TRH) in patients with primary hypothyroidism.

Reports of suppression of plasma prolactin (PRL) in humans by water loading led us to examine the effect of a 20 cc/kg water load on serum TSH in 21 normal volunteers. In addition, the effects of a water load on basal and TRH-stimulated TSH and PRL levels were evaluated in seven patients with primary hypothyroidism. The water load had no effect on pasal serum TSH levels in either normal or hypothyroid subjects, and did not alter the TSH response to TRH in hypothyroid subjects. Basal or TRH-stimulated plasma PRL was also unaffected by water loading in the hypothyrpid subjects. These data suggest that a water load of 20 cc/kg does not significantly affect TSH release by the anterior pituitary, and also provide further evidence that water loading does not consistently suppress PRL secretion.

Administration, Oral↗

PubMed1975

Nicotine-stimulated release of neurophysin and vasopressin in humans.

Nicotine stimulation, induced by cigarette smoking, has previously been identified as a potent stimulus for vasopressin release in humans. In this study, radioimmunoassay measurements of plasma vasopressin and human neurophysin were performed on samples taken from 14 normal subjects during cigarette smoking. Significant rises in vasopressin occurred in 10 of the 14 subjects and the same 10 had significant rises in neurophysin. Pretreatment with ethanol in 3 subjects either eliminated or greatly blunted the responses of both vasopressin and neurophysin to cigarette smoking. These studies indicate that the release mechanisms for vasopressin and neurophysin are closely linked in humans.

Adult↗

PubMed1975

Klinefelter's syndrome: examination of thyroid function, and the TSH and PRL responses to thyrotropin-releasing hormone prior to and after testosterone administration.

Thyroid function and prolactin (PRL) responsiveness to thyrotropin-releasing hormone (TRH) were examined in 6 patients with Klinefelter's syndrome prior to and after therapy with testosterone. The thyroid function tests, including serum triiodothyronine (T3), thyroxine (T4), thyroxine binding globulin (TBG), resin T3 uptake (RT3U), radioactive iodine uptake (RAIU), thyrotropin (TSH) stimulation and the TSH response to TRH were normal during both periods of study. Testosterone treatment had no significant effect on any of these parameters with the exception of the RT3U which increased. PRL response to TRH were significantly higher than those observed in normal men (P less than 0.05). Despite the fact that mean plasma PRL responses to TRH were decreased when the patients were restudied during testosterone therapy, they remained greater than those of normal men. Mean serum estradiol concentrations were normal and did not increase significantly during testosterone therapy. These studies suggest that: (1) thyroid function may be normal in patients with Klinefelter's syndrome more often than previously reported, and (2) patients with Klinefelter's syndrome may manifest PRL hyper-responsiveness to TRH that is decreased but not normalized during testosterone therapy. Because estradiol levels failed to increase despite a marked rise in testosterone, further studies are warranted to examine testosterone and estradiol clearance and conversion rates in patients with Klinefelter's syndrome.

Adolescent↗

PubMed1975

Dopamine antagonism by thioridazine in schizophrenia.

One of the leading current theories of the etiology of schizophrenia is excessive activity of some brain dopaminergic tracts. One of the major objections to the theory is that thioridazine is clinically as effective a treatment of schizophrenia as other neuroleptic drugs but appears to have much less dopamine-blocking properties than these agents in man and laboratory animals. Serum prolactin levels are increased by dopamine receptor-blocking drugs. We have found that thioridazine is as effective as chlorpromazine, trifluperazine, and prolixin enanthate in increasing serum prolactin levels in unmediated schizophrenic patients, indicating it is an effective dopamine-blocking agent.

Administration, Oral↗

PubMed1974