[Effects of naloxone and morphine on the proestrous surge of prolactin and gonadotropins in the rat (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Ieiri.
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A 50-day-old boy with severe lactose intolerance is described. In addition to vomiting, failure to thrive, dehydration, metabolic acidosis and amino aciduria, bilateral cataracts were also found. At three months of age, a computerized axial tomography scan and an electroencephalogram were abnormal, and myoclonic spasms began at the age of seven months.
The effects of morphine (M) and naloxone (N) on serum levels of luteinizing hormone (LH) and prolactin (PRL) in prepubertal male and female rats were investigated. N raised serum LH concentrations in female rats at 10, 15, 20, 25 and 30 days of age, but increased serum LH levels in male prepubertal rats only at 30 days of age. M significantly depressed serum LH values in both sexes only at 15 days of age. M increased serum PRL levels in immature rats of both sexes in all age groups, except in 25-day-old males, whereas N decreased serum PRL only in 25-day-old male rats. These data show that there are differences in the pituitary LH and PRL responses to M or N of immature as compared to the responses previously reported in mature rats, and suggest that the endogenous opioid peptides may have a role in regulating LH and PRL secretion in immature rats.
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A patient, 38-year-old man, with hemorrhage into a prolactin-secreting pituitary adenoma, or pituitary apoplexy, is reported. On his admission, clinical examinations revealed typical stigmata indicating that he suffered from an acute attack of pituitary apoplexy probably induced by acute meningitis. He survived the acute attack and recovered spontaneously without an urgent operation. Although there was no suspicious sign and symptom of hypopituitarism, the first study performed immediately after the attack suggested strongly that hypopituitarism might acutely developed during the hemorrhage into the tumor. Moreover, the follow-up studies indicated that TSH, LH and ADH recovered spontaneously from the initial damage following the resorption of hemorrhage for the next 3 months.
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Tracer doses of 131I- (Carrier free), 131I-T3 and 131-T4 were administered po to 19 healthy male volunteers at intervals 2 to 8 weeks to study whether or not part of the iodide generated in the kidney from T3 and T4 deiodination may enter the renal tubular lumen and be excreted in the urine without entering the blood stream. U(urine)/T(thyroid) ratios of the radioactivity from these materials were employed as the index of the comparison. U/T ratios were severalfold higher 24 h after 131I-T3 or 131I-T4 administration than after 131I-. The data indicate that the 131I- derived from T3 and T4 metabolism is more readily excreted into urine than 131I- which reaches the kidney as inorganic iodide.
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In order to compare the acute effects of three kinds of antithyroid agents of iodide (I-), propylthiouracil (PTU) and PTU combined with iodide (PTU+I-) on thyroid function in hyperthyroid patients with diffuse goiter, serum concentrations of thyroxine (T4), triiodothyronine (T3), T3-resin sponge uptake (T3-RU) and free thyroxine index (FT4I) were employed as thyroid function parameters. In the group given iodine (1 mg/day) as iodinated-lecithine, the initial values of T4, T3, T3-RU and FT4I were 20.9 +/- 1.6 microng/100 ml (T4), greater than 740 ng/100 ml (T3), 49.5 +/- 2.3% (T3-RU) and 14.7 +/- 1.8 (FT4I). At the end of one week of therapy, they decreased clearly to 15.6 +/- 2.2 microng/100 ml, 457 +/- 87 ng/100 ml, 42.2 +/- 4.0% and 9.7 +/- 2.4. The so-called "escape phenomenon" from iodide inhibition was observed in serum T4, T3-RU and FT4I values at the end of two weeks of iodide therapy, while serum T3 continued to decrease but the value of T3 was far outside of the normal range. In the PTU group (300 mg/day), thyroid function parameters were 22.5 +/- 0.8 microng/100 ml (T4), greater than 592 ng/100 ml (T3), 54.9 +/- 1.0% (T3-RU) and 18.7 +/- 1.0 (FT4I) before treatment. They decreased continually week by week. At the end of four-week treatment with PTU, the value of each thyroid function parameter was 11.1 +/- 1.9 microng/100 ml, 229 +/- 56 ng/100 ml, 36.6 +/- 4.4% and 5.7 +/- 1.7. In the group of hyperthyroidism simultaneously given both PTU and iodide (300 mg/PTU and 1 mg/iodine), these thyroid function parameters decreased as well as in the group treated with PTU alone for more than two weeks. More rapid or significant decrease of T4, T3, T3-RU and ft4i in PTU+I- group than in PTU group was observed in the present study. These results suggested strongly that iodide alone was not an adequate therapy for hyperthyroidism as well known and they were also compatible with the idea that the concomitant administration of PTU and iodide was more effective in the early phase of therapy of hyperthyroidism than PTU alone.
Recently, L-dopa has been known as one of drugs to stimulate the secretion of growth hormone from the pituitary gland through dopamine, which is a metabolic of L-dopa, without any changes of serum insulin levels, blood sugar values, fatty acids and amino acids concentrations in the serum of human being. The present study was thus designed to assess the effect of L-dopa on the pituitary gland to secrete the growth hormone in the normal subject and the study was further extended to compare the response of the pituitary secretion of the growth hormone following the administration of L-dopa between in the patient with diabetes mellitus and in the normal subject. In the present experiment, 5 normal subjects and 11 diabetes mellitus without obesity were employed and they received a 30 min infusion of 200 mg L-dopa dissolved in 200 ml physiological saline. In normal subjects, serum growth hormone concentration measured by radio-immunoassay was started to increase within 10 min after L-dopa administration and maximum value of serum growth hormone was obtained 60 min after the drug, mean values of it, 30 ng/ml of serum. Then it was declined sharply upto the values of 2-3 ng/ml. In the patients with diabetes mellitus, on the other hand, maximum value of serum concentration of the growth hormone was only approximately 5 ng/ml of serum obtained between 45 and 75 min after the administration of L-dopa. No changes in the serum concentration of IRI (Immunoreactive insulin) and of blood sugar values were observed by the infusion of L-dopa in both normal subjects and diabetes mellitus. From the above mentioned facts, it was concluded that the ability of pituitary gland to secrete the growth hormone was considerably impaired in diabetics when it was compared with normal subjects.
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