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Biomedical subjects

N Ofuji

Publications and source records attributed to N Ofuji.

9 recordsLinked to original sources
PubMed1978

[Studies on the effect of the therapeutic dosage of indomethacin on human gonadotropin secretion (author's transl)].

To investigate the effect of the therapeutic dosage (50 approximately 100 mg/day) of indomethacin (IDM), which is well-known to inhibit the synthesis of prostaglandins, on the human pituitary-gonadal axis, five experiments were performed. Exp. I and Exp. II: Six healthy male subjects pretreated with IDM for two days (Exp. I), and 12 male patients receiving IDM for 1 to 19 months (Exp. II) were examined. In these two IDM treated groups, resting levels of plasma LH did not change, and LH response to LH-RH (100 microgram i.v.) slightly increased as compared with nontreated control males (N=11). Resting levels of plasma FSH, and FSH response to LH-RH statistically and significantly suppressed in both IDM treated groups, except for FSH response to LH-RH in the IDM pretreated healthy male group. Exp. III: Two healthy women with regular menstrual cycles were treated with IDM for several days just before ovulation. These women's preovulatory LH surges were not blocked by IDM and were followed by a normal luteal pattern of basal body temperature. Exp. IV: Ten female patients receiving IDM for 1 to 10 months were examined. In 9 patients, normal preovulatory LH surges were observed. It was interesting that the duration of the luteal phase was shortened (less than 10 days) in 5 of the 10 patients, and mid-luteal plasma progesterone levels were less than 500 ng/dl even if some of those patients had a normal duration of the luteal phase. Exp. V: In five female patients treated with IDM for 1 to 9 months, mid-follicular gonadotropin secretions were estimated. Resting levels of plasma gonadotropins and their responses to LH-RH did not differ from the control female group (N=4). From these results, it was indicated that (1) the therapeutic dosage of IDM acted on the central nervous system and the anterior pituitary, and then suppressed FSH secretion in male subjects. There was sexual difference in the IDM effect on FSH secretion, that is, mid-follicular FSH secretion was not affected by IDM in female subjects. (2) LH secretion was not suppressed by IDM in either male or female subjects in the mid-follicular phase. (3) The therapeutic dosage of IDM did not block the preovulatory LH surge and ovulation in female subjects, but IDM might act on corpus luteum and cause luteal dysfunction.

Adolescent↗
PubMed1977

Influence of synthetic thyrotropin-releasing hormone tartrate monohydrate on plasma gonadotropin concentration of normal males.

Synthetic thyrotropin-releasing hormone (TRH) tartrate monohydrate was administered by rapid intravenous injection to nine normal males. Plasma thyroid-stimulating hormone (TSH), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured before and at selected periods after TRH injection. The mean plasma TSH value immediately prior to TRH injection was 3.5 muU/ml and the level 15 min after injection was 14.8 muU/ml. The mean plasma LH value immediately prior to TRH injection was 8.0 mIU/ml and the level 15 min after injection was 15.0 mIU/ml. The latter elevation was statistically significant (p less than 0.01), although it was just above the upper normal range. The mean plasma FSH value immediately prior to TRH injecion was 7.7 mIU/ml, and a significant difference was not observed after TRH administration. These results revealed that synthetic TRH tartrate monohydrate influenced the release of LH from the anterior pituitary.

Adult↗
PubMed1977

Effects of prostaglandin E1 and indomethacin on ACTH, prolactin, GH and LH from rat pituitary in vitro.

The effects of prostaglandin E1 (PGE1) and indomethacin (IDM) on the release of several pituitary hormones from the rat pituitary were investigated in vitro. An addition of 2 microng/ml of PGE1 to the medium elicited the release of growth hormone (GH) and prolactin, but not of adrenocorticotropin (ACTH) and luteinizing hormone (LH). Although the addition of 1 microng/ml of IDM alone resulted in no effect on the basal release of these hormones, IDM diminished the release of ACTH induced by crude rat hypothalamic extracts (HE) or lysine-8-vasopressin (LVP), and LH induced by HE or luteinizing hormone-releasing hormone (LH-RH). These findings implicate that a part of PGE1 action might be a direct one on the pituitary gland and PGE1 might release GH and prolactin, whereas IDM might have a direct action on the pituitary gland, and that blunt the release of these pituitary hormones induced by several stimuli.

Adrenocorticotropic Hormone↗
PubMed1976

[Plasma prolactin and thyroid-stimulating-hormone (TSH) in patients with breast cancer (author's transl)].

In order to investigate plasma prolactin and thyroid-stimulating-hormone (TSH) concentration and pituitary reserve of these two hormones in patients with breast cancer, following examinations were carried out. Plasma prolactin concentration was measured before and 15, 30, 60, 90 minutes after the 500mug of thyrotropin-releasing-hormone (TRH) i.v. injection in 22 patients with breast cancer and 4 patients with benign breast disease. All patients did not take any hormonal therapy and any medication inducing prolactin secretion. Ten healthy females were also tested as controls. Plasma prolactin concentration was estimated by a double antibody radioimmunoassay (RIA) technique using hPRL RIA kit provided by NIAMDD. The basal prolactin concentration in patients with breast cancer was 18.6 +/- ng/ml (Mean +/- SEM), and it was slightly higher than the control group (14.7 +/- 2.2 ng/ml), but not statistically significant. In 6 out of 22 patients with breast cancer, high plasma prolactin concentrations more than 25 ng/ml were observed. The maximal plasma prolactin concentration following the TRH injection was obtained at 15-30 minutes after TRH in most patients with breast cancer. The maximal value was 87.4 +/- 9.2 ng/ml, and it was near the upper limit of normal range of prolactin response, and not significantly higher than the maximal value in the control group (59.7 +/- 5.7 ng/ml). In 7 patients with breast cancer, the maximal prolactin values more than 100 ng/ml were obtained after TRH injection. There was no statistically significant difference between early breast cancer group (TNM: stage I & II, N=14) and advanced breast cancer group (TNM: stage III & IV, N=6) in both the plasma prolactin concentration and the pituitary prolactin reserve...

Adult↗
PubMed1976

[In vitro assay for ACTH-releasing activity using ACTH radioimmunoassay: ACTH releasing activities by various drugs (author's transl)].

Several procedures have been reported for the assay of corticotrophine-releasing factor (CRF), each having its advantages and disadvantages. This report deals with an in vitro assay of ACTH releasing activity utilizing pituitary incubation combined with ACTH radioimmunoassay. Rat half pituitary was preincubated in 2 ml Krebs Ringer bicarbonate buffer containing 0.2% glucose and 0.25 % BSA (KRBG-BSA) for 1.5 hr (45 min X 2). The medium was replaced by 1 ml KRBG-BSA and incubated for 30 min. Then the medium was again replaced by 1 ml KRBG-BSA or KRBG-BSA containing test materials and incubated for another 30 min. The amount of ACTH assayed by radioimmunoassay in the 2nd 30 min incubation was compared with in the 1st 30 min incubation and expressed as percentage. In ACTH radioimmunoassay, anti-ACTH serum was diluted to 1 : 1,500-3,000. The 125I-alpha 1-24ACTH-antibody system was not affected by lysine-vasopressin (LVP), arginine-vasopressin (AVP), rat's pituitary LH, GH and prolactin. Human 1-39ACTH was used as ACTH standard, and the dilution curve of incubation medium was paralleled with the standard curve. Repeatability of immunoassayable ACTH within-assay was 174 +/- 5.0 pg/tube (CV = 2.9%). A log dose-relationship was observed between the amounts of stalk median eminence extracts (SME ; NIAMDD) added to the incubation medium and its ACTH releasing activities. The sensitivity of this assay method was at least 0.1 SME or 10 mU of LVP and AVP. Using this method, it found that LVP, AVP, norepinephrine (100 ng/ml200 ng/ml) and 5-hydroxytryptophane (1 mug/ml) had ACTH releasing activities but LH-RH, TRH, glucagon, dopamine, phentolamine, propranolol, haloperidol, prostaglandin E1 and indomethacin did not affect the release of ACTH.

5-Hydroxytryptophan↗