Search PubMed⌕ Search

Biomedical subjects

T Kumasaka

Publications and source records attributed to T Kumasaka.

At least 73 records · Page 4Linked to original sources
PubMed1986

[Study of the correlation between gonadotropin- and prolactin-releasing systems in women in the luteal phase and early pregnancy].

The purpose of this study was to investigate the correlation between gonadotropin (Gn) and prolactin (PRL) releasing activities on the hypothalamo-pituitary axis in the luteal phase of the normal menstrual cycle and in the early gestational period. The plasma levels of LH-beta subunit (LH-beta) following an intravenous bolus of 100 micrograms LHRH did not change significantly in early pregnancy. The plasma PRL levels, as well as the Gn levels, were significantly elevated (p less than 0.05) after the administration of 100 micrograms LHRH in the luteal phase, but did not rise in early pregnancy. The intravenous bolus of 10mg metoclopramide (MCP) had no effect on plasma LH-beta, LH, FSH, estradiol or progesterone in the luteal phase or early pregnancy. The plasma PRL levels remained significantly (p less than 0.001) elevated after the administration of MCP. However, there was no significant difference between PRL response to MCP in the early pregnant and luteal phase groups. In the luteal phase, we could show the correlation between Gn and PRL releasing mechanisms on hypothalamo-pituitary axis, which could not be found in early pregnancy.

Estradiol↗
PubMed1986

Prolactin-releasing system in maternal, fetal, and amniotic compartments during labor.

The effect of a dopamine antagonist on prolactin concentrations was studied in maternal, fetal plasma, and amniotic fluid in term gestation. Twenty-three women with normal full-term pregnancies received 10 mg metoclopramide intravenously during labor. The prolactin levels in maternal plasma increased significantly after metoclopramide. However, the prolactin levels in amniotic fluid and fetal plasma did not change significantly after administration of this drug. Although the increased values of prolactin in maternal plasma were significantly correlated with metoclopramide concentrations after metoclopramide injection, there was no correlation between these two values in amniotic fluid. The authors conclude that the prolactin-releasing system in amniotic fluid is independent of the maternal hypothalamopituitary axis.

Adult↗
PubMed1985

[Restoration of pituitary-ovarian function by pulsatile administration of GnRH during the early puerperium].

In general, the hypogonadotropic hypogonadism seen during early puerperium is thought to be due to long-term deprivation of endogenous GnRH during the course of pregnancy. Recently, based on the pulsatile nature of hypothalamic GnRH section, it has been demonstrated that pulsatile administration of this decapeptide is effective in activation of the pituitary-ovarian function and induction of ovulation in patients with endogenous GnRH deficiency. Thus, we investigated whether this physiological replacement of GnRH can bring about the rapid restoration of the pituitary-ovarian function in early puerperal women. Fourteen postpartum women who had undergone cesarean section for obstetric reasons at 37-41 weeks of gestation volunteered for this study. Six of them received 10 micrograms (one subject received 5 micrograms) of GnRH in every 90 min from day 0-5 postpartum for 7-17 days duration by a portable auto-infusion pump. The remaining 8 subjects without treatment served as controls. On day 14 postpartum, serum baseline values of LH and FSH were significantly higher and their responses to the 100 micrograms GnRH challenge test were significantly greater in GnRH-treated subjects than those in the control subjects, respectively. Serum estradiol levels increased day by day, reaching more than 500 pg/ml at the end of the treatment in the 6 subjects. One of them ovulated within 3 weeks postpartum following GnRH treatment and subsequent hCG administration. These results demonstrate that the physiological replacement of pulsatile GnRH can restore the pituitary-ovarian function even within the first 2 weeks postpartum and in the presence of puerperal hyperprolactinemia. They also suggest that a deficiency of endogenous GnRH secretion may account for, at least in part, the pathophysiology of the hypogonadotropic hypogonadism during early puerperium.

Chorionic Gonadotropin↗
PubMed1985

[Effect of dopaminergic agents on the endocrine profile in labor and early puerperium].

The purpose of this study was to investigate the prolactin (PRL) releasing mechanism of the hypothalamo-pituitary axis during labor and early puerperium. Ten full-term gravidas during labor and 42 women in early puerperium were examined in this study. The plasma PRL levels rose significantly (p less than 0.001 approximately 0.05) after an intravenous bolus of 10mg metoclopramide (MCP). The peak values for PRL increase were 609.3 +/- 194.1ng/ml during labor and 447.0 +/- 62.3ng/ml in early puerperium. However, there were no significant differences in PRL response to MCP between these two groups. The plasma PRL levels dropped significantly (p less than 0.001 approximately 0.01) after an oral administration of 2.5mg bromocriptine (BRC), and the PRL release from the pituitary by MCP was suppressed significantly (p less than 0.001) by pretreatment with BRC in the puerperium. In addition, no significant changes in plasma 17 beta-estradiol (E2), progesterone (P) and cortisol levels could be observed after MCP. We concluded that the control mechanism of PRL secretion remained unchanged during labor and early puerperium.

Bromocriptine↗
PubMed1984

[Induction of ovulation with pulsatile LHRH in anovulatory women].

Nine anovulatory patients were treated by administering pulsatile LHRH (2-20 micrograms, i.v. at 90 min intervals) for 15-58 days. These patients consisted of 4 women with hypothalamic amenorrhea, one women with oligomenorrhea, 2 women with polycystic ovarian disease (PCOD) and 2 women with hyperprolactinemic amenorrhea. Four of them were involuntarily infertile. The pulsatile LHRH therapy induced follicular maturation and ovulation, as evidenced by increased plasma estradiol levels followed by a midcycle LH surge and subsequent rise in plasma progesterone (P) levels, in 8 of the 9 patients. One patient with PCOD failed to ovulate. All of 11 treatment cycles were ovulatory in the 8 patients. A maximal P level of below 10 ng/ml was seen in 3 of the 11 induced ovulatory cycles, indicating corpus luteum insufficiency. Luteolysis occurred soon after discontinuing the pulsatile LHRH administration at the mid to late luteal phase in 3 ovulatory cycles. One of the 4 infertile women became pregnant. The results indicate that chronic pulsatile administration of LHRH is useful in inducing ovulation not only in hypothalamic amenorrhea, but also in PCOD and hyperprolactinemic amenorrhea. They also suggest that although a possible augmentation of the hypothalamic LHRH release at the preovulatory phase cannot be denied, a series of endocrine events during the human menstrual cycle may be regulated by the feedback action of the ovarian signals on the pituitary under a fixed input of the hypothalamic LHRH.

Adult↗
PubMed1984

The prolactin-releasing mechanism of the hypothalamo-pituitary axis in pregnancy.

The purpose of this study was to investigate the prolactin (PRL)-releasing mechanism of the hypothalamo-pituitary axis in pregnancy. Forty-six gravidas in the first and second trimesters received bromocriptine (BRC), 2.5 mg orally, metoclopramide (MCP), 10 mg intravenously, or thyrotropin-releasing hormone (TRH), 500 micrograms intravenously. Additionally, BRC was given orally to another 42 gravidas 60 minutes prior to the intravenous injection of MCP or TRH. The plasma PRL levels decreased significantly after BRC and remained significantly elevated after MCP or TRH administration. However, there were no significant differences of PRL response to these agents between the first- and second-trimester groups. The PRL release from the pituitary by MCP or TRH was suppressed significantly by pretreatment of BRC in the gravidas. We concluded that the control mechanism of PRL secretion remained unchanged in the first and second trimesters.

Adult↗
PubMed1984

[Plasma prolactin response to suckling stimulation in puerperal women].

Plasma PRL response to suckling was studied during the 1st week, between the 1st and 2nd weeks and between the 4th and 5th weeks postpartum. During the 1st week, mean (+/-SE) basal PRL significantly rose from 201.9 +/- 27.5 ng/ml to 294.7 +/- 25.6 ng/ml at 15 min and 300.9 +/- 25.9 ng/ml at 30 min after suckling had begun. Between the 1st and 2nd weeks, mean basal levels and the responses to suckling were not significantly different from those during the 1st week. Between the 4th and 5th weeks, mean basal values were considerably lower and the responses to suckling were significantly greater [51.8 +/- 6.9 ng/ml at 0 min; 212.9 +/- 14.8 ng/ml at 15 min and 239.3 +/- 21.4 ng/ml at 30 min] than those within the 2nd week. Assessment of intersubject variations within the 5th week revealed that a significant inverse correlation existed between the basal levels and the suckling-induced maximum increments in PRL (r = -0.538, p less than 0.001). The effects of the oral administration of two serotonin antagonist (cyproheptadine and metergoline) and the dopamine infusion on plasma PRL levels and the response to suckling were investigated during the 1st week postpartum. Metergoline and dopamine suppressed basal PRL levels and abolished the response to suckling, whereas cyproheptadine suppressed the response less effectively without modifying the basal levels. These data suggest that in the early puerperal period an inverse relationship exists between the basal level and the response to suckling in plasma PRL. The suckling-induced PRL release may be mediated via a serotonergic as well as a dopaminergic pathway.

Cyproheptadine↗
PubMed1983

[Effect of a histamine H2-receptor antagonist, cimetidine, on prolactin secretion in women].

The effect of acute intravenous injection of 400mg cimetidine, a histamine H2-receptor antagonist, on prolactin (PRL) secretion was investigated in women with normal menstrual cycles (n = 12) and normoprolactinemic secondary amenorrhea (n = 10). In addition, the PRL response to cimetidine was also examined in women with puerperal (n = 10) and idiopathic (n = 10) hyperprolactinemia. The administration of cimetidine provoked a rapid rise in plasma PRL in both normal and amenorrheic women, with peak values occurring at 10-15 minutes, followed by a return toward the baseline by 2 hours. The PRL response was significantly greater (p less than 0.001) in normal women [mean (+/- SE) basal vs. peak values: 15.3 +/- 1.5 vs. 124.6 +/- 10.3 ng/ml (p less than 0.001)] than in amenorrheic women [13.5 +/- 1.3 vs. 71.7 +/- 7.2 ng/ml (p less than 0.001)]. There were no significant changes in plasma LH or FSH levels in any group. The cimetidine injection caused a remarkable increase in plasma PRL in women with puerperal hyperprolactinemia [110.8 +/- 31.1 vs. 288.8 +/- 39.6 ng/ml (p less than 0.001)], while the PRL response was diminished or absent in women with idiopathic hyperprolactinemia [103.3 +/- 19.3 vs. 122.9 +/- 14.6 ng/ml (p greater than 0.1)]. The mean incremental PRL response was 1.6 times greater than that observed in normal women. These results suggest that histamine may exert an inhibitory effect on PRL secretion through H2-receptors and that an altered central histaminergic tone may be involved in amenorrheic or pathological hyperprolactinemic state.

Adult↗
PubMed1983

[Suppression of puerperal lactation by metergoline].

Suppression of puerperal lactation by a potent serotonin antagonist, metergoline was studied in 33 puerperal women, i.e., abortion after sixteen weeks of gestation 6, premature labor 13, labor at term 13, and hydatiform mole 1. The drug was administered orally at a dose of 4 mg bid for 5 days to 26 subjects, starting within one week from delivery (group A). The remaining 7 subjects received 4 mg of metergoline bid for 7 days after more than 2 weeks from delivery (group B). Lactation was either rapidly suppressed or prevented in 22 out of the 26 subjects in group A and in all subjects in group B. After the therapy was stopped, rebound phenomena were observed in 4 subjects in group A and in 2 subjects in group B, but a further 5-7 days' treatment with metergoline produced satisfactory results. The mean plasma prolactin levels, studied in 10 subjects in group A at hourly intervals after the first metergoline dose, decreased significantly one hour later (p less than 0.05) and reached the nadir level, 19.9 +/- 2.6% of the mean basal value, 4 hours later. The daily plasma prolactin levels in 9 subjects were significantly lower than those of the control group during metergoline treatment (p less than 0.001). No side effects of metergoline medication were observed. Metergoline for a short course of administration is very effective in the suppression of puerperal lactation. In case of the suppression of lactation after the second week of puerperium, 10-14 days of metergoline treatment is recommended to avoid the rebound phenomena.

Adult↗
PubMed1982

[The effects of metoclopramide on maternal, umbilical and amniotic fluid prolactin at delivery].

Sixteen normal pregnant woman at delivery were administered 10 mg of Metoclopramide (MCP) intravenously, and the Prolactin (PRL) levels in the maternal plasma and in the amniotic fluid were measured by RIA before and after the administration, and in the umbilical plasma after the administration. Eight other pregnant women at term were studied similarly without the administration of MCP and served as the control. In this experiment, there was a significant increase only in the maternal plasma PRL but not in the amniotic fluid PRL nor in the umbilical plasma PRL. Furthermore, by using an intrauterine pressure catheter and a maternal intravenous cannula we measured the amniotic fluid PRL and the maternal plasma PRL about every 20 minutes during 3 hours before and after the intravenous administration of MCP 10mg. The maternal plasma PRL increased promptly and remained high for 150 minutes, while there was no significant change in the amniotic fluid PRL. This obvious discrepancy supports the hypothesis that decidua is the source of amniotic fluid PRL and suggests an independent regulation of amniotic fluid PRL.

Amniotic Fluid↗
PubMed1982

[Effects of bromocriptine and dopamine on pituitary hormone secretion in women].

The present study was designed to examine whether a dopamine agonist, bromocriptine (Brc) exerts similar effects as dopamine (DA) on the pituitary hormones secretion and also to investigate the interaction of these dopaminergic agents and a dopamine receptor antagonist, metoclopramide (MCP) on the DA receptors in the hypothalamic-pituitary axis. Thirty normal cycling women in the midfollicular phase volunteered for this study. Following the administration of Brc (2.5mg, orally) to 13 subjects, a partially significant fall in LH levels, but not in FSH levels, during 4h was observed. DA, infused at a rate of 5 micrograms/kg/min for 4h, induced a significant fall in LH levels between 1 and 4h, but in FSH levels only at 2.5h after the start of infusion in 9 subjects. The amplitude of the spontaneous pulsations of LH secretion which was observed in 8 control subjects, was diminished by DA, while the amplitude seemed to be augmented by Brc. The administration of MCP (10mg, i.v.) to all subjects at 3h during the 4h experimental period caused no observable change in LH and FSH levels. A significant and progressive decline in PRL levels was observed in both Brc-and DA-treated groups of subjects, and this PRL-lowering effect was markedly counteracted by MCP administration in DA-treated group, but not in Brc-treated group. Brc induced a widely varying but significant rise in GH levels, with which MCP did not appear to interfere, whereas DA failed to cause any significant changes in GH levels. These data suggest that Brc, in contrast with DA, seems to be able to increase the pulse amplitude, but not the basal level, of LH and to stimulate GH secretion. Brc is also regarded to be a potent and unique PRL inhibitor, because its PRL-lowering effect cannot be easily antagonized by MCP.

Adult↗