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Biomedical subjects

O Murakami

Publications and source records attributed to O Murakami.

At least 109 records · Page 6Linked to original sources
PubMed1985

Modulation of postinhibitory increase in plasma prolactin by domperidone in patients with prolactin secreting adenoma.

To evaluate the PRL secretory mechanism in patients with PRL-secreting adenoma (PRL-oma), plasma PRL responses to dopamine (DA) were studied in these cases and in normal subjects. Plasma PRL values showed clear decreases during the infusion of DA (5 micrograms/kg/min for 90 min) in both 6 normal and 7 PRL-oma subjects (%decrease: 43.8 +/- 3.9% vs. 53.9 +/- 5.6%; NS) and postinhibitory increases after the termination. However, the postinhibitory increase occurred more promptly and markedly in PRL-oma patients than in normal subjects, i.e. the postinhibitory increase exceeded the basal level 45 min after the termination of DA infusion in PRL-oma patients, whereas the increase in normal subjects did not exceed the basal level even 90 min after the infusion. When domperidone was injected at the termination of DA infusion, the postinhibitory increases were significantly enhanced in either PRL-oma or normal subjects. The maximal increments in plasma PRL in the combination test of DA plus domperidone were significantly larger in PRL-oma patients, but were almost the same in normal controls, compared to the single domperidone test. In contrast, TRH did not modify the postinhibitory rises in 9 PRL-oma patients. These results indicate that the secretory properties and the sensitivities of lactotrophs to decreasing action of DA might be different between PRL-oma patients and normal controls. Further, the postinhibitory rebound phenomenon in PRL-oma patients is possibly determined by an overshoot of PRL storage concomitantly with a decreasing DA action.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1985

Comparative study on the responses of plasma GH to synthetic GH-releasing factor and other stimulatory and inhibitory agents in patients with acromegaly.

Ten patients with active acromegaly received synthetic human pancreatic GH releasing factor (hpGHRF-44), and the GH responses to GHRF were compared with the basal GH levels and with the GH responses to arginine, TRH, LH-RH, somatostatin, and L-dopa. There were no significant relationships between the plasma GH responses to GHRF and the results of the stimulatory and inhibitory tests mentioned above, except that the responses to GHRF showed weak positive or negative correlations with the responses to LH-RH (r = +0.56) or with the basal GH levels (r = -0.57). These results indicate that acromegalic somatotrophs would have GHRF receptors as well as several other receptors to hypothalamic hormones and to dopamine, and that there might be no distinct relationship between the somatotroph sensitivities to GHRF and to other stimulatory or inhibitory stimuli. Further studies are required regarding the weak correlations between the response to GHRF and that to LH-RH or basal GH value.

Acromegaly↗
PubMed1985

GHRF test in acromegalic patients for the evaluation of therapeutic results.

We studied here the clinical significance of GHRF test in evaluating therapeutic results in patients with acromegaly. Three cases of acromegaly were studied at pre- and posttreatment. Case 1 is a 42 year old woman, and her plasma GH showed slight increases responding to TRH and arginine administration before therapy. Eleven years after the pituitary irradiation, basal plasma GH decreased to low normal ranges and showed no response to the above two agents. Only an insufficient increase in plasma GH was observed after GHRF injection. This case would have pituitary lesions not only in the tumor somatotrophs but also in the normal somatotrophs. Case 2 is a 38 year old man. His plasma GH showed a marked increase after TRH injection. To GHRF administration, however, no clear response was observed. After transsphenoidal adenomectomy, the aberrant responses to TRH was still observed despite the marked GH decrease to the near normal ranges. Interestingly, plasma GH became responsive to GHRF after the operation. It seems that the adenomectomy was inadequate in this case and the normal somatotrophs recovered the responsiveness to GHRF. Case 3 is a 53 year old woman, and she showed aberrant GH responses to TRH and to L-dopa. Her plasma GH clearly increased after GHRF injection. Postoperatively, the abnormal responses of plasma GH disappeared completely, while a normal GH response was observed following GHRF injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

Modulation of postinhibitory rebound rise in plasma GH by hypothalamic hormones in patients with acromegaly.

To evaluate the GH regulating mechanism in acromegalic patients, post-inhibitory rebound rise in GH secretion induced by somatostatin was studied in these cases and normal subjects, and was compared with the rebound GH rise induced by dopamine. After somatostatin infusion (500 micrograms/75 min) both 5 normal and 9 acromegalic subjects showed prompt GH decreases during the infusion (% decrease: 69.1 +/- 10.4 vs 74.4 +/- 5.1) and showed rebound rises after its termination. However, the rebound rises occurred more promptly and markedly in normal controls than in acromegalic patients, i.e. the rebound peak appeared at 45 min in normal controls and at 75 min in acromegalic patients after the cessation of somatostatin infusion. Dopamine (DA) infusion (5 micrograms/kg/min for 90 min) also induced similar inhibition and postinhibitory rebound rises in GH secretion in 7 patients with acromegaly. Although the maximum inhibition (65.6 +/- 6.4% vs 74.4 +/- 5.1%) and the inhibitory area (4338.0 +/- 481.5% X min vs 3682.5 +/- 295.5% X min) during the DA or somatostatin infusion were not different, the rebound at 15 min was significantly greater after DA than after somatostatin (p less than 0.02). When TRH was injected at the termination of somatostatin infusion, the rebound increase was significantly enhanced and the rebound peak appeared 45 min earlier than after a single somatostatin administration. Similarly, hp GRF (1-44)-NH2 enhanced the postinhibitory rebound rises in 4 patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

Immunocytochemical identification of CRF in the human hypothalamus.

Immunoreactive ovine corticotropin-releasing factor (CRF) was revealed in the cell bodies of parvocellular neurons in the paraventricular nucleus of the human hypothalamus by an immunocytochemical technique. The immunoreactivity was negative in magnocellular neurons. Immunoreactive nerve fibers were found in the subependymal layers of the third ventricle and in the perivascular space of the primary plexus in the lower hypothalamus. No CRF immunoreactive cell bodies were found in the supraoptic nucleus.

Corticotropin-Releasing Hormone↗
PubMed1984

Plasma growth hormone responses to sulpiride in patients with acromegaly.

The role of endogenous dopamine (DA) on plasma GH secretion was studied in 12 patients with active acromegaly. After intramuscular administration of 100 mg sulpiride, 3 out of 12 patients showed distinct increases in their plasma GH (cases 1-3: sulpiride-responders). The GH increases far exceeded the ranges of physiological fluctuation in two cases studied (case 1 & 3). After domperidone administration, case 3 showed a quite similar GH increase as after sulpiride. Plasma GH responses to TRH and sulpiride were still observed in case 2 even after the basal GH levels were normalized by the transsphenoidal hypophysectomy. The three sulpiride-responders showed so-called paradoxical GH decreases following the administration of L-dopa (500 mg, p.o.) or DA (5 micrograms/kg/min over 90 min, i.v.). However, the basal plasma PRL levels and the responses to sulpiride in these 3 cases were not homogeneous. These results indicate that endogenous DA has a tonic inhibitory effect on GH secretion in some cases of acromegaly, and that tumorous somatotrophs rather than elevated GH levels are the critical factor for such inhibition. Further, the sensitivities of somatotrophs and lactotrophs to DA appeared to be heterogeneous in acromegalic patients.

Acromegaly↗
PubMed1984

The mechanism of postinhibitory rebound increases in plasma gh in acromegalic patients.

The mechanism of postinhibitory rebound increase in GH secretion was studied in 5 normal and 7 acromegalic subjects. Both normal and acromegalic subjects showed prompt GH decreases during the infusion of somatostatin (500 micrograms/75 min) (% decrease: 69.1 +/- 10.4 vs. 73.9 +/- 6.5) and rebound rises after its termination. The rebound rises occurred more promptly and markedly in normal controls than in acromegalic subjects, i.e. the rebound peak appeared at 15 min in normal controls and at 45 min in acromegalic patients after the cessation of somatostatin infusion. Dopamine (DA) infusion (5 micrograms/kg/min for 90 min) also induced similar inhibition and postinhibitory rebound rises in GH secretion in 6 patients with acromegaly. Although the maximum inhibitions (67.1 +/- 7.3% vs. 73.7 +/- 7.1%) and the inhibitory areas (4354.5 +/- 471.0% . min vs. 3796.5 +/- 322.5% . min) during the DA and somatostatin infusions were not different, the rebound at 15 min was significantly greater after DA than after somatostatin (p less than 0.05). All seven patients with acromegaly were TRH responsive in their plasma GH (% of basal: 93.5 to 944.3). When TRH was injected at the termination of somatostatin infusion, the rebound increase was significantly enhanced and the rebound peak appeared 30 min earlier than after single somatostatin administration. These results indicate that the mechanisms participating in the postinhibitory rebound rise are different in normal controls and acromegalic patients, and that the magnitude of the rebound differs with agents employed. Also, it is evident that the rebound phenomenon in acromegaly is possibly modified by exogenous hypothalamic releasing factors.

Acromegaly↗
PubMed1984

Rapid radioimmunoassay of plasma GH and its application to the judgement of surgical results in patients with acromegaly.

To improve the surgical results in patients with acromegaly, rapid radioimmunoassay (RIA) of plasma GH was developed and this method was applied for quick judgement of whether transsphenoidal hypophysectomy was performed successfully or not. The best reaction temperature and the shortest incubation time were proved to be 40 degrees C and 16 min, respectively. The GH values obtained by this method and the usual RIA method were correlated well (r = 0.9, p less than 0.001). Using the rapid RIA it became possible within 35 min just after the termination of the hypophysectomy to report the data to the neurosurgeons. This RIA method was applied for 5 patients with acromegaly undergoing transsphenoidal hypophysectomy. In two cases plasma GH decreased markedly (62.0-71.4% decreases from preoperative value) at the termination of the hypophysectomy, and later fell to normal ranges. The other three cases showed only slight decreases (7.7-17.3%), and the operation was judged as unsuccessful. Therefore, two of these cases were followed by further removal of residual tumors which resulted in steep declines of GH. In the remaining one the further operation was not performed, because surgical removal of the adenoma was believed by the surgeons to be complete. In conclusion, rapid RIA of plasma GH is possible within 16 min and this method is of significant value to improve the surgical results of acromegalic patients.

Acromegaly↗
PubMed1984

Evidence for endogenous dopaminergic control of mineralocorticoids secretion in normal subjects and in patients with hyperaldosteronism.

The role of endogenous dopamine (DA) in the secretion of several mineralocorticoids was studied in six normal subjects, eight patients with primary aldosteronism (PA), two patients with non-familial idiopathic hyperaldosteronism (NF-IHA), and four patients with familial IHA (F-IHA). To these subjects 10 mg metoclopramide (MCP) was administered intravenously, and plasma aldosterone (Ald), 18-OH-corticosterone (18-OH-B), 18-OH-11-deoxycorticosterone (18-OH-DOC), and DOC were measured by RIA. Further, five normal subjects were studied with MCP test after pretreatment with DA infusion (5 micrograms/kg/min over 90 min). After the administration of MCP, normal subjects showed significant increases in their plasma Ald and 18-OH-B, and slight increases in plasma 18-OH-DOC and DOC. However, no significant changes were observed in plasma ACTH, cortisol, PRA, or serum K, Na or Cl. In patients with PA and NF-IHA, plasma Ald and the three precursors were increased after administration of MCP. Especially, marked increases in plasma 18-OH-DOC were seen in PA patients. In contrast, F-IHA patients showed increases in the above mineralocorticoids except 18-OH-B. Following DA infusion in normal subjects neither basal plasma Ald secretion nor the responsivenesses to MCP were modified. These results suggest that endogenous DA plays an inhibitory role in the terminal stages of mineralocorticoids production in man. However, the degrees of the dopaminergic inhibition may be different in normal subjects and the patients with mineralocorticoids excess, and among the three groups of aldosteronism mentioned above.

18-Hydroxycorticosterone↗
PubMed1984

Enhanced prolactin secretion in patients with primary hypothyroidism during thyroid replacement.

Thyroid hormones are known to exert some influence on prolactin (PRL) secretion indirectly via the hypothalamic dopaminergic system and directly at the level of pituitary gland. In order to study the effect of thyroid hormones on the activity of hypothalamic dopamine neurons, lactotrophs and thyrotrophs, we administered increasing doses of thyroid hormones to patients with primary hypothyroidism, and examined the changes of basal PRL, TSH and PRL responses to a dopamine receptor blocker (sulpiride). Among 24 patients with primary hypothyroidism, hyperprolactinemia was observed in 10 cases (18.0-236 ng/ml, mean +/- S.E. 58.6 +/- 20.0 ng/ml), while elevated TSH levels were observed in all of them (6.6-972 microU/ml, mean +/- S.E. 231.4 +/- 53.9 microU/ml). There was a significant negative relationship between plasma T3 or T4 levels and basal plasma TSH levels (p less than 0.05), whereas a poor correlation was observed between the thyroid hormones and basal plasma PRL levels (r = -0.25, p greater than 0.05). Following the administration of gradually increasing doses of thyroid hormones, plasma PRL showed paradoxical and transient increases, while plasma TSH decreased steadily. Plasma PRL response to sulpiride also became exaggerated during the treatment. The elevated basal PRL level and the enhanced response to sulpiride turned to be within the normal range when the patients became euthyroid by treatment. These results may indicate that thyroid hormones stimulate not only hypothalamic dopaminergic activity, but also the lactotroph activity in a long term hypothyroid state. Regarding the paradoxical elevation of basal PRL, one can postulate that the activation of lactotroph by a small dose of thyroid hormone may be able to overcome the hypothalamic dopaminergic inhibition.

Adult↗
PubMed1983

Persistence of impaired PRL responses to sulpiride in patients with PRL secreting pituitary adenomas after successful hypophysectomy.

TRH, arginine, L-dopa, and sulpiride tests for PRL secretion were carried out in 18 control subjects and 20 patients with pituitary PRL-secreting adenomas before and after hypophysectomy. After the hypophysectomy PRL levels fell to normal ranges in 9 cases (categorized as Group I), and remained high in 11 other cases (categorized as Group II). After the operation, there were no alterations of PRL responsiveness to TRH, arginine, or to L-dopa in terms of percent change from the basal value, in either Group I or Group II. No significant differences were found in PRL responses to the above three agents between operated Group I patients and normal subjects even when expressed in absolute values. On the other hand, the PRL responses to sulpiride in both Groups I and II improved markedly after the hypophysectomy, but the absolute response in operated Group I patients was still lower than that in normal subjects. The mean PRL value in operated Group I (mean +/- S.E., 13.2 +/- 0.8 ng/ml, n = 9) was significantly (p less than 0.01) higher than in normal subjects (5.1 +/- 0.4 ng/ml, n = 18). It is concluded 1) that even in hypophysectomized normoprolactinemic patients the circulating PRL may originate mainly from the residual tumor cells, and 2) that the sulpiride test is useful to detect the abnormalities of hypothalamo-pituitary axis in operated patients with PRL-secreting adenomas, whereas TRH, arginine, and L-dopa tests are less useful for such purposes.

Adenoma↗
PubMed1982

The autonomy of prolactin secretion in patients with prolactin producing tumor.

To examine the responsiveness of prolactin (PRL) secretion in patients with PRL-producing tumor (PRL-noma), TRH (500 micrograms), arginine (0.5 g/kg, b. wt.), and sulpiride (100 mg) were administered to 13 patients with PRL-noma. Seven of these patients responded to TRH or other agents with an increase in their plasma PRL levels of 50% or more above the basal values (categorized as Group I). The remaining six patients, however, showed no response to any of these agents (categorized as Group II). After the administration of L-dopa (500 mg, p.o.), Group I patients showed significantly greater decreases in plasma PRL (-68.9 +/- 6.6%) from the basal value than did Group II (-37.4 +/- 8.6%; p less than 0.02). The mean basal PRL levels were higher in Group II than in Group I, although these differences failed to reach statistical significance. Moreover, there were no differences in age, sellar volume, or the presence of bitemporal hemianopsia between the two groups of patients. It is concluded that there are two patterns of PRL-secretory responses to pharmacological stimuli in patients with PRL-noma. The differences between the two patterns might be characterized by the properties of the lactotroph cells themselves rather than by the relation of these cells to the hypothalamus.

Adult↗