巻号一覧
前身誌
63 巻, 8 号
選択された号の論文の6件中1～6を表示しています
- |<
- <
- 1
- >
- >|
-
二川原 和男, 鈴木 唯司, 小野寺 孝夫, 福井 耕三, 冨樫 繁也, 舟生 富寿, 山谷 金光, 寺山 百合子, 山口 建1987 年 63 巻 8 号 p. 923-933
発行日: 1987/08/20
公開日: 2012/09/24
ジャーナル フリーA case of malignant pheochromocytoma, with a recurrence 15 years after adrenalectomy and with an associated watery diarrhea, hypokalemia, achlorhydria syndrome, is reported. Histological evaluation of the tumors revealed composite malignant pheochromocytoma-ganglioneuroblastoma (well differentiated type). Vasoactive intestinal polypeptide and catecholamine levels were high both in the plasma and in the tumors. Somatostatin was also rich in the metastatic tumor of the liver, but not in the plasma. Immunohistochemical studies have demonstrated that immunoreactive vasoactive intestinal polypeptide is present in the ganglioneuroblastoma component, and that immunoreactive somatostatin is present in the pheochromocytoma component. Literature on the watery diarrhea, hypokalemia, achlorhydria syndrome associated with pheochromocytoma was reviewed.抄録全体を表示PDF形式でダウンロード (1996K) -
三橋 信次, 山崎 柳一, 宮崎 修一, 斎藤 晴比古, 斎藤 史郎1987 年 63 巻 8 号 p. 934-946
発行日: 1987/08/20
公開日: 2012/09/24
ジャーナル フリーThe responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis.
In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8±1.4pg/ml (mean±SE) to 34.8±3.1pg/ml at 30-90 min after oral administration of 500mg L-dopa, followed by a rise of GH release (plasma GH level from <1ng/ml to 21.7±4.7ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypo-thalamic GHRH.
On L-dopa administration, no apparent increases in both plasma GHRH and GH concentrations were observed in patients with hypothalamic hypopituitarism, whereas GHRH administration induced almost normal GH response.
In patients with acromegaly, the plasma levels of GHRH remained stationary after the L-dopa administration and did not correlate with plasma GH levels.
In subjects with simple obesity, the responses of plasma GHRH (peak 13.2±1.2pg/ml) and GH (peak 4.3±1.7ng/ml) to L-dopa were significantly lower than those in normal subjects (p<0.01).
In patients with primary hypothyroidism, peak levels of plasma GHRH (12.6±1.3pg/ ml) and GH (2.4±0.6ng/ml) were significantly lower than those in normal subjects (p<0.01).
In patients with non-insulin dependent diabetes mellitus (NIDDM), the responses of GHRH and GH were divided into 2 groups; in the responder the peak values of GHRH and GH were 19.4±8.6pg/m and 12.2±1.4ng/ml and in the low or non responder 14.7±1.5pg/ml and 2.0±0.6ng/ml, respectively. Between both groups, there was a significant difference in the values of fasting blood sugar and HbA1 and mean suffering period.
These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states.抄録全体を表示PDF形式でダウンロード (1396K) -
佐藤 秀一1987 年 63 巻 8 号 p. 947-960
発行日: 1987/08/20
公開日: 2012/09/24
ジャーナル フリーPlasma prolactin (PRL) responses to several exogenous agents are variable in patients with prolactinomas. In this study the factors determining the responsiveness to exogenous stimuli were investigated in 35 patients with prolactinomas. Among these patients, 14 patients were responder (>150% increase of basal value) to TRH, sulpiride (DA D2-receptor blocker) and arginine, and remaining 21 were non-responder to these three agents. Plasma TSH responses to sulpiride, an indirect indicator of hypothalamic dopaminergic tone on pituitary gland, were similar between responder (ΔATSH : M SEM; 5.3±0.2μU/ml) and non-responder (ΔTSH : 5.6±0.2μU/ml), and were greater than those in normal subjects (ΔTSH : 0.7±0.2μU/ml, n=18) (P<0.001).
The plasma PRL responses to dopaminergic agents (L-dopa, CB-154, dopamine) were greater in responders than in non-responders (% of basal : L-dopa, 33.7±3.7% vs 51.6±5.6% at 150 min, P<0.05; CB-154, 16.5±2.6% vs 30.9±2.8% at 6hr, P<0.05; dopamine, 31.7±5.6% vs 44.9±4.3% at 90 min, P<0.05). When all patients were divided into microadenoma (n=12) and macroadenoma patients (n=23), there were no differences in plasma PRL responses to these agents between the two groups. Again, there were no differences in the duration of illness between the responder and non-responder patients (61.9±13.7 vs 54.1±12.0 months). During the short term CB-154 treatment (7.5mg/day for 3-5 weeks) in 8 responders and 15 non-responders, all responder patients showed normalization of plasma PRL levels, while such normalization was observed in only 6 non-responder patients.
These results suggest that in prolactinoma patients variable responsiveness to several exogenous agents are depending on the sensitivity to several exogenous agents are depending on the sensitivity of prolactinoma itself, regardless of the endogenous hypothalamic dopaminergic tone, tumor size or duration of the illness.抄録全体を表示PDF形式でダウンロード (1532K) -
坂中 昭典, 宮崎 青爾, 小坂 譲二, 地守 研三, 百々 修司, 五井 麗司, 三浦 清1987 年 63 巻 8 号 p. 961-977
発行日: 1987/08/20
公開日: 2012/09/24
ジャーナル フリーIn this study we outlined the development of an enzymatic technique to activate plasma inactive renin by trypsin in rat plasma. Using this method, we reported the releasing mechanism of the trypsin-activable inactive renin which has not yet been clarified. Adult male Wistar rats (260-300g) were kept on regular diet (Na : 260mg/100g) unless explained and underwent operation under pentobarbital anesthesia (50mg/kg). Blood samples were obtained from conscious rats through the cannulae, which had been inserted into the left femoral arteries 24h before the experiments. After addition of excessive renin substrate which had been obtained from the 24 h-nephrectomized rat plasma, renin was measured by the commercial RIA-kit (Dainabot). Trypsin (Worthington) treatment (20mg/ml plasma for 10 min at 4°C) was followed by addition of SBTI (Sigma) (20mg/ml plasma). This condition maximally increased the rate of angiotensin I generation and did not alter the Km or optimum pH of the renin reaction. In this condition, trypsin reaction was completely inhibited by adding these concentrations of SBTI. The molecular weight of inactive renin (51,000) in the normal rat plasma estimated by Sephadex G-100 column (Pharmacia) was the same as that in the nephrectomized rat plasma. In conclusion, trypsin treatment of plasma (20mg/ml plasma for 10 min at 4°C) followed by SBTI (20mg/ml plasma) was justified for trypsin activation of rat plasma.
Using this method, we investigated the changes in active and inactive renin after bilateral nephrectomy in the salt-depleted rat. Active renin decreased rapidly after bilateral nephrectomy with a half life of 23.6±4.0 min. Inactive renin, on the other hand, increased gradually and reached to a plateau 24h after bilateral nephrectomy, and was kept unchanged during the following 24h. The infusion of mouse submandibular gland active renin or angiotensin II could not prevent the increase of plasma inactive renin in the nephrectomized rat. These suggest that there may be no feedback mechanisms between plasma inactive and active renin or angiotensin II.
Furthermore, we investigated the organ-related sources of plasma inactive renin which markedly increased after total nephrectomy. Simultaneous removals of submandibular glands but not of adrenal glands completely prevented the postnephrectomy increases of plasma inactive renin. But, removals of submandibular glands or adrenal glands alone were followed by no changes in the basal levels of plasma inactive renin. It is concluded that the increases of plasma inactive renin may be dependent on the presence of the submandibular glands, but not of the adrenal glands. However, the real sources of plasma inactive renin are still unknown.抄録全体を表示PDF形式でダウンロード (1826K) -
坂本 長逸, 的崎 尚, 長尾 宗彦, 西崎 朗, 馬場 茂明1987 年 63 巻 8 号 p. 978-986
発行日: 1987/08/20
公開日: 2012/09/24
ジャーナル フリーTo investigate whether somatostatin receptors couple to guanine nucleotide inhibitory protein, Ni, on rat pancreatic acinar membranes, the effects of guanine nucleotide analogs or pretreatment of acini with islet activating protein (IAP), pertussis toxin on labeled somatostatin binding were examined. Guanine nucleotides reduced labeled somatostatin binding to acinar membranes up to 80%, with rank order of potency being guanyl-5′-yl imidodiphosphate (Gpp(NH)p)>GTP>GDP>GMP. Scatchard analysis of the labeled somatostatin binding revealed that the decrease in somatostatin binding caused by Gpp(NH)p was due to the decrease in the maximum binding capacity without a significant change in the binding affinity. The inhibitory effect of Gpp(NH)p was partially abolished in the absence of Mg2+ and Na+ also reduced labeled somatostatin binding. Furthermore, inhibitory effects of 100mM Na+ and Gpp(NH)p were additive in reducing labeled somatostatin binding. A half maximal inhibitory concentration of Gpp(NH)p was decreased to 10-7M in the presence of 100mM Na+ and 5mM Mg2+ as compared to 10-6M in the presence of 5mM Mg2+ alone. Results therefore suggest that Gpp(NH)p requires Mg2+ for Ni activation and Na+ increases sensitivity of Ni to guanine nucleotide analogs.
When pancreatic acini were treated for 4 hours with varying concentrations of IAP, which has been shown to uncouple Ni-mediated communication between inhibitory receptors and adenylate cyclase catalytic unit, subsequent labeled somatostatin binding to the acinar membranes was decreased in a dose dependent manner.
These results indicate that somatostatin receptors on pancreatic acinar membranes couple to guanine nucleotide inhibitory protein, Ni and thus somatostatin probably functions in the pancreas to regulate intracellular signal transduction via Ni.抄録全体を表示PDF形式でダウンロード (798K) -
関東 繁1987 年 63 巻 8 号 p. 987-999
発行日: 1987/08/20
公開日: 2012/09/24
ジャーナル フリーFor the purpose of screening of thyroidal dysfunction in adult, we have collected blood of 15,905 (male 11,559, female 4,346) adult normal workers and school students on filter papers at the time of the annual health examination. Both TSH and total T4 were measured by radioimmunoassay. Either TSH or total T4 or both showed abnormal values in 148 cases. For these subjects, serum TSH, total T4 and T3, free T4, TBG, antimicrosomal and antithyroglobulin antibody were estimated. From these results, diagnosis was made as follows : 6 hyperthyroidism, 12 primary hypothyroidism (including 3 subclinical hypothyroidism who showed elevated TSH and normal free T4 values) and 29 TBG abnormality (increase : 8, decrease or deficiently : 21). The incidence by this study was : hyperthyroidism 0.038% (1/2650), primary hypothyroidism 0.075% (1/1330), TBG increase or deficiency 0.132% (1/760). Sex ratio of thyroidal dysfunction were higher in female than male. In hyperthyroidism, ratio of male to female was 1 : 2.66, and in hypothyroidism, it was 1 : 133. Most of these patients were not diagnosed before this screening. The fact that the incidence of hypothyroidism was higher than hyperthyroidism in this population was apparent in this study. TBG abnormality was noted more in male than female. This report is important to show the incidence of thyroidal abnormalities and the necessity of the screening test of thyroid in adult.抄録全体を表示PDF形式でダウンロード (1335K)
- |<
- <
- 1
- >
- >|