巻号一覧
前身誌
65 巻, 5 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
- >
- >|
-
交感神経系の関与について石崎 元久, 黒田 一明, 梶原 長雄1989 年 65 巻 5 号 p. 473-482
発行日: 1989/05/20
公開日: 2012/09/24
ジャーナル フリーHistamine H2-receptor antagonists administered into the central nervous system have been shown to increase arterial pressure (AP) in anaesthetized animals (Paakkari et al., 1982). Few studies have been reported on the effects of centrally administered cimetidine (CIM), one of the histamine H2-receptor antagonists, in conscious animals. However, the mechanism of the pressor action of histamine H2-receptor antagonists remains unclear. The present study was designed to investigate the hemodynamic effects of intracerebroventricular (i.c.v.) CIM and the interaction between the sympathetic nervous system and histamine receptor system in conscious rats.
Male Wistar rats weighing 200 gr were prepared for the experiment under a conscious and minimally restricted state. Five μg of i.c.v. saline (SAL-ICV group, n=5) did not produce significant changes in mean arterial pressure (MAP) or heart rate (HR) (MAP from 85.6±3.4 to 86.0±4.3 mmHg and HR from 395.0±13.9 to 395.2±8.2 bpm, respectively). Twenty μg of i.c.v. phenoxybenzamine (POB-ICV group, n=6) decreased MAP from 95.8 ±4.1 to 85.2 ±3.1 mmHg, -10.7±2.2 mmHg as ΔMAP, and increased HR from 392.5±8.5 to 435.3± 13.9 bpm, +42.8±6.8 bpm as ΔHR. Two-hundred μg of intravenous (i.v.) POB (POB-IV group, n=5) also decreased MAP from 96.0±4.3 to 71.0±5.1 mmHg, -25.0±2.7 mmHg as ΔMAP, and increased HR from 395.8±10.5 to 473.0±12.4 bpm, +77.2±7.6 bpm as ΔHR. The changes in MAP and HR were much greater in the POB-IV group than those in the other two groups. The subsequent i.c.v. administration of 250μg of CIM induced an increase in MAP (+19.4± 1.7 mmHg as ΔMAP) and a decrease in HR (-36.4±3.1 bpm as ΔHR) in the SAL-ICV group, which continued for at least 30 minutes producing peak effects 2 minutes after i.c.v. administration of CIM. However, an elevation of MAP caused by i.c.v. CIM was much more inhibited in the POB-ICV group than in the POB-IV group (+2.5± 0.7 mmHg as AMAP in the POB-ICV group and +5.0± 1.3 mmHg as AMAP in the POB-IV group, respectively). Reflex bradycardia produced by i.c.v. CIM was also inhibited in the POB-ICV group, while an initial increases of HR was observed (+44.0± 7.7 bpm as ΔHR) at 2-10 minutes after i.c.v. administration of CIM in the POB-IV group. Plasma noradrenaline (PNA) and adrena-line (PA) increased significantly after i.c.v. administration of CIM (from 143.0± 37.0 to 332.4±86.2 pg/ml and from 305.7±72.1 to 1136.8±278.0 pg/ml, respectively).
I.c.v. administration of CIM has been reported to produce an increase in AP and HR in anaesthetized rats. HR decreased, however, in conscious rats, while AP was elevated as in anesthetized rats. A change in HR seems to be brought through a baroreflex system. I.c.v. administration of CIM caused an elevation of AP and brought about a significant increase of PNA and PA, which were inhibited by the pretreatment of POB either i.c.v. or i.v. Therefore, the mechanisms for an increase in AP are thought to be mediated through the central sympathetic nervous system, and to be partly due to an augmentation of discharge in the efferent sympathetic outflow as well as an increase of catecholamine release from the adrenals.抄録全体を表示PDF形式でダウンロード (1024K) -
若杉 和義1989 年 65 巻 5 号 p. 483-496
発行日: 1989/05/20
公開日: 2012/09/24
ジャーナル フリーTo evaluate the effect of glucagon degrading activity (GDA) on radioimmunoassay (RIA) of glucagon, I measured GDAs in plasma, serum, lysed red blood cells (RBC), and suspension of mononuclear cells and granulocytes. Serum levels of GDA in patients with various diseases were also examined.
1. Serum GDA values in normal subjects (control) measured by TCA precipitation method were 4.6±2.2% (mean±S.D.). GDA values in plasma treated with citrate and those in serum treated with aprotinin were not different from those in nontreated serum. GDAs in plasma treated either with EDTA and aprotinin or with EDTA alone were significantly lower than those in control serum, but the values in plasma treated with heparin were markedly higher than those in control serum.
2. GDAs in RBC lysate and suspension of mononuclear cells and granulocytes re-mained low up to the concentration of 23 ×104 RBC/μl and 5000 mononuclear cells or granulocytes/μl, respectively. GDAs in RBC lysate and mononuclear cells were markedly suppressed by the treatment with EDTA, whereas GDAs in granulocytes were inhibited by the treatment with aprotinin.
3. Markedly high values of GDA were obtained in serum of patients with pancreas diseases, liver diseases, renal diseases and hyperthyroidism. However, in four patients these elevated levels were restored to normal value after recovery from these disorders. The elevated GDA values in serum were suppressed to normal value by the addition of EDTA and aprotinin.
4. On Bio-Gel P-6 column chromatography, 125I-glucagon incubated with patient serum containing high GDA values revealed several peaks eluted after 125I-glucagon.
5. In healthy subjects, immunoreactive glucagon (IRG) levels in nontreated serum were not different from those in plasma treated either with EDTA and aprotinin or with heparin.
6. In patients showing high serum GDA levels, serum GDA levels were not significantly related to IRG levels in plasma treated with EDTA and aprotinin.
These results indicate that a series of treatment of blood samples before assay : addition of EDTA and aprotinin to the blood samples, immediate separation of plasma from blood cells, and storage at 4°C is recommended to avoid breakdown of glucagon by GDAs.抄録全体を表示PDF形式でダウンロード (1119K) -
山辺 晋吾, 片山 和明, 望月 眞人1989 年 65 巻 5 号 p. 497-511
発行日: 1989/05/20
公開日: 2012/09/24
ジャーナル フリーIn order to investigate the role of progesterone in the maintenance of pregnancy, an anti-progesterone agent, RU486 (RU) was injected subcutaneously into pregnant rats on day12 (D12), and morphological changes of the uterus as well as endocrinological changes were observed.
In all rats injected with RU, abortion occurred with macroscopic and microscopic intrauterine hemorrhage and degeneration or delivery of conceptuses. Endocrinologically, the levels of progesterone decreased rapidly 48 hours after the injection, while the levels of estradiol showed a tendency to increase.
As progesterone is mainly produced by the corpus luteum but not by the placenta in rats, the decrease in progesterone is suspected to be due to luteolysis. Then in order to clarify the mechanism of luteolysis induced by RU and the effects of progesterone on this phenomenon, the dynamics of the luteotrophic factors (estradiol, LH, PRL) and specific binding capacity of the ovaries to LH/hCG were investigated in D7 pregnant rats treated with RU 1 mg/kg alone (RU group) or with both RU 1mg/kg and progesterone 50mg/kg (RU+P group).
The serum levels of progesterone in the RU group decreased significantly after 72 hours of administration, while those in the RU+P group remained within the levels of the control group. However, serum levels of luteotrophic factors in the RU group did not de-crease, and some of them were even higher than those in the control group. In the RU+P group, luteotrophic factors remained within control levels.
On the other hand, the specific bindings of LH/hCG to ovarian homogenates decreased significantly after 72 hours in the RU group. But in the RU+P group, the specific bindings were kept at the same levels as the controls. Scatchard analysis of these results disclosed that in the RU group, both affinity and numbers of receptors decreased compared to the controls, and that in the RU+P group only affinity decreased transiently and afterwards recovered quickly.
From these results, it is concluded that deterioration of affinity and numbers of ovarian LH/hCG receptors seems to be one of the factors which induce luteolysis in pregnant rats treated with RU, and that progesterone can spare the effect of RU on the corpus luteum during pregnancy.抄録全体を表示PDF形式でダウンロード (1969K) -
小島 章裕, 西内 健, 山崎 保寛, 斎藤 史郎1989 年 65 巻 5 号 p. 512-524
発行日: 1989/05/20
公開日: 2012/09/24
ジャーナル フリーIn order to clarify the mode of atrial natriuretic peptide (ANP) release and the effect of autonomic nerve function on ANP release, we measured plasma ANP concentrations in response to hypertonic saline infusion in patients with non-insulin-dependent diabetes mellitus (NIDDM) having or not having autonomic neuropathy (AN).
Studies were made on 72 normal subjects (male 44, female 28; 53.0±0.9 yr.), and 63 patients with NIDDM (male 36, female 27; 56.9±2.1 yr.). The patients with NIDDM were divided into two groups : Group A was 48 diabetics without AN, and Group B was 15 diabetics with AN. Six patients selected randomly from each group and 6 normal subjects were given an infusion of hypertonic saline (2.5% NaCl) at a rate of 0.25 ml/min/kg over 45 min. Autonomic nerve function was estimated by clinical symptoms, coefficient of variation of R-R intervals (CVR-R), Valsalva test and Schellong test. Plasma ANP concentration was measured by a sensitive and specific radioimmunoassay (RIA) after extraction using SEP-PAK C18 cartridge reported previously.
The mean plasma concentration of ANP was 20.7±1.8 pg/ml (mean±SEM) in normal subjects, 24.3±2.4 pg/ml in NIDDM patients without AN, and 26.4±3.6 pg/ml in NIDDM patients with AN. There was no significant difference in these levels among the 3 groups. The fasting plasma concentration of ANP in diabetics as well as in normal subjects increased parallel with age.
In 12 diabetics, plasma concentrations of ANP significantly elevated from 27.6 ±2.0 pg/ml to 149.4± 29.8 pg/ml at 60 min after start of hypertonic saline infusion as compared with 6 normal subjects in whom the levels increased from 15.6± 2.9 pg/ml to 34.1±5.7 pg/ml at 75 min. On the other hand, the plasma ANP concentration in response to hypertonic saline infusion in NIDDM patients with AN (71.8±14.4pg/ml, at 60 min) was lower than that in NIDDM patients without AN (224.2± 38.2 pg/ml, at 60 min). Area under the curve (AUC) of plasma ANP of NIDDM patients with AN after hypertonic saline infusion was 6560± 879.6 pg·min/ml (normal subjects, 2575.6 ±444.6 pg·min/ml), which was significantly lower than that of NIDDM patients without AN (13757.8± 1148.4 pg·min/ml). Moreover, there was a positive correlation between AUC and CVR-R in patients with NIDDM.
These results indicate that the response of plasma ANP to hypertonic saline infusion in NIDDM patients is significantly higher than in normal subjects. In addition, the response of plasma ANP in NIDDM patients having AN is lower than that in NIDDM patients without AN, suggesting that autonomic neuropathy impairs the release of ANP.抄録全体を表示PDF形式でダウンロード (1150K) -
須永 恭司, 西川 光重, 稲葉 潔, 廣實 伸郎, 井上 昇, 四方 伸明, 稲田 満夫1989 年 65 巻 5 号 p. 525-536
発行日: 1989/05/20
公開日: 2012/09/24
ジャーナル フリーDescribed herein are two brothers with 21-hydroxylase deficiency (21-OHD) associated with adrenal tumors, and these possible mechanisms are discussed. A 34-year-old male was admitted on Jan. 9, 1984 because of an enlarged and tender left breast. Physical examination revealed short stature (152cm, 76.5kg), gynecomastia and shortening of meta-carpal bone. His testes were small (2.6×1.6× 1.9cm). Urinary excretion of 17-OHCS was within normal range (5.9mg/day), but those of 17-KS, 17-KGS and pregnanetriol were markedly increased (44.4,110 and 22.6mg/day, respectively). Plasma concentrations of progesterone and ACTH and urinary excretions of estrone, estradiol and estriol were also increased. Urinary excretions of 17-KS were decreased to 11.7mg/day and 17-KGS to 22.3mg/day after the ingestion of 2mg/day dexamethasone for two days.
The computed tomography and a scintigraphy with 131I-Adosterol® revealed a tumor in the left adrenal gland, and the adrenal arteriography revealed a neovascularity and a tumor stain in the tumor. These data indicated that the patient was suffering from both 21-OHD and the left adrenal tumor. At this point, adenoma or adenocarcinoma of the adrenal gland was suspected. The left adrenal tumor (85g) was resected on April 10, 1984, and the patho-logical diagnosis was adrenal adenoma. The patient's endocrinological abnormalities, how-ever, did not improve after the operation.
Urinary excretions of 17-KS and KGS were increased to 57.9 and 108.5mg/day, respectively, in the patient's elder brother, and 63.3 and 127.9mg/day, respectively, in his younger brother, indicating that they also had 21-OHD. Interestingly, an adrenal tumor was diagnosed by abdominal computed tomography in the elder brother who had the same HLA typing as the present case. The three brothers had 21-OHD, and two of them had both 21-OHD and adrenal tumor. To our knowledge, this is the first report documenting the co-existence of adrenal tumors in brothers with 21-OHD. This suggests that adenoma can be one of the complications of 21-OHD, probably due to the chronic stimulation by ACTH, and that a possible linkage to HLA may exist in such cases.抄録全体を表示PDF形式でダウンロード (2146K) -
近藤 国和, 大竹 千生, 岩崎 泰正, 大磯 ユタカ, 高槻 健介1989 年 65 巻 5 号 p. 537-548
発行日: 1989/05/20
公開日: 2012/09/24
ジャーナル フリーThe concentration of unextracted urinary arginine vasopressin (UAVP) was directly measured by high-sensitive radioimmunoassay (AVP-RIA Kit, Mitsubishi Petrochemical Co., Ltd.). Urine was diluted to eliminate interference of nonspecific substance without prior extraction. When urine aliquots were diluted in 4 to 32 fold in assay buffer, the relationship between UAVP concentration and dilution ratio corresponded exactly in a linear regression line. The elution pattern on Sephadex G-25 of UAVP immunoreactivity was identical with that of synthesized AVP. The AVP concentration in unextracted urine was not significantly different from that of extracted urine by Sep-Pak C18 column (Water Associates, Milford MA). The mean recovery of added AVP to urine specimens was 101.1±9.8% (mean±SD). The immunoreactivity of UAVP was not modified by either albuminuria (50 and 100mg/dl) or glycosuria (1000mg/dl). Mean coefficients of variance between-assay and within-assay were 8.3% and 6.6% respectively.
In normal subjects (n=28), significant correlation was observed between UAVP con-centration and simultaneously measured plasma AVP (r=0.701, p<0.001). Moreover, AVP concentration in random urine was significantly correlated with AVP excretion in 24hr-urine (r=0.703, p<0.05, n=9), and this suggested that random UAVP concentration may indicate daily UAVP secretion.
In normal subjects, AVP concentration in random urine was widely scattered from 9.2 to 470.6pg/mg Cr (89.5±76.4pg/mg Cr, n=211). In patients with diabetes insipidus (DI), UAVP concentration (1.6 to 13.0pg/mg Cr, 6.94±2.77pg/mg Cr, n=25) was significantly lower (p<0.001) than that of normal subjects. UAVP concentration in a patient with primary polydipsia (43.2 pg/mg Cr) was not similar to that of ID but to that of normal subjects. UAVP concentration in 2 patients with SIADH was not more than that of normal subjects, indicating that random UAVP concentration is not suitable for detecting inappropriate AVP secretion.
In this study, it is suggested that patients of random UAVP concentration below 13.0 pg/mg Cr should be recommended other intensive examination to diagnose DI, even though 2 normal subjects (0.9%) were incorrectly estimated as DI.
In conclusion, radioimmunoassay of AVP in unextracted random urine is easy to sample and assay, and useful in screening polyuric patients.抄録全体を表示PDF形式でダウンロード (981K)
- |<
- <
- 1
- >
- >|