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Biomedical subjects

A Morimoto

Publications and source records attributed to A Morimoto.

At least 109 records · Page 6Linked to original sources
PubMed1992

Running training attenuates the ACTH responses in rats to swimming and cage-switch stress.

The present study was carried out to investigate the effect of running training on adrenocorticotrophic hormone (ACTH) response in rats to swimming or cage-switch stress to determine whether, after physical training, a cross-adaptation develops in the ACTH responses induced by different types of stresses. Rats were trained by two different kinds of exercises and for two different periods of training: 1) swimming for 4 wk (4W-swimming), 2) running for 4 wk (4W-running), and 3) running for 10 wk (10W-running). Remaining rats were used for control for 4 wk (4W-control) and 10 wk (10W-control). The ACTH response induced by swimming stress was reduced after training by swimming (62.4%) or by running (13.8-16.4%). These training periods also attenuated the ACTH response induced by cage-switch stress (62.4% in the swimming group, 23.8-34.6% in the running groups). After swimming stress, the 4W-swimming and 10W-running groups showed smaller increases in blood glucose than the control groups. In addition, the increased levels of blood lactate in all the trained rats were significantly smaller than those in the control groups, suggesting that an adaptation was achieved after physical training. These results suggest that after running training, cross-adaptation is developed in the ACTH response induced by different types of physical (swimming) or psychological (cage-switch) stresses.

Adrenocorticotropic Hormone↗
PubMed1992

A binding profile of manganese to the nucleus of rat liver cells, and manganese-induced aberrations in thyroid hormone content and RNA synthesis in the nucleus.

Manganese (Mn) is accumulated in the nuclear and mitochondrial fractions when excess Mn is administered. However, little is known with respect to the behaviors of Mn in nuclei. In the present study, rats were given excess Mn and the nuclei were purified from liver cells by differential and sucrose gradient centrifugations. Being subjected to equilibrium dialysis with a radioactive 54Mn, the binding capacity of Mn in nuclei from the control rat was five-fold higher than BSA, which was used as a reference protein; and the capacity of 54Mn-binding rose in the nuclei from the Mn-treated animals in comparison with those from the control. On the analyses of nuclear materials with partial solubilization, sepharose column chromatography and HPLC, there were two major fractions which associated with a lot of Mn; one fraction was of large molecules of DNA, and the other fraction seemed to be peptides with small molecular weights. Therefore, Mn may open up a superhelical structure of DNA to provide more negatively charged phosphate moiety as a binding-site for a positively charged Mn. The results also disclosed a possible aberration in biological functions due to excess Mn in nuclei; the apparent association constant of triiodothyronine, a physiologically active thyroid hormone, to the nucleus was reduced by 75% and the uptake of 14C-labelled orotic acid to a newly synthesized RNA in the liver was severely inhibited.

Animals↗
PubMed1992

Clinical evaluation of interventional radiology for renal cell carcinoma in 100 patients.

One hundred of 160 patients with renal cell carcinoma (RCC) were treated by interventional radiology (IVR) in the period from 1978 to 1989. The number and kind of interventions done each year were classified retrospectively. More than half of the patients underwent therapeutic arterial embolization or intraarterial infusion of anticancer drugs during the first half of the period. More recently, about half of the patients have had nephrectomies without IVR. One patient with advanced RCC by IVR 18 times lived 8 years and three months after diagnosis, but that was exceptionally long. IVR has been more effective against hepatocellular carcinoma than RCC, for several reasons.

Angiography↗
PubMed1991

Hepatocyte growth factor modulates migration and proliferation of human microvascular endothelial cells in culture.

Epidermal growth factor (EGF) induces tubular formation of cultured human omental microvascular endothelial (HOME) cells and EGF also stimulates cell migration as well as expression of tissue type plasminogen activator (t-PA). Here we studied the effects of hepatocyte growth factor (HGF) on cell proliferation, cell migration and expression of t-PA and other related genes. Migration of confluent HOME cells into the denuded space was stimulated by HGF after being wounded with razor blade, but at a reduced rate in comparison with EGF. HOME cells could be proliferated in response to exogenous 100 ng/ml of HGF at rates comparable to that of 20 ng/ml EGF. The chemotactic activity of HOME cells was significantly stimulated by HGF in a dose-dependent manner when assayed by Boyden chamber. HGF did not efficiently enhance expression of both the t-PA gene and a tissue inhibitor of metalloproteinase gene whereas it stimulated expression of plasminogen activator inhibitor-1. Our present study provides a new evidence that some of the biological effects of HGF on HOME cells in culture are similar to those of EGF.

Bilirubin↗
PubMed1991

Threshold dose of interleukin-1 beta for induction of an ACTH response is higher than of a febrile response.

The present study was carried out to compare the threshold doses of interleukin-1 beta (IL-1 beta) necessary to elicit febrile and adrenocorticotrophic hormone (ACTH) responses. The results show that intravenous injection of a small dose of IL-1 beta (0.2 micrograms/kg) did not stimulate ACTH secretion but induced a significant febrile response. However, intravenous injection of a higher dose of IL-1 beta (2.0 micrograms/kg) induced significant increases in plasma ACTH accompanying the fever. These results suggest that the rise in body temperature per se is not responsible for the ACTH response and that the threshold dose of IL-1 beta to induce the ACTH response is higher than that to elicit the febrile response.

Adrenocorticotropic Hormone↗
PubMed1991

The effect of prostaglandin E2 on the body temperature of restrained rats.

We examined the effects of intravenous (IV) or intracerebro-ventricular (ICV) injection of prostaglandin E2 (PGE2) on the rectal temperature of restrained rats. The IV injection of PGE2 (0.5 mg/kg) caused hypothermia in rats with high initial rectal temperatures, but caused an elevation in rectal temperature in those animals whose starting temperatures were low. In contrast, the ICV injection of PGE2 induced fever, regardless of the rectal temperature at the time of injection. We also examined whether temperature changes due to the IV injection of endotoxin (lipopolysaccharide, LPS, 10 micrograms/kg) or interleukin-1 beta(IL-1 beta, 0.2 micrograms/kg) were dependent upon the rats' initial rectal temperatures. Rats with low rectal temperatures developed fevers in response to LPS, while animals with high starting temperatures showed hypothermia. In contrast, the IV injection of IL-1 beta produced fever regardless of initial rectal temperature. These data suggest that PGE2 acts centrally to cause fever and peripherally to cause hypothermia, and that following the injection of LPS, these opposing actions of PGE2 may act together to determine the thermoregulatory response.

Animals↗
PubMed1991

The effect of physical restraint on IL-1 beta- and LPS-induced fever.

The stress of physical restraint has been shown to cause an elevation in the body temperature of rats. In this study, we compared the febrile responses of restrained and unrestrained animals to the injection of interleukin-1 beta (IL-1 beta) and lipopolysaccharide (LPS). We found that, prior to injection, the body temperature of the restrained animals was about 1 degree C higher than that of the unrestrained rats. The restrained rats showed significantly smaller increases in body temperature in response to the injection of either pyrogen than did the unrestrained animals.

Animals↗
PubMed1991

Fever and acute-phase response induced in rabbits by intravenous and intracerebroventricular injection of interleukin-6.

We investigated the effect of human recombinant interleukin-6 (IL-6) on body temperature and acute-phase response, including changes in plasma levels of iron, zinc, copper, and fibrinogen and in circulating leukocyte count. The intravenous (IV) injection of IL-6 (2 micrograms/kg) produced a monophasic fever. The intracerebroventricular (ICV) injection of IL-6 produced a dose-dependent fever that developed gradually and remained elevated throughout the 5-h recording period. The IV injection of IL-6 decreased the plasma concentration of iron and zinc and increased the circulating leukocyte count. The ICV injection of IL-6 resulted in similar trace metal and leukocyte changes, and increased plasma levels of fibrinogen. These results show that IL-6 can cause fever when injected IV or ICV and induces some acute-phase responses through its action on peripheral target organs and in the central nervous system.

Animals↗
PubMed1991

Prostaglandin E2 is involved in adrenocorticotrophic hormone release during swimming exercise in rats.

1. We found that adrenocorticotrophic hormone (ACTH) release in rats induced by acute swimming exercise or by an intravenous injection of human recombinant interleukin-1 beta (IL-1 beta) was significantly attenuated after chronic exercise. 2. Since involvement of prostaglandins in the ACTH response induced by IL-1 is well known, we investigated the effect of indomethacin, an inhibitor of prostaglandin synthesis, on the ACTH response induced in rats by acute swimming exercise. Pretreatment with an intravenous injection of indomethacin significantly suppressed the ACTH response induced by exercise. The effect of indomethacin (1 and 10 mg/kg) on the ACTH response was dose-dependent. 3. The effect of chronic exercise on the exercise-induced changes in the plasma concentration of prostaglandin E2 was investigated. The plasma concentration of prostaglandin E2 significantly increased after acute exercise in both the control and the chronically exercised rats. However, the increase in the plasma level of prostaglandin E2 was significantly smaller in the chronically exercised group than in the control group. 4. Intravenous injections of prostaglandin E2 produced dose-dependent increases in the plasma concentration of ACTH in rats. 5. The present results suggest that an increase in prostaglandin E2 levels in plasma is involved in the development of the ACTH response induced by exercise.

Adrenocorticotropic Hormone↗
PubMed1991

The effect of chronic exercise on the pituitary-adrenocortical response in conscious rats.

1. This study was designed to investigate the effect of chronic exercise on exercise-induced changes in plasma concentrations of adrenocorticotrophic hormone (ACTH) and corticosterone in rats. Corticotrophin releasing factor (CRF) and ACTH were injected I.V. in order to assess the responsiveness of the pituitary and adrenal glands after chronic exercise. 2. The concentrations of ACTH and corticosterone in the plasma increased significantly after acute exercise in both the control and the exercised groups but both responses were significantly smaller in the exercised group. 3. The ACTH response to I.V. CRF was also significantly smaller in the exercised rats. However, both groups of animals showed similar increases in plasma corticosterone levels after the administration of exogenous ACTH. 4. The ACTH response to CRF attenuated by repeated administration of CRF. 5. These results suggest that attenuated ACTH and corticosterone responses to acute exercise after chronic exercise result from reduced responsiveness of the pituitary gland to CRF.

Adrenal Glands↗
PubMed1991

Possible involvement of prostaglandins in psychological stress-induced responses in rats.

1. We investigated the effect of pre-treatment with intraperitoneal (I.P.) injection of indomethacin, an inhibitor of prostaglandin synthesis, on psychological stress-induced responses including cardiovascular, thermoregulatory and hormonal responses in free-moving rats. 2. Psychological stress was induced by cage-switch stress. After the rats were placed in the novel environment, blood pressure, heart rate and body temperature significantly increased. Plasma levels of adrenocorticotrophic hormone (ACTH) and prostaglandin E2 were significantly higher 30 min after exposure to stress, in comparison to normal levels. 3. Pre-treatment with I.P. indomethacin significantly suppressed the increases in body temperature induced by cage-switch stress, but had no effect on increases in blood pressure and heart rate induced by this stress. Indomethacin also significantly suppressed the increases in the plasma levels of ACTH and prostaglandin E2 induced by cage-switch stress. 4. The present results suggest that prostaglandins are involved in the development of hyperthermia and the ACTH response induced by psychological stress.

Adrenocorticotropic Hormone↗
PubMed1991

ACTH release induced in rats by noradrenaline is mediated by prostaglandin E2.

1. We investigated the involvement of prostaglandin E2 in the development of the adrenocorticotrophic hormone (ACTH) response induced by noradrenaline (NA) in rats. 2. Intravenous (i.v.) injection of NA produced dose-dependent increases in the plasma concentration of ACTH and prostaglandin E2. However, pre-treatment with systemic administration of indomethacin, an inhibitor of prostaglandin synthesis, significantly suppressed this increase in plasma ACTH. 3. The i.v. injection of prostaglandin E2 significantly increased the plasma concentration of ACTH in a dose-dependent manner. In contrast, ACTH responses induced by the i.v. injection of prostaglandin E2 were significantly suppressed by systemic pre-treatment with anti-corticotrophin-releasing factor antibody (anti-CRF), although the plasma level of ACTH still increased in comparison to the basal level. 4. These results suggest that NA-stimulated prostaglandin release is involved in the ACTH response induced by NA. In addition, it is likely that CRF may be responsible for a portion of the ACTH response induced by i.v. injection of prostaglandin E2.

Adrenocorticotropic Hormone↗
PubMed1991

Intraperitoneal injections of prostaglandin E2 attenuate hyperthermia induced by restraint or interleukin-1 in rats.

1. The purpose of this study was to investigate the effect of the intraperitoneal (I.P.), intravenous (I.V.) or intrapreoptic area (POA) injection of prostaglandin E2 (PGE2) on the body temperature of restrained and unrestrained rats. The effect of I.P. PGE2 on the body temperature of rats during fever induced by I.P. injection of interleukin-1 beta (IL-1 beta) was also investigated. 2. Prior to injection, restrained rats had body temperatures of approximately 1 degree C higher than unrestrained rats. The I.P. injection of PGE2 (0.05 and 0.5 mg kg-1) caused body temperature to fall towards the pre-restraint levels in a dose-dependent manner. This fall in body temperature was preceded by a sharp increase in tail skin temperature that was also dependent on dose. The I.P. injection of PGE2 had no effect on the body temperature of unrestrained animals. 3. The I.V. injection of PGE2 caused very little change in the body temperature of restrained rats. However, when injected I.V. into unrestrained animals, PGE2 caused dose-dependent fevers. The injection of PGE2 (50 ng) into the POA resulted in fever in both restrained and unrestrained animals. 4. The I.P. injection of IL-1 beta (10 micrograms kg-1) caused a biphasic fever that lasted at least 420 min. The I.P. injection of PGE2 180 min after the injection of IL-1 beta caused a transient decrease in the rats' body temperature. This drop in body temperature was not associated with a decrease in metabolic rate. 5. These data support the hypothesis that during restraint stress hyperthermia and IL-1 beta fever, the I.P. injection of PGE2 acts peripherally to lower the body temperature of rats.

Animals↗
PubMed1991

ACTH response in rats during biphasic fever induced by interleukin-1.

Injection of a low concentration (0.3 micrograms/kg iv) of interleukin-1 beta (IL-1 beta) produced monophasic fever, but high concentrations (15 micrograms/kg iv) produced biphasic fever in rats. Treatment with IL-1 beta caused dose-dependent rises in the plasma concentration of adrenocorticotropic hormone (ACTH) 30 min after injection. Moreover, significant increases in plasma levels of ACTH were observed 90 and 180 min after injection of the high dose of IL-1 beta. ACTH response induced by IL-1 beta (15 micrograms/kg iv) was suppressed by pretreatment with injection of indomethacin (Indo), a potent inhibitor of prostaglandin (PG) synthesis, in a dose-dependent manner (1 and 10 mg/kg iv). Also, biphasic fever induced by the high dose of IL-1 beta was completely abolished by pretreatment with the intravenous injection of Indo. Intracerebroventricular (icv) injection of Indo (50 micrograms) did not affect febrile and ACTH responses induced by intravenous IL-1 beta, whereas those responses induced by IL-1 beta (2 ng icv) were significantly suppressed by injection of Indo (50 micrograms icv). Although it is possible that intracerebroventricular Indo does not reach the site of intravenous IL-1 beta action within the brain, these results suggest that in rats febrile and ACTH responses induced by intravenous IL-1 beta are caused by IL-1 beta-acting structures outside the blood-brain barrier. It is likely that these structures subsequently synthesize and release PGE2, which in turn induces ACTH and febrile responses in rats.

Adrenocorticotropic Hormone↗
PubMed1991

[Two routes chemotherapy by CDDP and STS against liver tumor].

Nine (eight males, one female) patients with unresectable liver tumor (seven HCC and two metastasis) were treated by two-routes chemotherapy using cis-diamminedichloroplatinum (CDDP) and sodium thiosulfate (STS). In these patients, 50-100 mg/body of CDDP was administered through the proper hepatic artery or right hepatic artery by one shot infusion or the balloon-occluded arterial infusion (BOAI) at 10 mg/min, and during administration, intra-inferior vena cava injection of STS (4 g/body) was given. None of 9 patients suffered nausea and vomiting during the treatment, 3 of 9 patients suffered nausea and vomiting to a mild degree after the treatment, none of 9 patients showed significant side effects, such as bone marrow suppression and/or renal disfunction. In conclusion, this study demonstrated the protection effect of STS injected in inferior vena cava against the toxicity of CDDP were well indicated.

Aged↗
PubMed1990

ACTH response induced by interleukin-1 is mediated by CRF secretion stimulated by hypothalamic PGE.

We investigated whether hypothalamic prostaglandin E2 (PGE2) and corticotropin releasing factor (CRF) are responsible for the development of the adrenocorticotropic hormone (ACTH) response induced by interleukin-1 alpha (IL-1 alpha). The present results show that ACTH responses induced by intravenous injection of IL-1 alpha were suppressed by systemic pretreatment with indomethacin and that intrahypothalamic injection of PGE2 stimulates the secretion of ACTH. Furthermore, systemic pretreatment with anti-CRF antibody significantly suppressed the ACTH response induced by intrahypothalamic injection of PGE2. These data suggest that the ACTH response induced by IL-1 is mediated by CRF secretion stimulated by hypothalamic PGE2.

Adrenocorticotropic Hormone↗
PubMed1990

Maternal thermal stimulation changes metabolic activity in fetal hypothalamus.

To study whether the central nervous system in the perinatal fetal rat can operate during maternal cooling and warming, we examined the 2-deoxy-D-[14C]glucose ([14C]DG) uptake in the fetal brain. Full-term pregnant rats were placed at three different ambient temperatures of 35-37 degrees C, 24-25 degrees C and 0-10 degrees C. Saline containing 20 microCi/100 g of [14C]DG was injected into the superior caval vein in the pregnant rats. Forty-five min after the injection, the mother rats were decapitated and the fetal brains were taken out for autoradiography. The [14C]DG uptake was significantly influenced by maternal thermal stimulation in the hypothalamus and not in other brain regions examined such as the cerebral cortex, the basal ganglia and the limbic nuclei. Glucose utilization in the fetal anterior hypothalamus, paraventricular hypothalamus and dorsomedial hypothalamus significantly increased when the mother rat was exposed to heat compared to when the mother rat was in the thermoneutral condition. During maternal cooling, glucose utilization in the ventromedial hypothalamus and dorsomedial hypothalamus significantly decreased. There was no area activated by cooling and/or inhibited by warming. Compared to a similar study in adult rats (Am. J. Physiol., 248 (1985) R84-92), the present results suggest that although the perinatal fetal brain does not respond to thermal stimulation in terms of glucose utilization as fully as the adults, a few hypothalamic nuclei have already acquired thermal responses, which might be a possible neuronal basis for the thermoregulatory responses just after birth in rats.

Animals↗