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Biomedical subjects

H Amano

Publications and source records attributed to H Amano.

At least 199 records · Page 11Linked to original sources
PubMed1989

Evidence for tonic activation of prejunctional beta-adrenoceptors in guinea-pig pulmonary arteries by adrenaline derived from the adrenal medulla.

1. The effects of (+/-)-carteolol 10(-8) M to 10(-6) M, a non-selective beta-antagonist, applied cumulatively, on stimulation-evoked 3H-release at 1 Hz were studied in pulmonary arteries isolated from guinea-pigs. The guinea-pigs were subjected to either bilateral adrenalectomy, adrenalectomy followed by injections of deoxycorticosterone acetate (DOCA) and hydrocortisone, bilateral adrenodemedullation or a sham operation, and then loaded in vitro with [3H]-noradrenaline. 2. Carteolol inhibited 3H-output in arteries from sham-operated animals in a concentration-dependent manner. This inhibitory effect was not found in pulmonary arteries from animals subjected to adrenalectomy or adrenodemedullation. However, DOCA and hydrocortisone pretreatment, did not prevent the disappearance of the carteolol-induced inhibition of 3H-release. 3. Adrenalectomy and adrenodemedullation depleted or markedly reduced the endogenous contents of adrenaline in pulmonary arteries without altering the levels of dopamine and noradrenaline. 4. It is concluded that adrenaline, mainly derived from the adrenal medulla, acts as an endogenous agonist for tonically functioning prejunctional beta-adrenoceptors in guinea-pig pulmonary arteries, probably by being taken up and co-released with noradrenaline.

Adrenal Medulla↗
PubMed1989

Nicotine-induced regional changes in brain noradrenaline and dopamine turnover in rats.

Using high performance liquid chromatography with electrochemical detection, the levels of 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3,4-dihydroxyphenylalanine (DOPA) were determined in various brain regions of the rat 1 h after nicotine administration. Nicotine (1 mg/kg, s.c.) produced an increase in MHPG concentrations in the occipital cortex, hippocampus, striatum, hypothalamus, thalamus, midbrain, pons/medulla and cerebellum. This alkaloid at the same dose also caused an increase in DOPAC concentrations in the hypothalamus, thalamus and pons/medulla. The nicotine-induced increase in MHPG and DOPAC concentrations in the brain regions was inhibited by pretreatment with mecamylamine (5 mg/kg, i.p.) but not by hexamethonium (10 mg/kg, i.p.). Nicotine (1 mg/kg, s.c.) produced an increase in DOPA concentrations under DOPA decarboxylase inhibition with NSD-1015 (200 mg/kg, i.p.) in the hypothalamus, thalamus and pons/medulla. These results indicate that nicotine can increase the turnover of noradrenaline and dopamine in various brain regions of the rat and this effect is mediated via activation of central nicotinic receptors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Effects of acute nicotine on catecholamine turnover in various rat brain regions.

Acute effects of in vivo nicotine application on turnover rates of noradrenaline (NA), adrenaline (AD) and dopamine (DA) in rat occipital cortex, hippocampus, striatum, hypothalamus, thalamus, midbrain, pons/medulla and cerebellum were examined by determining the amine concentrations by high performance liquid chromatography. The regional turnover rates of catecholamines were evaluated by comparing the decline in concentrations produced by blockade of synthesis. Intraperitoneally injected fusaric acid (80 mg/kg), an inhibitor of dopamine-beta-hydroxylase, significantly decreased NA concentration in all eight regions examined, and AD concentration in the hypothalamus and pons/medulla. alpha-Methyl-p-tyrosine methylester (alpha-MPT, 400 mg/kg), an inhibitor of the tyrosine hydroxylase, induced significant and uneven decreases in regional DA concentrations 1 h after the i.p. injection. alpha-MPT also significantly decreased NA concentration in all the regions except the striatum. Subcutaneously injected nicotine 0.4-1 mg/kg significantly enhanced the fusaric acid-induced decline in NA concentrations in the hippocampus and cerebellum. AD decline in the midbrain by fusaric acid was significantly accelerated by nicotine (0.4 mg/kg), but was not affected by a larger dose (1 mg/kg). In the hippocampus, nicotine (1 mg/kg) significantly enhanced the alpha-MPT-induced decrease in NA concentration, while it reduced the decrease in DA concentration. These findings suggest that nicotine can affect the turnover of brain catecholamine in a regionally specific manner.

Animals↗
PubMed1989

A histomorphometric analysis of the alveolar bone resorption process in calcium-deficient rats.

The present study was carried out to investigate the morphological changes in the alveolar bone in rats fed a low calcium diet, in order to establish an experimental model of alveolar bone resorption. Male Wistar rats (70-85 g in body weight) were either fed a low calcium diet (0.05% Ca, 0.35% P) or a control diet (0.5% Ca, 0.35% P) by using a pair feeding technique. The rats were sacrificed at intervals of 3, 6, 9 and 20 days. No difference was found in the growth rate between the control and the low calcium group. In the low calcium group, the bone area significantly reduced at day 3 and progressively decreased to 46% of that of the controls by the end of the experiment. The bone resorption was obvious in the cancellous bone during the early period of the experiment and then the cortical bone was seen to resorb. However, the contour of bone and the rate of bone apposition did not change. At day 20, bone still remained in three regions: the alveolar bone proper that surrounds the tooth sockets, a few cancellous bones and a thin wall-like cortical bone. These results suggest that the process of alveolar bone resorption is related to the mechanical forces induced by the occlusal function of the tooth and, further, that this experimental model might be useful for investigating the mechanism of alveolar bone resorption and disorders of the alveolar bone.

Alveolar Bone Loss↗
PubMed1989

[The pharmacokinetics of cisplatin and its influence on renal function according to different infusion methods (report II)--alleviation of renal impairment by bismuth subnitrate combined with ginseng and tang-koui ten].

In the previous report, we discussed in vivo dynamics and renal impairment resulting from the difference in cisplatin CDDP administration. In the present study, we investigated in vivo dynamics and renal impairment under 1 h of continuous drip infusion of CDDP. The free-type Pt concentration ratio, which is considered to indicate antitumor activity in the overall plasma Pt concentration at the end of the administration, was noted to be approximately 64%. This was significantly higher than other administration methods, making this an effective administration procedure. However, NAG, which is considered to be an index of renal impairment along with the amount of beta 2-microglobulin urine excretion, showed higher values than those by other administration methods. Thus, using the 1-hr continuous CDDP drip infusion, we attempted to alleviate the renal impairment, combining bismuth subnitrate with ginseng and Tang-koui ten. As a result, the amount of beta 2-microglobulin excretion in the urine was diminished as well as NAG, and a reduction of the renal impairment was noted. These alleviational effects of the renal impairment were attributed to the method of consistent oral administration by which alleviation could take place with little load on the patient.

Acetylglucosaminidase↗
PubMed1989

[Successful management of massive hemoptysis, following pulmonary mycosis by bronchial artery embolization in a patient with acute lymphoblastic leukemia].

In June 1987, a 20-year-old man was diagnosed as T-cell acute lymphoblastic leukemia. In August, at a nadir period of the remission induction chemotherapy, he complained of high fever and dry cough. A chest roentgenogram also showed a nodular area of increased density in the left upper lobe. Since his clinical state deteriorated progressively despite the administration of broad-spectrum antibiotics, amphotericin B was administered intravenously (with an initial dose of 5 mg/day, increased up to 25 mg/day). Concomitant with bone marrow recovery and continued antifungal therapy, he became soon afebrile and improved over the next 2 months. The infiltrates also began to resolve. Then he abruptly coughed up about 800 ml of blood and suffered from acute respiratory failure. Bronchial arteriographic studies demonstrated active extravasation of contrast medium in the region of the cavity. After therapeutic embolization with Gelfoam, the extravasation was no longer observed. Active bleeding abruptly ceased and had not recurred until the left upper lobectomy which was performed 10 days after the embolization. This case typically demonstrates the value of bronchial arterial embolization in treating massive hemoptysis.

Adult↗
PubMed1988

Nucleotide sequence homology of the tetracycline-resistance determinant naturally maintained in Bacillus subtilis Marburg 168 chromosome and the tetracycline-resistance gene of B. subtilis plasmid pNS1981.

The nucleotide sequence (1579 bp) of tetracycline-resistance determinant and flanking regions of the cloned 5.1 kb DNA fragment from Bacillus subtilis GSY908 chromosome (Sakaguchi, R. and Shishido, K. (1988) Biochim. Biophys. Acta 949, 49-57) were determined and compared with those of the B. subtilis tetracycline-resistance plasmid pNS1981. The tetracycline-resistance structural (tet) genes of the B. subtilis GSY908 chromosome (tetBS908) and pNS1981 (tetpNS1981) were found to be highly homologous (80% identical). Both tet genes were composed of 1374 bp and 458 amino-acid residues initiating from a GTG codon preceded by a ribosome-binding site (RBS-2). Upstream from tetBS908 there exists a short open reading frame (20 amino acids) initiating from a ATG codon preceded by its own RBS (RBS-1). This leader sequence was also highly homologous to that of tetpNS1981 except for a deletion of one bp between the RBS-1 and the ATG codon.

Bacillus subtilis↗
PubMed1988

Adrenaline as an endogenous agonist for presynaptic beta-adrenoceptors and their relevance to the development of hypertension in spontaneously hypertensive rats.

We attempted to identify an endogenous agonist for presynaptic facilitatory beta-adrenoceptors. Pulmonary arteries isolated from guinea pigs 5 days after bilateral adrenalectomy and renal arteries from 4-week-old spontaneously hypertensive rats (SHR) exposed to swimming stress for 1 h were preloaded with 3H-noradrenaline and superfused with Krebs medium. Electrical field stimulation was carried out four times at 15-min intervals (S1 to S4). Beta-antagonist carteolol at 10(-8), 10(-7) and 10(-6) mol/l was cumulatively applied after S1, S2 and S3 and the effect was estimated as the evoked 3H release ratio, Sx:S1. Catecholamine contents in arteries were measured by high performance liquid chromatography with electron capture. In sham-operated pulmonary arteries, carteolol inhibited evoked 3H release in a concentration-dependent manner. This inhibition was completely abolished by adrenalectomy. Adrenalectomy depleted adrenaline contents without modification of noradrenaline and dopamine. In renal arteries, swimming stress potentiated carteolol-induced concentration-dependent inhibition of evoked 3H release and increased adrenaline and dopamine contents without modification of noradrenaline. Adrenaline derived from adrenals and probably stored and coreleased with noradrenaline acts as an endogenous agonist for presynaptic beta-adrenoceptors.

Animals↗
PubMed1988

Regional changes in brain noradrenergic activity elicited by a decrease in blood pressure.

Using high performance liquid chromatography with electrochemical detection, the level of 3-methoxy-4-hydroxyphenylethylene glycol (MHPG), an index of noradrenaline release, was determined in regions of the brainstem and hypothalamus of rats after acute hypotension induced by hydralazine. In hypotensive rats, an increase in MHPG concentrations was observed in the posterior hypothalamus, while no significant changes were seen for all the other regions. These results suggest that hypotension results in an enhancement of noradrenaline release in the posterior hypothalamus in rats.

Animals↗
PubMed1987

Biotransformation of 1-nitropyrene and 2-nitrofluorene to novel metabolites, the corresponding formylamino compounds, in animal bodies.

The present study provides the first evidence that nitropolycyclic aromatic hydrocarbons such as 1-nitropyrene and 2-nitrofluorene are metabolized to the corresponding formylamino compounds in animal bodies. The study shows that the formation of such novel metabolites, 1-formylaminopyrene and 2-formylaminofluorene, is due to N-formylation of the nitroreduction products, 1-aminopyrene and 2-aminofluorene, by liver formamidase in the presence of N-formyl-L-kynurenine.

Animals↗