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Biomedical subjects

M Kusunoki

Publications and source records attributed to M Kusunoki.

At least 217 records · Page 12Linked to original sources

Impaired contractile motility of the gallbladder after gastrectomy.

Contractile motility of the gallbladder was compared using a real-time ultrasonography in 13 patients with gastric ulcer and 31 patients with gastric cancer who had undergone either subtotal or total gastrectomy within 1 month previously. Contractile motility of the gallbladder after oral administration of dried egg yolk (Daiyan, Maruishi, Osaka), which was slightly but not significantly reduced in patients with gastric ulcer, was remarkedly impaired in patients with gastric cancer who had either subtotal or total gastrectomy including radical lymph node dissection. Especially, maximum contractile rate after Daiyan in Billroth II patients was significantly reduced than that of Billroth I patients. Intramuscular injection of naloxone (0.4 mg), which had no effects on contractions after Daiyan in healthy subjects, significantly improved the hypomotility in response to Daiyan in these gastric cancer patients. It was suggested, therefore, that the possible roles of various anatomical and mechanical changes resulting from gastrectomy including vagotomy and sympathectomy, and in particular exclusion of duodenum from digestive circuits and relative or absolute excess of endogenous opioids, were involved in the control of the gallbladder motility within 1 month after gastrectomy including lymphadenectomy.

Colectomy↗

Some pharmacological effects of tizanidine on smooth muscle organs and alpha 2-adrenoceptor.

Microsomal and crude synaptosomal fractions were prepared from the longitudinal muscle of guinea-pig ileum. A specific binding of [3H]yohimbine (10 nM) to alpha 2-adrenoceptor in the crude synaptosomal fraction was inhibited by tizanidine and clonidine. Tizanidine is about one-third as potent as clonidine. A specific binding of [3H]QNB (0.3 nM) to muscarine receptor in the microsomal fraction was inhibited by atropine (10(-8)-10(-7) M) but not by tizanidine (up to 10(-4) M). Tizanidine inhibited spontaneous movements of guinea pig ileum and rat stomach (in situ) and intestinal transit in mice, and induced mydriasis in mice. These effects induced by tizanidine might be due to activation of alpha 2-adrenoceptor but not to atropine like action.

Animals↗

Dopamine regulation of [3H]acetylcholine release from guinea-pig stomach.

The involvement of dopamine receptors in cholinergic transmission of guinea-pig stomach was investigated by analyzing the effects of dopamine receptor agonists and antagonists on acetylcholine (ACh) release from this organ. Electrical stimulation (1-20 Hz) of strips of guinea-pig stomach preloaded with [3H] choline induced a [3H]ACh release that was calcium dependent and tetrodotoxin sensitive. Dopamine inhibited this transmural stimulation-induced [3H]ACh release in a concentration-dependent manner (10(-8)-10(-4) M). This effect of dopamine was not altered by 10(-5) M hexamethonium, thereby suggesting that the major dopamine receptors are located on the postganglionic cholinergic neurons. Concentration-response curves for dopamine on [3H]ACh release were inhibited by haloperidol, sulpiride and domperidone but not by prazosin, yohimbine, propranolol and ketanserin. LY 171555, an agonist for the D2 dopamine receptor, but not SKF 38-393, an agonist for the D1 dopamine receptor, to some extent decreased the release of [3H]ACh induced by transmural stimulation. In view of the results, the release of ACh from postganglionic cholinergic neurons is probably required through dopamine receptors antagonized by D2 antagonists but not by adrenergic or serotonin receptor antagonists.

Acetylcholine↗

Inhibitory histamine H2-receptor in the guinea-pig urinary bladder.

The histamine H2-receptor in the guinea-pig urinary bladder was characterized by determining the effects of histamine and impromidine on contractions induced by electrical transmural stimulation (ETS). The contractile responses to ETS (0.5 ms, 15 V, for 15 s) at frequencies of 1 to 30 Hz were abolished by treatment with tetrodotoxin, and were partly inhibited by scopolamine, indicating that the ETS-induced contraction has scopolamine-sensitive and -resistant components. Histamine and impromidine inhibited the scopolamine-resistant contraction induced by ETS but not the ETS-induced scopolamine-sensitive contraction and nicotine- and acetylcholine (ACh)-induced contractions. The inhibitory effects of histamine and impromidine were antagonized by cimetidine, but not by diphenhydramine and mepyramine. Thus, the inhibitory effect of histamine may be mediated through H2-receptors. As impromidine did not affect the tetrodotoxin-sensitive and Ca2+-dependent ETS-evoked release of ACh and noradrenaline (NA) from the isolated urinary bladder preloaded with [3H]choline and [3H]NA, respectively, the H2-receptor may not be involved in the cholinergic and adrenergic mechanisms. These results indicate that histamine H2-receptors are present in the guinea-pig urinary bladder. The H2-receptor located on non-cholinergic excitatory neurons may be involved in the inhibitory action produced by histamine.

Acetylcholine↗

A phorbol ester and A23187 act synergistically to release acetylcholine from the guinea pig ileum.

Electrical stimulation of guinea pig ileum preloaded with [3H]choline provokes the release of [3H]acetylcholine (ACh) in a Ca2+-dependent manner. This release was markedly increased by the tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA). The combination of the ionophore A23187 and TPA produced the release of [3H]ACh up to a level equal to or exceeding a maximal response induced by electrical stimulation. A23187 alone gave only a minor response and TPA alone had no apparent effect on the [3H]ACh release. Thus, protein kinase C probably plays a role in cell surface signal transduction related to the release of transmitters from nerve endings.

Acetylcholine↗

Refined structure of cytochrome c3 at 1.8 A resolution.

The structure of cytochrome c3 from the sulfate-reducing bacterium Desulfovibrio vulgaris Miyazaki has been successfully refined at 1.8 A resolution. The crystallographic R factor is 0.176 for 9907 significant reflections. The isotropic temperature factors of individual atoms were refined and a total of 47 water molecules located on the difference map were incorporated in the refinement. The four heme groups are closely packed, with adjacent pairs of heme planes being nearly perpendicular to each other. The fifth and the sixth ligands of the heme iron atoms are histidine residues with N epsilon 2-Fe distances ranging from 1.88 A to 2.12 A. The histidine co-ordination to the heme iron is different for each heme group. The heme groups are all highly exposed to solvent, although the actual regions exposed differ among the hemes. The four heme groups are located in different environments, and the heme planes are deformed from planarity. The differences in the heme structures and their environments indicate that the four heme groups are non-equivalent. The chemical as well as the physical properties of cytochrome c3 should be interpreted in terms of the structural non-equivalence of the heme groups. The characteristic secondary structural non-equivalence of the heme groups. The characteristic secondary structures of the polypeptide chain of this molecule are three short alpha-helices, two short beta-strands and ten reverse turns.

Binding Sites↗

Telencephalic and preoptic areas integrate sexual behavior in hime salmon (landlocked red salmon, Oncorhynchus nerka): results of electrical brain stimulation experiments.

Various patterns of sexual behavior were evoked in freely swimming hime salmon by electrical stimulation of specific loci in the telencephalon and the preoptic area (POA) using chronically implanted electrodes. Furthermore, co-ordinated sexual behavior corresponding to stages of the natural spawning sequence was elicited from some of these brain regions. These results suggest that (1) sexual behavior is integrated in specific parts of the telencephalon and POA, and (2) within these regions there is a hierarchy of neural systems which mediate progressively more complete components of normal sexual behavior.

Animals↗

Successful replantation of a leg--a 7-year follow-up.

This paper presents the 7-year follow-up of successful replantation in a patient whose right leg was amputated. The patient's daily activities surpass those that would have otherwise been attained by the use of an artificial leg. The authors believe that this patient is one of the most successful cases of replantation of the leg, with a long follow-up period.

Adult↗

Structure and possible catalytic residues of Taka-amylase A.

A complete molecular model of Taka-amylase A consisting of 478 amino acid residues was built with the aid of amino acid sequence data. Some typical structural features of the molecule are described. A model fitting of an amylose chain in the catalytic site of the enzyme showed a possible productive binding mode between substrate and enzyme. On the basis of the difference Fourier analysis and the model fitting study, glutamic acid (Glu230) and aspartic acid (Asp297), which are located at the bottom of the cleft, were concluded to be the catalytic residues, serving as the general acid and base, respectively.

Binding Sites↗

Neuronal GABA release and GABA inhibition of ACh release in guinea pig urinary bladder.

gamma-Aminobutyric acid (GABA) and glutamate decarboxylase (GAD) are present in the urinary bladder of guinea pigs, and the possible correlation in regional distribution between GABA, GAD, and the number of vesical ganglion cells was studied. Electrical stimulation of the bladder strips produced an increase in the calcium-dependent and tetrodotoxin-sensitive [3H]GABA release and contractions in the strips preloaded with [3H]GABA. Nicotine, acetylcholine chloride (ACh), and hexamethonium did not significantly alter the release of [3H]GABA. Bicuculline significantly enhanced [3H]ACh release and cholinergic components of contractions evoked by electrical stimulation of the bladder strips preloaded with [3H]choline, thereby suggesting that this compound antagonizes the effect of endogenous GABA released during stimulation. GABA and muscimol but not baclofen reduced both the [3H]ACh release and contractions evoked by nicotine. These effects of GABA were antagonized by bicuculline and furosemide but not by alpha- and beta-adrenergic blockers. These findings suggest that GABA may be a noncholinergic nonadrenergic inhibitory neurotransmitter in the urinary bladder. The motility of the urinary bladder is thus inhibited by reducing the release of ACh from the postganglionic cholinergic neurons through bicuculline-sensitive GABA receptors probably associated with the chloride ion channel.

Acetylcholine↗

Platelet accumulation in carotid atherosclerotic lesions: semiquantitative analysis with indium-111 platelets and technetium-99m human serum albumin.

To evaluate platelet accumulation in carotid atherosclerotic lesions semiquantitatively, a dual-tracer technique was applied, using In-111 platelets and Tc-99m human serum albumin. With this approach, we investigated the ratio of radioactivity in In-111 platelets deposited on the vascular wall to those circulating in the blood pool, platelet accumulation index ( PAI ). This study included 12 normal subjects and 25 patients with ischemic cerebrovascular disease (CVD). Angiographic abnormalities were observed at 34 of 50 carotid bifurcations in the CVD patients. The mean PAI value was significantly higher at the carotid bifurcations with angiographic abnormality than at the normal ones (p less than 0.001). Furthermore, elevations of mean PAI were prominent at the lesions with severe stenosis or ulceration. The degree of platelet accumulation was well demonstrated by this technique, which can also yield information on thrombogenicity and efficiency of antiplatelet therapy in carotid atherosclerotic disease.

Adult↗

GABA evoked ACH release from isolated guinea pig ileum.

To identify the target cells of GABAergic neurons located in the myenteric plexus, the action of gamma-aminobutyric acid (GABA) on the release of acetylcholine (ACh) and on the contractions was studied using the isolated guinea pig ileum. GABA evoked a release of 3H-ACh from the contracting ileum, under conditions of loading with 3H-choline. As both the GABA-evoked release of 3H-ACh and the contractions were inhibited by bicuculline, tetrodotoxin and furosemide, but not by hexamethonium, this release seems to be evoked through GABA receptors which are bicuculline sensitive and associated with the Cl- ion channel.

Acetylcholine↗

Role of prostacyclin in the response of cerebral blood flow to CO2.

The prostacyclin (PGI2) formation in cerebral vessels, as reflected by the difference in concentration of internal carotid arterial and internal jugular venous radioimmunoassayed 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), was determined under normocapnic and hypercapnic conditions in 5 patients with mild cerebral thrombotic infarction. There was no evidence that endogenous PGI formation in cerebral vessels was stimulated at mild hypercapnia, while an increase of cerebral blood flow (CBF) induced by hypercapnia was observed. These results suggest that endogenous PGI2 may not be a mediator for the response of CBF to CO2.

6-Ketoprostaglandin F1 alpha↗

Release of endogenous and labeled GABA from isolated guinea pig ileum.

The release of gamma-aminobutyric acid (GABA) was studied by comparing the properties of labeled GABA released from preloaded preparations to those of endogenous GABA released from the isolated guinea pig ileum. The spontaneous release of endogenous GABA was 4.46 +/- 0.10 pmol X min-1 X g wet wt-1, and the fractional rate of endogenous GABA release was much lower. The ratio of evoked to spontaneous release of endogenous GABA was high compared with that of labeled GABA. The electrical transmural stimulation-evoked release of labeled and endogenous GABA was inhibited by superfusion with tetrodotoxin and Ca2+-free Krebs-Ringer solution containing 1 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid. Thus the nature of the stimulation-evoked release of labeled GABA was similar to that of endogenous GABA. These results indicate that the released GABA is neuronal in origin and provide additional evidence for the presence of GABA-ergic neurons in the guinea pig ileum.

Animals↗

Platelet hyperaggregability in ischemic cerebrovascular disease and effects of aspirin.

Platelet aggregation was studied in 24 patients in the chronic stage of ischemic cerebrovascular disease (CVD), with cerebral affluent and effluent blood, i.e., carotid arterial and internal jugular venous blood, and also with peripheral venous blood. Aggregation tests were performed at various final concentrations of sodium arachidonate (A.A.) and ADP. In 17 patients, not taking aspirin, platelet aggregability in jugular venous blood was significantly accentuated compared with that in arterial and peripheral venous blood. This tendency was more marked in the patients with cerebral artery stenosis and/or occlusion than in those with normal cerebral angiogram. In 7 patients taking 500 mg or more oral aspirin, aggregation differences across the brain were not observed and A.A. aggregation and the second phase of ADP aggregation were completely suppressed. These results suggest that a prophylactic administration of aspirin may be beneficial for patients in chronic stage of CVD.

Arteries↗

[Release of gamma-aminobutyric acid from cat colon].

The release of gamma-aminobutyric acid was confirmed in isolated cat colon loaded with tritiated gamma-aminobutyric acid. Thirty to 180 minutes after loading the spontaneous efflux of tritium appeared to fit a single exponential curve with an efflux rate coefficient of 0.002 per minute. Electrical stimulation produced frequency-dependent increases in the tritium efflux and in the contractions. Even 120 minutes later over 91 percent of the total radioactivity in the superfusates was attributable to tritiated gamma-aminobutyric acid. The acid release and the contractions induced by electrical transmural stimulation were inhibited by tetrodotoxin and by a calcium-free medium. Release of the acid was not significant during contractions elicited by nicotine and acetylcholine. These findings indicate that gamma-aminobutyric acid is released from the terminals of neurons in the myenteric plexus of the colon.

Acetylcholine↗