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Biomedical subjects

Y Osumi

Publications and source records attributed to Y Osumi.

At least 73 records · Page 4Linked to original sources
PubMed1984

Effects of intracerebroventricularly applied nicotine on enhanced gastric acid secretion and mucosal blood flow in rats.

The effects of intracerebroventricularly administered nicotine on the elevated levels of gastric acid output and mucosal blood flow (MBF) were examined in anesthetized rats. Intravenous administration of both 2-deoxy-D-glucose (2-DG) and pentagastrin induced marked increases in gastric function and the intraventricularly applied nicotine diminished the increases induced by 2-DG but not those due to pentagastrin. This effect of nicotine was inhibited when hexamethonium was given concomitantly. In reserpinized rats, this inhibitory effect of nicotine on the 2-DG-induced increases in gastric function was abolished. Electrical stimulation of the lateral hypothalamic area induced increases in gastric function and these increases were also inhibited by intraventricularly administered nicotine. These results indicate that centrally administered nicotine has an inhibitory effect on both acid secretion and MBF, when these gastric parameters are maintained at relatively higher levels by central activation. Central noradrenergic inhibitory mechanisms in the regulation of gastric function may relate to the inhibitory effects of nicotine.

Animals↗
PubMed1983

Neurotensin potentiates the potassium-induced release of endogenous dopamine from rat striatal slices.

The effects of neurotensin on the release of endogenous dopamine (DA) from rat striatal slices were investigated. DA was extracted by the aluminium adsorption method and assayed electrochemically by high-performance liquid chromatography. Neurotensin (2-100 microM) potentiated the potassium-induced release of striatal endogenous DA in a concentration-dependent manner. This neurotensin-induced release of DA was completely abolished in calcium-free medium containing EGTA 1 mM. The presence of tetrodotoxin 2 microM did not alter the effect of neurotensin 10 microM. On the other hand, neurotensin did not affect the uptake of [3H]DA into the striatal slices. In additional experiments, we confirmed that the KCl-induced release of DA in the nucleus accumbens was also potentiated b neurotensin. These results suggest that neurotensin has a direct effect on the central DA nerve terminals and releases DA in a Ca2+-dependent manner.

Animals↗
PubMed1983

Central noradrenergic-cholinergic interaction in regulation of gastric acid secretion in rats.

Possible roles of noradrenaline (NA) and acetylcholine (ACh) within the lateral hypothalamic area (LHA) in regulation of gastric acid secretion were examined in urethane anesthetized rats. When NA 30 nmoles was given into the LHA, the gastric acid output decreased and this inhibitory effect of NA was potentiated in rats pretreated with reserpine (2 mg/kg, i.p., 20 hr). Even in a dose of 3 nmoles which was without effect in non-treated control animals, there was a remarkable decrease in acid output. In these reserpinized animals, ACh in a dose of 30 nmoles induced a remarkable increase in acid output, while in the controls this ACh-induced increase was observed only with a 10 times higher dose. In the rats not given reserpine, the cholinergic muscarinic agonist bethanechol (10 nmoles) increased the gastric acid output while nicotine (30 nmoles) was without effect. Therefore, in rats, the central noradrenergic inhibitory mechanisms related to regulation of gastric function may be present at the level of LHA as well as at the ala cinerea (area of the dorsal motor nucleus of vagi and the nucleus tractus solitarius). In addition, in the LHA, a cholinergic muscarinic mechanism which elevates gastric acid secretion may be antagonized by a noradrenergic inhibitory mechanism.

Acetylcholine↗
PubMed1983

Dual effects of electrical stimulation of ventromedial hypothalamic neurons on gastric acid secretion in rats.

Effects of electrical stimulation of the ventromedial hypothalamus (VMH) on gastric acid output and mucosal blood flow were examined in rats anesthetized with urethan. With stimulation of this area, a significant increase in acid output and mucosal blood flow occurred in 8 out of 16 animals. In these eight rats, the tip of the electrode had been placed mainly within the caudal portion of VMH. When the basal acid output was maintained at a relatively high level by pretreating the rats with 2-deoxy-D-glucose, electrical stimulation of the VMH significantly reduced the levels of these gastric parameters in 9 out of 12 animals. In the remaining three animals, the tip of the electrode had been placed in an area outside the VMH. These findings suggest that VMH is not a homogeneous neuron group, and both excitatory and inhibitory neurons probably play a role in regulating gastric functions.

Animals↗
PubMed1983

Effects of the sympathoadrenal system on vagally induced gastric acid secretion and mucosal blood flow in rats.

Effects of the sympathoadrenal system on vagally induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized, gastric fistula rats. Greater splanchnic nerve stimulation reduced significantly both the gastric acid secretion and MBF. Stimulation of the splanchnic postganglionic nerve reduced to a greater extent the acid secretion than the MBF, while stimulation of the adrenal branch reduced both the acid secretion and MBF. Infusion of epinephrine also reduced both the acid secretion and MBF, but the reduction of MBF was the more prominent. Phentolamine, but not propranolol and alprenolol, reduced the inhibitory effects on both gastric functions of the splanchnic postganglionic nerve stimulation and adrenal branch stimulation or epinephrine infusion. These results suggest that catecholamines released from the splanchnic postganglionic nerve terminals inhibit gastric acid secretion through alpha adrenergic receptors in the stomach, independent of MBF, and that circulating catecholamines released from the adrenal medulla inhibit both the acid secretion and MBF through alpha adrenergic receptors in the stomach. The inhibition by greater splanchnic nerve stimulation is probably the sum of the effects induced by catecholamines released from the splanchnic postganglionic nerve terminals and from the adrenal medulla.

Animals↗
PubMed1982

Possible roles of central cholinergic nicotinic mechanisms in regulation of gastric functions.

The effect of nicotine microinjected into various hypothalamic regions and ala cinerea on gastric acid output and mucosal blood flow was examined in rats anesthetized with urethane. After administration of nicotine, 3 nmol, a marked increase in gastric acid output was observed in rats in which the tip of the micropipette was applied to the caudal portion of the ventromedial hypothalamus (VMH) and ala cinerea. Microinjection of physiological saline into ala cinerea also enhanced gastric acid output. Nicotine was without effect when microinjected into other hypothalamic regions. The increase in gastric acid output induced by microinjection of nicotine into the caudal portion of VMH was completely blocked by the concomitant administration of hexamethonium, 50 nmol, but was not modified in reserpine-pretreated animals. Intraventricularly applied nicotine increased the gastric acid output; this increase was abolished following bilateral destruction of VMH. The increase in gastric acid output was always in parallel with the increase in mucosal blood flow. These results suggest that cholinergic nicotinic receptors in the VMH are concerned with central regulation of gastric functions.

Animals↗
PubMed1982

Neurotensin-induced release of endogenous noradrenaline from rat hypothalamic slices.

Effects of neurotensin on the release of endogenous noradrenaline (NA) from rat hypothalamic slices were investigated. NA was extracted by the aluminum adsorption method, and assayed electrochemically by high-performance liquid chromatography. Neurotensin (30-300 microM) enhanced the release of NA, in a dose dependent manner. Neurotensin 2 and 10 microM, doses without effect on the spontaneous release of NA, potentiated the potassium-induced release of this amine. Neurotensin 100 microM repetitively added to tbe medium at 40 min intervals induced a consistent and reproducible increase in the release of NA. This neurotensin-induced release of NA was completely abolished in calcium free medium containing EGTA 1 mM. The presence of tetrodotoxin 2 microM did not alter the effect of neurotensin 100 microM. These results of in vitro investigations suggest that neurotensin has a direct effect on NA nerve terminals in the hypothalamus and releases NA, in a Ca++-dependent manner.

Animals↗
PubMed1981

Inhibition of gastric functions by stimulation of rat locus coeruleus.

To investigate the possible role of central noradrenergic neurons in the regulation of gastric functions, electrical stimulation of the locus coeruleus [LC] and microinjection of noradrenaline [NA] into the ala cinerea (area of the dorsal motor nucleus of the vagi [NDV] and the nucleus tractus solitarius [NTS]) were given to urethane-anesthetized rats. Unilateral electrical stimulation of the LC decreased both the basal levels and the lateral hypothalamic area [LHA]-induced increases in gastric acid output and mucosal blood flow. Microinjection of NA 0.1 and 0.5 micrograms/animal into the ala cinerea also decreased the basal levels of these gastric parameters. From these results, combined with neuroanatomical data from the literature, it is concluded that central noradrenergic inhibitory mechanisms originating from the LC seem to be involved in the regulation of gastric functions, probably at the level of the brain-stem ala cinerea.

Animals↗
PubMed1981

Prostaglandins and the contractility of the guinea pig biliary system.

The effects of exogenously applied prostaglandins on the contractile responses of the gallbladder and sphincter of Oddi isolated from guinea pigs were examined in normal and indomethacin-treated preparations. Indomethacin reduced the tone and the contractile responses to transmural stimulation and to exogenously applied ACh of the gallbladder, while the tone and contractile responses of the sphincter of Oddi were little affected by indomethacin. Prostaglandins E1, E2 and F2 alpha potentiated the contractile responses of the gallbladder to transmural stimulation and ACh, and furthermore, treatment with indomethacin enhanced the potentiating effects of prostaglandins E1 and E2 but not the effect of PGF2 alpha. The reduced tone and contractility of the gallbladder were restored to the control level by addition of PGE1 and PGE2 but not by PGF2 alpha. These results suggest that endogenous PGE1 and PGE2 may play an important role in neurogenic control of contractility of the gallbladder, but not of the sphincter of Oddi.

Acetylcholine↗
PubMed1980

Central effect of nicotine on gastric acid secretion in rats.

The central effect of nicotine on gastric acid secretion was examined in rats anesthetized with urethane. Intraventricular administration of nicotine 5 and 20 microgram/animal induced a dose-related increase in acid output. This nicotine-induced increase was blocked by treatment with hexamethonium 50 microgram/animal given intraventricularly or atropine 100 microgram/kg given intravenously. Changes in acid output after intravenous administration of nicotine 100 microgram/kg were inconsistent; however, a significant increase was observed with 500 microgram/kg of this alkaloid given by the same route. This increase was also blocked by hexamethonium 50 microgram/animal given intraventricularly. The level of gastrin in the gastric juice, after the intraventricular administration of nicotine 20 microgram/animal, did not significantly differ from the control. These results suggest that nicotine administered intraventricularly stimulates nicotinic receptors in the brain, and that there is a subsequent excitation of cholinergic muscarinic receptors in the stomach after which the secretion of acid increases.

Animals↗
PubMed1980

Left unilateral agraphia and tactile anomia. Disturbances seen after occulusion of the anterior cerebral artery.

A 53-year-old right-handed Japanese man had a callosal disconnection syndrome associated with an occlusion of the left pericallosal artery. Computerized tomography scan confirmed a left medial lesion affecting the cingulate gyrus, the paracentral lobule, the precuneus of the left hemisphere, and most probably the corpus callosum. This anterior cerebral artery syndrome was characterized by right hemiparesis with predominant crural involvement, unilateral left-sided "disconnection" agraphia, and left unilateral "disconnection" tactile naming deficit. To our knowledge, this is the first case in the literature of the anterior cerebral artery syndrome in which unilateral leftsided apraxia was not associated with agraphia. The case is also the first in which Kanji-Kana dissociation of an aphasic nature has been reported as a feature of isolated left agraphia.

Agraphia↗
PubMed1980

Elevated homovanillic acid in cerebrospinal fluid of children with infantile spasms.

To determine the role of noradrenaline, dopamine, and serotonin in the brain of patients with infantile spasms, levels of respective major metabolites in cerebrospinal fluid were examined. Homovanillic acid levels were significantly increased in these patients, while 3-methoxy-4-hydroxyphenylethylene glycol and 5-hydroxyindoleacetic acid were not significantly altered, as compared with controls. In patients with febrile convulsion and status epilepticus who were examined during or within a few hours after convulsions the same phenomenon was evident. The increased level of dopamine metabolite was closely related to the occurrrence of convulsions and is considered to be a secondary phenomenon.

Adrenocorticotropic Hormone↗
PubMed1979

Effects of water-immersion stress on gastric secretion and mucosal blood flow in rats.

The correlation between acid secretion and mucosal blood flow in the rat stomach during stress loading was determined to provide clues to the etiology of the gastric ulceration which thus occurs. The gastric acid output was increased remarkably by water-immersion stress at 23 degrees C, and this increase lasted while the stress was given, yet the mucosal blood flow did not show a corresponding increase. In rats stressed for 3 hr, ulcerative changes were observed in the glandular portion of the stomach. The stress-induced increase in acid output correlated well with the severity of erosions. Pretreatment of animals with atropine 10 microgram/kg, given subcutaneously, or vagotomy, inhibited the increase in acid output and also inhibited the ulcer formation caused by the stress: however, the mucosal blood flow in these animals decreased significantly. These results suggest that when there is an elevation of gastric acid secretion with no parallel increase in mucosal blood flow, gastric ulceration may occur under conditions of stress.

Animals↗