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Biomedical subjects

Y Okuma

Publications and source records attributed to Y Okuma.

At least 91 records · Page 5Linked to original sources
PubMed1987

Sympatho-adrenomedullary system mediation of the bombesin-induced central inhibition of gastric acid secretion.

Possible mechanisms of the inhibitory effect of bombesin on gastric acid secretion were examined in rats anesthetized with urethane. Intracerebroventricular (i.c.v.) administration of bombesin (0.1-3 nmol) dose dependently inhibited the increase in gastric acid secretion induced by both intravenous (i.v.) administration of 2-deoxy-D-glucose 60 mg/kg and electrical stimulation of the vagus nerve (1 mA, 0.5 ms, 3 Hz), but not increase due to i.v. infusion of bethanechol (10 micrograms/kg per min). Such an inhibitory effect of bombesin on the gastric response was markedly reduced by bilateral cutting of the greater splanchnic nerves. The inhibitory effect of bombesin on gastric acid secretion induced by stimulation of the vagus nerve was not modified either by chemical sympathectomy with 6-hydroxydopamine or by bilateral adrenalectomy alone. However, this inhibitory effect of bombesin was abolished under conditions of combined chemical sympathectomy and adrenalectomy. These results suggest that bombesin (i.c.v.) probably excites the sympatho-adrenomedullary system and thus induces inhibition of gastric acid secretion. Furthermore, a dysfunction of the sympathetic or of the adrenomedullary system may well be functionally compensated for by the system with unaltered function.

Adrenal Medulla↗
PubMed1987

Enhancement of gastric acid output and mucosal blood flow by tripeptide thyrotropin releasing hormone microinjected into the dorsal motor nucleus of the vagus in rats.

Central effect of thyrotropin releasing hormone (TRH) on gastric acid output and mucosal blood flow (MBF) was examined in urethane anesthetized rats. TRH, microinjected into the dorsal vagal complex [the dorsal motor nucleus of the vagus (NDV), the nucleus tractus solitarius and area postrema] induced dose-dependent (0.5-50 pmole) increases in gastric acid output and MBF. In contrast, 5 pmole TRH microinjected into various hypothalamic regions had no effect on these gastric parameters. Administration of TRH intraventricularly (i.c.v.) also increased these gastric parameters; however, about a 10 times higher dose of TRH was required to obtain the same order of excitatory effects seen with microinjection to the dorsal vagal complex. Application of anti-TRH serum to the dorsal vagal complex inhibited the increases in gastric acid output and MBF induced by TRH (i.c.v.). The effect of TRH applied to the dorsal vagal complex and i.c.v. were not modified by a concomitant administration of atropine. These results suggests that NDV is probably the site of action of TRH in inducing gastric hyper-functions. The mode of action of TRH seems to be independent of cholinergic muscarinic mechanisms present in the NDV.

Animals↗
PubMed1987

Central site of inhibitory action of bombesin on gastric acid secretion in rats.

Sites of inhibitory action of bombesin on gastric acid secretion were examined in rats anesthetized with urethane. Intracerebroventricular administration of bombesin (3-1000 pmole) dose-dependently inhibited the increase in gastric acid secretion induced by electrical stimulation of the vagus nerve (1 mA, 0.5 msec, 3 Hz). On the other hand, intrathecal (direct lumbar puncture) administration of bombesin, even in the large dose of 1 nmole, had no effect on the vagally stimulated gastric acid secretion. Three pmoles of bombesin microinjected into the preoptic area, the anterior hypothalamus and the paraventricular nucleus inhibited the vagus stimulated gastric acid secretion. Microinjection of this peptide into the ventromedial nucleus, the dorsomedial nucleus and the lateral hypothalamic area were without effect. A large electrolytic lesion of the anterior hypothalamus, including the preoptic-anterior hypothalamic area and the paraventricular nucleus, abolished the inhibitory effect of intracerebroventricularly applied bombesin, but a lesion restricted to the preoptic-anterior hypothalamus or the paraventricular nucleus was without effect. We propose that the preoptic area, the anterior hypothalamus and the paraventricular nucleus are all involved in the inhibitory effect of bombesin on gastric acid secretion.

Animals↗
PubMed1987

Intracerebroventricularly administered nicotine inhibits vagally stimulated gastric acid output in rats by activating the central sympatho-adrenal outflow.

The effect of intracerebroventricularly (i.c.v.) administered nicotine was investigated in urethane-anesthetized rats. I.c.v., but not intravenously, administered nicotine (300 and 600 nmole/animal) inhibited the increase in gastric acid output induced by electrical stimulation of the vagus nerve. This antisecretory effect of nicotine was abolished by combined pretreatment with adrenalectomy and 6-hydroxydopamine (50 mg/kg, i.v., 3 days before). I.c.v.-administered nicotine also raised the blood levels of catecholamines. These observations suggest that i.c.v. administered nicotine leads to excitation of the central sympatho-adrenomedullary outflow and inhibits gastric acid output induced by stimulation of the vagus nerve.

Adrenalectomy↗
PubMed1986

Sympatho-adrenal system involved in the inhibitory effects of nicotine on the vagally stimulated gastric acid output and mucosal blood flow in rats.

The peripheral effects of nicotine on gastric functions were examined in anesthetized rats. The intravenous infusion of nicotine inhibited the increase in vagally stimulated gastric acid output. This inhibitory effect was abolished by phentolamine or by a combined treatment with bilateral adrenalectomy and reserpine. Nicotine had a dual effect on the gastric mucosal blood flow (MBF): inhibition followed by an increase. The inhibitory effect was abolished by phentolamine or by the combination with reserpine and adrenalectomy. Propranolol or adrenalectomy abolished the increase. These various effects of nicotine on the gastric acid output and MBF were not attenuated by bilateral splanchnicectomy. These results suggest that nicotine acts directly on both the adrenal medulla and postganglionic sympathetic neurons in the gastric wall, namely by acting on alpha-adrenoceptors, thus decreasing acid output and MBF, and by activating beta-adrenoceptors thus slightly increasing MBF.

Adrenal Glands↗
PubMed1986

Nicotine applied into the dorsal motor nucleus of the vagus inhibits enhanced gastric acid output and mucosal blood flow in rats.

The effects of nicotine microinjected into several brain regions on the centrally elevated gastric acid output and mucosal blood flow (MBF) were examined in anesthetized rats. Intravenous administration of 2-deoxy-D-glucose (2-DG) induced increases in gastric acid output and MBF. These increases were inhibited dose dependently by nicotine microinjected into the dorsal motor nucleus of the vagus (NDV) but not into various hypothalamic regions. This effect of nicotine was abolished with concomitantly administered hexamethonium and was not observed in reserpine-pretreated animals. Electrical stimulation of the lateral hypothalamic area (LHA) induced an increase in gastric acid output. This increase was completely inhibited when nicotine was microinjected into the NDV 5 min before stimulation. This inhibitory effect of nicotine was abolished by concomitantly administered hexamethonium and by intraventricular pretreatment with phentolamine, but not with propranolol. These results suggest that activation of nicotinic receptors within the NDV releases noradrenaline and that there is a resultant inhibition of gastric acid output and MBF.

Animals↗
PubMed1986

KCl-induced calcium-independent release of endogenous dopamine from rat brain slices.

Effects of the absence of calcium on the KCl- and electrical stimulation-induced releases of endogenous dopamine (DA) from rat brain slices were studied and the findings were compared with the effects on the release of endogenous noradrenaline (NA). DA and NA were extracted by the aluminum-adsorption method and assayed electrochemically by high-performance liquid chromatography. KCl, 15 mM, induced a significant increase in the release of DA from both the striatum and the hypothalamus, even in the Ca2+-free medium containing 1 mM EGTA. In the normal medium, the KCl-induced release of DA was concentration-dependent (15, 30 and 50 mM), while that in the Ca2+-free medium showed a plateau at 30 mM of KCl. The release of DA induced by electrical stimulation (10 cycles/s, 2 ms, 30 mA, for 5 min) was abolished in the Ca2+-free medium as was NA induced by both KCl and electrical stimulation. Nomifensine, 10 microM, a DA transport inhibitor, abolished the 15 mM KCl-induced release of DA in the Ca2+-free medium. On the other hand, the release of DA induced by electrical stimulation was considerably enhanced by nomifensine. Therefore, the mode of DA release induced by KCl sometimes differed from that induced by electrical stimulation. The present results also suggest that DA released by KCl in the Ca2+-free medium originates from cytoplasmic DA storage sites, through a carrier-mediated process.

Animals↗
PubMed1986

Central cholinergic descending pathway to the dorsal motor nucleus of the vagus in regulation of gastric functions.

A possible role of the cholinergic mechanism within the dorsal motor nucleus of the vagus (NDV) in the regulation of gastric functions was examined in urethane anesthetized rats. Pretreatment with atropine (1-5 nmole), intracerebroventricularly inhibited the increase in both gastric acid output and mucosal blood flow (MBF), as induced by electrical stimulation of the lateral hypothalamic area (LHA). Bethanechol, microinjected into the dorsal vagal complex (the NDV, the nucleus tractus solitarius and area postrema) induced dose-dependent (5-30 nmole) increases in gastric acid output and MBF, while nicotine was without effect. Pretreatment with atropine 3 nmole microinjected into the dorsal vagal complex completely blocked the increases induced by electrical stimulation of the LHA. Furthermore, the increases in these gastric parameters induced by the administration of 2-deoxy-D-glucose (2-DG) were also significantly inhibited by atropine microinjected into the dorsal vagal complex. These results suggest that neurotransmission of the central descending pathway to the NDV in excitatory regulation of gastric functions is probably mediated through cholinergic muscarinic receptors.

Animals↗
PubMed1985

Endometriosis associated with ascites.

Pelvic endometriosis associated with massive ascites is an unusual occurrence. Only 12 cases have been reported since 1954 when Brews first described this entity. The authors present two cases recently encountered at Saga Medical School Hospital. Clinical courses and operative findings are described and other cases from the literature are reviewed. The possible etiologic mechanisms of the ascites are explored and the possibility of conservative surgery and hormonal therapy with danazol is discussed.

Adult↗
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↗
PubMed1984

[Clinical experience with cefoxitin in the surgical field].

Cefoxitin (CFX) was administered to 49 hospitalized patients in the surgical field, and the following results were obtained: Clinical results of the 12 patients with surgical infections were excellent in 1 patient, good in 10, and poor in 1, with the efficacy rate of 91.7%. CFX was also administered to 37 patients for prophylaxis of postoperative infections, and the clinical efficacy rate was 91.7%. No side effects were seen besides mild eruption in 1 patient. The above results indicate that CFX is exceeding useful in surgical field.

Adolescent↗
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↗
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

Comparison of synaptosomal and glial uptake of pipecolic acid and GABA in rat brain.

The active uptake of [3H]pipecolic acid increased with incubation time and its uptake at 3 min was half of that at 20 min. On the other hand, a ratio (pellet/medium) of [3H]pipecolic acid uptake into glial cell-enriched fractions, was much less (0.4 - 0.6) than that of [14C]GABA (25.8 - 74.1). GABA, 10(-4) M, and pipecolic acid, 10(-4) M, produced a significant inhibitor of [3H]pipecolic acid uptake into P2 fractions. Pipecolic acid, 10(-4) M, significantly reduced the synaptosomal and glial uptake of [14C]GABA. GABA, 10(-4) M, affected neither spontaneous nor high K+-induced release of [3H]pipecolic acid from brain slices. It is suggested that pipecolic acid is involved in either synaptic transmission or in its modulation at GABA synapses in the central nervous system.

Animals↗