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Biomedical subjects

T Kubo

Publications and source records attributed to T Kubo.

At least 793 records · Page 44Linked to original sources
PubMed1988

Involvement of spinal alpha adrenoceptors in mediation of the hypotensive action of guanabenz in rats.

The effects of intrathecal, intracisternal and intravenous injections of yohimbine (10 micrograms) on hypotensive and bradycardic responses to the alpha agonist guanabenz (10 micrograms/kg, i.v.) were studied in anesthetized rats. The depressor response to guanabenz was inhibited by intrathecal pretreatment with yohimbine, while this pretreatment did not affect the bradycardic response to guanabenz. Intracisternal pretreatment with yohimbine inhibited both cardiovascular responses to guanabenz, whereas intravenous pretreatment with yohimbine affected neither. Guanabenz (1 microgram) decreased blood pressure when injected intrathecally but did not affect it when injected intravenously. These results suggest that in rats spinal alpha adrenoceptors are involved in mediation of the hypotensive action of the alpha agonist guanabenz injected systemically.

Animals↗
PubMed1988

Immunohistochemical studies of complement receptor (CR1) in cases with normal sinus mucosa and chronic sinusitis.

The complement receptor (CR1) in the maxillary sinus mucosa of normal patients and in cases of chronic sinusitis was studied with the peroxidase-antiperoxidase, avidin-biotin peroxidase and immunofluorescent methods. CR1 was localized on the ciliary surface and in the cytoplasm of the covering epithelium in both normal controls and the cases of chronic sinusitis. CR1 tended to be denser in the mucosa of chronic sinusitis than in normal mucosa. CR1-binding capacity was also studied with the immunofluorescent method, using C3b-conjugated zymosan. Although CR1 did not bind to C3b in vivo, it was found to bind to C3b in the normal maxillary mucosa when it was treated with C3b-conjugated zymosan. CR1-binding capacity could not be detected in the mucosa from cases with chronic sinusitis, indicating that CR1 was already bound to activated C3b in these cases.

Chronic Disease↗
PubMed1988

GABA transaminase inhibitors enhance the release of endogenous GABA but decrease the release of beta-alanine evoked by electrical stimulation of slices of the rat medulla oblongata.

Slices of the rat medulla oblongata were superfused and electrically stimulated. The amount of endogenous GABA, beta-alanine and glutamate release from the slices was determined by high performance liquid chromatography with fluorometric detection. Inhibitors of GABA-transaminase (GABA-T), aminooxyacetic acid (10(-5) M), gamma-acetylenic GABA (10(-4) and 10(-3) M) and gabaculine (10(-5) M), enhanced the stimulus-evoked release of GABA and reduced that of beta-alanine, while no change was observed in the release of glutamate. These changes in amino acid release from the slices were accompanied by an increase in the content of GABA and a decrease in that of beta-alanine. The stimulus-evoked release of these amino acids was abolished by Ca2+-deprivation, in either the presence or absence of GABA-T inhibitors. These results suggest a modulatory role of GABA-T for synaptically releasable GABA and involvement of this enzyme in the synthesis of releasable beta-alanine.

4-Aminobutyrate Transaminase↗
PubMed1988

Portacaval anastomosis attenuates the impairing effect of cyproheptadine on avoidance learning in rats--an involvement of the serotonergic system.

Portacaval-anastomized (PCA) rats were used to demonstrate the involvement of the serotonergic system in long-term memory formation. Significant increases in the concentration of 5-hydroxyindoleacetic acid, a metabolite of 5-hydroxytryptamine (5-HT), in all regions examined and the turnover rate of this indoleamine transmitter in the hippocampus, hypothalamus, midbrain and medulla oblongata were observed in PCA rats in comparison with sham-operated controls. Cyproheptadine, a 5-HT receptor blocking agent, impaired the retention of two-way avoidance learning reinforced by light stimuli when the drug was intraperitoneally injected immediately after the completion of training. PCA treatment attenuated the impairing effect of cyproheptadine. When cyproheptadine was injected 2 h after the completion of training, the correct response in the retention test period was not decreased. The present results suggest that memory formation is a time-requiring process and is mediated by the central serotonergic mechanism.

Animals↗
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

Determination of Abscisic Acid in Pinus densiflora by Selected Ion Monitoring.

Abscisic acid (ABA) in the stem of akamatsu (Pinus densiflora) was identified and quantified by gas chromatography-mass spectrometry-selected ion monitoring using hexadeuterated ABA as an internal standard. tert-Butyldimethylsilyl ester was used as a derivative of ABA. This derivative had high sensitivity and selectivity for ABA determination. ABA concentrations in cambial region scrapings were independent of the cessation of cambial activity.

Journal Article↗
PubMed1988

Transmitter-like release of endogenous 3,4-dihydroxyphenylalanine from rat striatal slices.

Biphasic electrical field stimulation (0.5-5 Hz, 2 ms, 25 V, 3 min) and high K+ (10-30 mM, 5 min) released endogenous 3,4-dihydroxyphenylalanine (DOPA) from superfused rat striatal slices. Characteristics of the DOPA release were compared with those of 3,4-dihydroxyphenylethylamine (dopamine, DA). Electrical stimulation at 2 Hz evoked DOPA and DA over similar time courses. alpha-Methyl-p-tyrosine (0.2 mM) markedly reduced release of DOPA but not of DA. Maximal release (0.3 pmol) of DOPA was obtained at 2 Hz and at 15 mM K+. The impulse-evoked release of DOPA and DA was completely tetrodotoxin (0.3 microM) sensitive and Ca2+ dependent and the 15 mM K+-evoked release was also Ca2+ dependent. On L-[3,5-3H]tyrosine (1 microM) superfusion, high K+ (15 and 60 mM) released DOPA and DA together with concentration-dependent decreases in tyrosine 3-monooxygenase (EC 1.14.16.2) activity as indicated by [3H]H2O formation, followed by concentration-dependent increases after DOPA and DA release ended. These findings suggest that striatal DOPA is released by a Ca2+-dependent excitation-secretion coupling process similar to that involved in transmitter release.

Animals↗
PubMed1988

Pica as an index of motion sickness in rats.

Rats eat kaolin after treatment with poisons or rotation. Thus, eating of nonnutritive substances such as kaolin, so-called pica, is an illness-response behavior of rats analogous to vomiting in humans. For use of rotation-induced pica as a behavioral index of motion sickness in rats we examined what kind of rotation was effective for inducing pica in rats and whether the vestibular apparatus was necessary for its induction. Rats ate much kaolin after double rotation with continuously changing centrifugal and angular accelerations, but little after single rotation with no accelerative changes. However, even double rotation failed to induce pica in bilaterally labyrinthectomized rats. Thus, rotation-induced pica in rats was induced in the same way as motion sickness in humans, suggesting that it resulted from motion sickness in rats. We conclude that pica can be used as a behavioral index of motion sickness in rats.

Animals↗
PubMed1988

Effects of anti-motion sickness drugs on motion sickness in rats.

Pica, the eating of nonnutritive substances such as kaolin, can be induced by rotation in rats. We used this rotation-induced pica as a behavioral index of motion sickness in rats and examined whether diphenhydramine, methamphetamine and scopolamine, which are anti-motion sickness drugs for humans, are effective for reducing motion sickness in rats. Intraperitoneal injection of diphenhydramine or methamphetamine suppressed the rotation-induced kaolin intake of rats. Intraperitoneal injection of scopolamine had no effect on the rotation-induced kaolin intake, but its transdermal administration reduced this kaolin intake. These findings show that human anti-motion sickness drugs also prevent motion sickness in rats. Since the pharmacological mechanisms for preventing motion sickness in rats and humans are similar, we conclude that rats are a suitable animal model for use in studies on putative anti-motion sickness drugs.

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↗
PubMed1988

Effects of blood pressure change upon brain-stem pO2 in rabbits with surgically removed baroreceptor nerve. Possible mechanisms for vertigo due to autonomic nerve dysfunction.

The effect of denervation of carotid sinus nerve (CSD) on the brain-stem tissue pO2 tension was studied in the awake rabbit. Tissue pO2 around the vestibular nuclei was measured in two groups of rabbits, normal and CSD, under two experimental conditions, viz. blood pressure (BP) modulation and tilt stimulation. BP was either depressed by hemorrhage (up to 50 mmHg) or elevated by intravenous injection of phenylephrine (up to 160 mmHg). In the normal rabbit, tissue pO2 showed minimum change during BP modulation (ranging between 70 and 160 mmHg. In contrast, CSD surgery resulted in the failure to maintain pO2 at a constant level when BP was elevated. However, tissue pO2 did not change when BP decreased. Head-up tilt stimulation (up to 40 degrees) also induced a transient decrease in BP and pO2 in the CSD rabbit; however, these were maintained at a constant level in the normal rabbit. These conditions were assumed to be due to the decrease in autoregulation of cerebral blood flow (CBF), which resulted in CSD. In these experiments, tissue pO2 recovered first, even when BP still remained low. Therefore, it can be proposed that the carotid baroreceptor reflex works for CBF autoregulation of brain stem primarily during an early phase of BP change. Therefore a disturbed carotid sinus reflex, as shown in the present experiment, may be a possible explanation for the mechanism of stress-related vertigo and/or orthostatic vertigo.

Animals↗
PubMed1988

Clinical observations in the acute phase of cerebellar hemorrhage and infarction.

Three cases of cerebellar hemorrhage and 5 of cerebellar infarction, diagnosed by brain CT, were examined from the early phase of the onset. All of our cases were mild to moderate in severity and were cured satisfactorily within 3 to 8 weeks of medical treatment. Dizziness and nausea were the commonest symptoms and cerebellar and other CNS signs could be detected only for a short period in some of the cases. Although neuro-otological examinations, especially gaze nystagmus, eye tracking and positional nystagmus tests, were useful for diagnosing the central vestibular lesion, no definite indication could be drawn in order to differentiate between cerebellar hemorrhage and infarction. Therefore, it is considered difficult in such mild cerebellar strokes to establish correct diagnosis by physical examinations alone. It was concluded that if central vestibular disorder is suspected, prompt brain CT examination is necessary in order to diagnose mild cases of cerebellar vascular diseases.

Cerebellar Diseases↗