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Biomedical subjects

Y Hiyoshi

Publications and source records attributed to Y Hiyoshi.

At least 19 recordsLinked to original sources
PubMed2001

Expression profiling of sulfotransferases in human cell lines derived from extra-hepatic tissues.

To explore the physiological roles of sulfotransferases (SULTs) in extra-hepatic tissues, we examined the expression of eight SULT genes by reverse transcription (RT)-PCR in human cell lines that were established from various tissues. Expression levels of SULTs were low in neural cell lines such as NB-1 and GI-1, and high in epithelial cell lines, such as Caco-2 and BeWo. SULT1C2 expression was abundant in all cell types, whereas that of SULT1E1, SULTIBI or SULT2B1 was restricted to a specific cell type. SULT1C1, which can catalyze the sulfation of N-hydroxy-2-acetylaminofluorene, was expressed in Caco-2, BeWo and KB562. Induction of differentiation did not generally affect SULT expression, although that of SULT1C2 was reduced after differentiation of the neuroblastoma cell line, NB-1, was induced. The profile of SULT expression in the culture cells obtained here gives clues to understanding the physiological roles of SULT enzymes in extra-hepatic tissues or organs.

Caco-2 Cells↗
PubMed1998

Supernormal conduction in a case of Mobitz type II atrioventricular block.

A 52-year-old woman exhibited Mobitz type II atrioventricular block with right bundle branch block and 1:1 atrioventricular conduction at or slower than 80 beats/min. Electrophysiologic study revealed transient HV interval block followed by recovery from the block at shorter coupling intervals without prolongation of the H1H2 and H2V2 intervals, suggesting true supernormal conduction. Isoproterenol enhanced the supernormal conduction, with shortening of blocked intervals and recovery of atrioventricular conduction, while atropine caused their less marked enhancement. Linking (ie, retrograde concealment of the impulse to the distal His bundle region through the blocked right bundle branch) is considered a possible mechanism of supernormal conduction in this case.

Atrioventricular Node↗
PubMed1998

Non-dipolarity of heart potentials estimated by magnetocardiography in normal subjects.

We studied non-dipolarity characteristics during ventricular excitation in normal adults and children by magnetocardiography (MCG) by recording magnetic field on the thorax. The source and currents of the electrical dipole from the onset up to 60 ms of ventricular excitation were analyzed in 16 adults and 5 children. A single equivalent current dipole (ECD) was estimated by Sarvas' formula for the sphere model at 1 ms intervals. The non-dipole value (NDV) was calculated from the magnetic field strength at each recording point and theoretically estimated by ECD, representing an index for the non-dipolarity. At 32-34 ms from the beginning of QRS, the mean NDV was a minimum in all subjects suggesting at least a non-dipole component during this period. High NDV (over 5%) were present in most subjects in both the early and late phase compared to this period. Thirteen of 16 adults had a high NDV in the early phase (9.3 +/- 3.0%, mean +/- SD) and all 16 subjects had a high NDV in the late phase (21.5 +/- 10.5%). All 5 children had high NDV in both the early (10.5 +/- 5.4%) and late phases (16.8 +/- 7.9%). A single ECD estimation by MCG showed a relatively low non dipolar component and MCG could be applied to the clinical evaluation of cardiac excitation in both normal and pathological conditions.

Adult↗
PubMed1995

Effects of imidazoline antagonists of alpha 2-adrenoceptors on endogenous adrenaline-induced inhibition of insulin release.

We studied the effects of adrenoceptor antagonists and imidazoline derivatives on endogenous adrenaline-induced inhibition of insulin release in anesthetized rats. The intracerebroventricular injection of neostigmine increased plasma levels of catecholamines and glucose but not insulin. Pretreatment with an i.p. injection with phentolamine caused a dose-dependent increase in insulin secretion. When atropine was coadministered with phentolamine, the phentolamine-induced increase in insulin secretion was inhibited. Neither phentolamine nor atropine affected plasma levels of catecholamine. Yohimbine and idazoxan, which are alpha 2-adrenoceptor antagonists, and tolazoline, a non-selective alpha-adrenoceptor antagonist, also reversed adrenaline-induced inhibition of insulin secretion. Phenoxybenzamine, prazosin, propranolol, and antazoline, an imidazoline without alpha 2-adrenoceptor activity, did not affect insulin levels. When agents were preinjected i.p. in rats that were given saline into the third cerebral ventricle, phentolamine and antazoline, but not yohimbine and idazoxan, increased plasma levels of insulin. The results suggest that the inhibition of insulin release induced by adrenaline was reversed by antagonism of alpha 2-adrenoceptors. Phentolamine and antazoline, both of which are imidazoline derivatives, induced insulin secretion independently of the adrenoceptors only under the resting conditions.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1994

CNS regulation of blood lactate concentration in anesthetized rats.

This study evaluated the effect of stimulating the central nervous system (CNS) with neostigmine, an inhibitor of acetylcholinesterase, on the blood lactate concentration in fed rats and in rats fasted for 48 hours. After the rat was anesthetized with pentobarbital, neostigmine was stereotaxically injected into the third cerebral ventricle. In fed rats, the central injection of neostigmine significantly increased the blood lactate level, while concomitantly increasing plasma glucagon, epinephrine and norepinephrine concentrations. Constant infusion of somatostatin throughout the experiments, to inhibit glucagon secretion from the pancreas, did not affect alterations in blood lactate by central injection of neostigmine. In adreno-medullated rats, CNS-stimulation by neostigmine still increased plasma norepinephrine significantly, however, the alteration in blood lactate was only one-third of that in intact rats. Intraperitoneal propranolol, but not phentolamine, prevented the rise in lactate. Neostigmine increased lactate in fasted rats as well as in fed rats. We conclude that in anesthetized rats, stimulation of the CNS by neostigmine increases blood lactate mainly through circulating epinephrine and partially through circulating norepinephrine or direct sympathetic nervous stimulation; glucagon does not appear to be involved in the increase in blood lactate.

Anesthesia, General↗
PubMed1993

Factors for transient entrainment of ventricular tachycardias by rapid atrial pacing.

Thirteen patients with sustained ventricular tachycardia (VT) were studied to elucidate predisposing factors for the development of constant and progressive fusion by rapid atrial pacing. All patients demonstrated transient entrainment by rapid ventricular pacing during VT. Constant and progressive fusion were observed in 7 patients (positive group) during rapid atrial pacing, but not in 6 (negative group). In the positive group, VT was induced by atrial pacing in 2 patients. The demonstration of constant and progressive fusion by atrial pacing was not dependent on QRS morphology or ventriculoatrial conduction during VT. VT cycle length in the positive group (363 +/- 59 ms) was longer than in the negative group (297 +/- 31 ms; p = 0.033). The maximal atrial pacing rate producing 1:1 atrioventricular (AV) conduction in the positive group was 171 +/- 18 beats/min compared with 125 +/- 22 beats/min in the negative group (p = 0.002). There were distinct differences between the positive and negative groups in the ratio of VT cycle length to minimal atrial cycle length causing 1:1 AV conduction (1.02 +/- 0.12 vs 0.61 +/- 0.12; p = 0.0001). It is concluded that AV conduction, VT cycle length and especially their ratio are important factors for the development of transient entrainment by rapid atrial pacing during VT. Therefore, atrial pacing can be used as an easy and useful method to examine transient entrainment during VT.

Adult↗
PubMed1993

Intrahypothalamic, but not hippocampal, administration of muscimol suppresses hyperglycemia induced by hippocampal neostigmine in anesthetized rats.

We investigated the effects of intrahypothalamic or hippocampal injection of GABA receptor agonists on hyperglycemia induced by hippocampal neostigmine. Prior to the injection of neostigmine (50 nmol) into the hippocampus (HPC), muscimol (0.01-1 nmol) or baclofen (1 nmol) was injected into the bilateral ventromedial hypothalamus (VMH). Muscimol suppressed the hyperglycemia in a dose-dependent manner, but baclofen affected it only minimally. In contrast, neither hippocampal muscimol (1 or 2.5 nmol) nor baclofen (1 nmol) suppressed the hippocampal neostigmine-dependent hyperglycemia. Intrahypothalamic muscimol (1 nmol) also decreased the changes in hepatic venous plasma glucagon and epinephrine significantly. These results indicate that intrahypothalamic muscimol suppresses hyperglycemia caused by cholinergic neurons originating from the HPC, indicating existence of the location specificity.

Analysis of Variance↗
PubMed1993

Histamine-induced, central nervous system-mediated hyperglycemia is suppressed by atropine in the brain.

We investigated the relationship between histamine and muscarinic cholinergic neurons in central nervous system (CNS)-mediated glucose regulation in anesthetized fed rats. The injection of pyrilamine (5 x 10(-7) mol) into the third cerebral ventricle suppressed the hyperglycemia induced by intraventricular injection of histamine (5 x 10(-7) mol). Ranitidine (5 x 10(-7) mol), however, did not suppress this hyperglycemia. The injection of atropine (5 x 10(-9)-5 x 10(-7) mol) into the third cerebral ventricle suppressed the histamine-induced hyperglycemia in a dose-dependent manner. These findings suggest that histamine induction of CNS-mediated hyperglycemia involves neuronal transmission not only via H1 receptors but also, at least in part, by muscarinic cholinergic neurons.

Animals↗
PubMed1993

Activation of GABAA receptor in the brain suppresses neostigmine or histamine-induced central nervous system-mediated hyperglycemia.

We investigated the effect of GABA receptor agonists on the central nervous system (CNS)-mediated hyperglycemia induced by neostigmine or histamine in anesthetized fed rats. The injection of muscimol, GABAA receptor agonist (1, 2.5 nmol) into the third cerebral ventricle suppressed the hyperglycemia induced by intraventricular injection of neostigmine (1 x 10(-8) mol) or histamine (5 x 10(-7) mol). Baclofen, GABAB receptor agonist (1, 2.5 nmol), however, did not suppress these hyperglycemia. Neither muscimol nor baclofen (2.5 nmol) affected plasma glucose levels. These findings suggest that activation of GABAA receptor in the CNS suppresses the hyperglycemia induced by the stimulation of cholinoceptive neuron or histaminergic neuron, but activation of GABAB receptor does not affect them.

Animals↗
PubMed1992

Role of brain histamine H1- and H2-receptors in neostigmine-induced hyperglycemia in rats.

We previously reported that when neostigmine, an inhibitor of acetylcholine esterase, was injected into the third cerebral ventricle, the concentration of hepatic venous plasma glucose was increased via central muscarinic receptors in anesthetized rats. To determine whether brain histamine receptors are involved in cholinergic system transmission with regard to central nervous system (CNS)-mediated glucoregulation, we examined the effects of the H1 receptor antagonist pyrilamine and the H2 receptor antagonist ranitidine on neostigmine-induced hyperglycemia in anesthetized rats. The injection of pyrilamine (5 x 10(-9)-5 x 10(-7) mol) into the third cerebral ventricle suppressed hyperglycemia induced by intraventricular injection of neostigmine (1 x 10(-9) mol) in a dose-dependent manner. Injection of ranitidine (5 x 10(-9)-5 x 10(-7) mol) into the third cerebral ventricle did not suppress the hyperglycemia induced by neostigmine, but enhanced it in a dose-dependent manner. These findings suggest that neostigmine-induced CNS-mediated hyperglycemia is transmitted by not only brain cholinergic muscarinic receptors but also in part by histamine H1 receptors.

Animals↗
PubMed1992

Double ventricular responses to a single atrial depolarization in a patient with dual AV nodal pathways.

Electrophysiological study was performed in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). Double ventricular responses through dual AV nodal pathways were observed by atrial extrastimulus technique followed by initiation of AVNRT. The difference in conduction time between the slow and fast AV nodal pathways was longer than 320 msec. A ventricular extrastimulus delivered during sinus rhythm, which was not followed by ventriculoatrial conduction, also induced AVNRT. These findings indicated the presence of an antegrade critical delay and retrograde block in the slow AV nodal pathway, criteria necessary for the occurrence of a double ventricular response.

Adult↗
PubMed1991

Association of humps on monophasic action potentials and ST-T alternans in a patient with Romano-Ward syndrome.

A case of Romano-Ward syndrome had episodes of torsade de pointes preceded by ST-T alternans. ST-T alternans was induced by isoproterenol and abolished by verapamil, lidocaine, mexiletine and MgSO4. A monophasic action potential (MAP) showed humps in MAPs at the right ventricular outflow tract but not at the right ventricular apex in alternate beats. Differences in the MAP duration were noted between the two areas and were associated with ST-T alternans. Atrial pacing abolished both humps and ST-T alternans. These results suggest that humps are a possible reflection of early afterdepolarizations and their appearance is limited to localized regions of the ventricles, which produces regional disparity of repolarization and ST-T alternans.

Action Potentials↗
PubMed1990

Cellular roles in physiological root resorption of deciduous teeth in the cat.

This study has attempted to assess the importance of mesenchymal cells, fibroblasts, cementoblasts, and mononuclear phagocytes (i.e., macrophages) in physiological root resorption of feline deciduous teeth. Deciduous incisors of three- to six-month-old kittens undergoing root resorption were investigated by means of electron microscopy. In an early phase of root resorption, the resorption organ consisted of many fibroblasts and relatively few macrophages and odontoclasts, the last with a wide, clear zone and narrow, immature, ruffled border. In the active phase of root resorption, the resorption organ contained many odontoclasts with a well-developed ruffled border and a reduced clear zone, cementoblasts, fibroblasts, macrophages, neutrophils, and many blood vessels. Cementoblasts were present usually on the resorbing dentin surface adjacent to odontoclasts and, in many cases, these cells communicated with each other via gap junctions. Cementoblasts frequently extended broad cell processes with secretion granules and with phagosomes containing collagen fibrils into the dentinal tubules exposed to resorption lacunae. Some macrophages exhibiting a clear zone-like structure also appeared on resorbing dentin surfaces. In the resting phase of root resorption, the dentin surface was covered mostly with cementoblasts resembling bone lining cells. There was an occasional macrophage, but no odontoclasts were observed during this phase. During removal of the periodontal ligament concomitant with root resorption, many fibroblasts phagocytosed mature collagen fibrils, as well as amorphous fluffy material. These results suggest that these mesenchymal cells, as well as odontoclasts, are essential for the cellular removal of dental hard and soft tissues during shedding of feline deciduous teeth.

Animals↗
PubMed1990

[Effects of oral flecainide treatment of refractory tachyarrhythmias].

Oral flecainide treatment was given to five patients who were refractory to conventional antiarrhythmic agents. The five patients included one with atrioventricular reentrant tachycardia (AVRT), one with non-sustained ventricular tachycardia (nsVT) and three with sustained VT (sVT). Flecainide produced favorable responses in patients of AVRT, nsVT and sVT with arrhythmogenic right ventricular dysplasia (ARVD). In the case of AVRT, flecainide exhibited a preventive effect on tachycardia induced by programmed electrical stimulation (PES). In the case of nsVT, flecainide markedly reduced the number of VPC and abolished the VT on the Holter ECG. In the case of sVT with ARVD, sVT was not induced by PES after the flecainide. Long-term treatment with flecainide on these three cases produced complete prevention of tachycardias. As an adverse effect of flecainide, an aggravation of congestive heart failure was recognized in one case with cardiac sarcoidosis. PQ interval and QRS interval in all the cases were prolonged after flecainide. The results indicate that flecainide is a useful antiarrhythmic agent for tachyarrhythmias refractory to treatment with conventional drugs.

Administration, Oral↗