Biomedical subjects

H Satoh

Publications and source records attributed to H Satoh.

At least 451 records · Page 25Linked to original sources

PubMed1995

Consistent relationship between selenium and apolipoprotein A-II concentrations in the sera of fasting middle-aged male abstainers and regular consumers of alcohol.

Several studies have suggested that selenium serum levels may be associated with serum lipids and apolipoproteins. In the present study, 99 clerical workers aged 40-49 yr were selected based on their drinking and smoking habits. The serum concentration of selenium was not affected by these lifestyle factors. The regular drinkers had raised serum high-density lipoprotein cholesterol, apo A-I, and apo A-II concentrations. Correlation analysis showed that serum selenium was positively and consistently associated with apo A-II regardless of alcohol consumption. Factor analysis revealed that serum selenium had no association with factors that represented each lipoprotein fraction (LDL, HDL, and VLDL). The present study indicates that serum selenium is positively correlated only with apo A-II levels.

Adult↗

PubMed1995

Inhibition of gamma-glutamyltranspeptidase decreases renal deposition of mercury after mercury vapor exposure.

The alteration of renal deposition of mercury (Hg) after mercury vapor (Hg0) exposure was studied in mice pretreated with acivicin, a potent and irreversible inhibitor of gamma-glutamyltranspeptidase (GGT). Pretreatment with acivicin decreased renal Hg concentration by about 60% and significantly increased Hg concentration in the urine compared with the non-treated group. The results suggest that renal deposition of Hg after Hg0 exposure depends on renal GGT, which plays an important role in the uptake of GSH or GSH conjugates filtered through the glomeruli. It seems that the mechanism of renal Hg deposition after Hg0 exposure is similar to that after exposure to ionic Hg: a GGT-mediated incorporation of an Hg-GSH complex into renal tubular cells. The acivicin pretreatment after Hg0 exposure did not affect Hg concentrations in the liver and erythrocytes.

Administration, Inhalation↗

PubMed1995

Invasive aspergilloma of the frontal base causing internal carotid artery occlusion.

BACKGROUND: Aspergilloma of the nasal cavity or paranasal sinuses rarely extends through the skull base into the intracranial space. PATIENT: The patient was a 79-year-old man in a nonimmunosuppressive state who had an invasive aspergilloma of the base of the frontal lobe. CLINICAL COURSE: The patient, whose initial symptom was a visual disturbance, eventually developed an occlusion of the right internal carotid artery and died. The diagnosis was established by a transsphenoidal biopsy. CONCLUSIONS: A rare case of invasive aspergilloma of the frontal base is described with emphasis on the findings of low-intensity mass on the T2-weighted magnetic resonance imaging (MRI). The prognosis in this disease is very poor. Early diagnosis and surgical treatment, combined with postoperative antifungal drug therapy, would have improved the outcome.

Aged↗

PubMed1995

Effects of prolonged selenium deficiency on open field behavior and Morris water maze performance in mice.

Neurobehavioral effects of prolonged Se deficiency were evaluated using ICR mice. Dams were fed Se-deficient or Se-adequate diet starting at 4 weeks before conception through the suckling period. After weaning, offspring of both groups were given the same diet as their dams were given. The behavior of these offspring was evaluated with open field apparatus (OPF) and Morris water maze. In OPF, Se-deficient females exhibited less locomotor activity, more defecation, and less entry to the center square areas than did the control females. No such difference was found in males. In the Morris maze, Se-deficient females showed slight but significant impairment during the initial phase of the trials. The behavioral changes in OPF and the maze might have been due to an altered reactivity to a novel environment, although this possibility needs further confirmation. The obtained data showed that the altered behavior was unlikely to be due to the changes in thyroid hormones. Mechanism of these behavioral effects is discussed in relation to possible neurochemical changes induced by Se deficiency.

Animals↗

PubMed1995

Modulation of L-type Ca2+ current by isoprenaline, carbachol and phorbol ester in cultured rat aortic vascular smooth muscle (A7r5) cells.

1. Effects of isoprenaline (ISO), carbachol and phorbol ester (a stimulator of protein kinase C) on L-type Ca2+ channels in single cultured rat aortic vascular smooth muscle (A7r5) cells were examined using whole-cell voltage clamp (at room temperature 22 degrees C). 2. With 20 mmol/l Ca2+ in the bath solution and 10 mmol/l EGTA in the pipette solution, a slow ICa (L-type) current was observed in the A7r5 cell line, which was blocked by nifedipine (2 mumol/l). 3. ISO (5 mumol/l) inhibited ICa by 18.3 +/- 2.2% (P < 0.001), and carbachol (1 mumol/l) also decreased ICa by 15.0 +/- 3.2% (P < 0.01). 8-Br-cAMP (1 mmol/l) and 8-Br-cGMP (1 mmol/l) both inhibited ICa by 30.1 +/- 2.8% (P < 0.001) and 18.8 +/- 3.8% (P < 0.01), respectively. 4. Phorbol ester, 4-beta-phorbol-12, 13-dibutyrate (PDB), at 0.1-1 mumol/l, had almost no effect on ICa in most cells, but slightly potentiated (or slightly enhanced) the inhibitory effects of ISO. 5. Time decay (inactivation) of ICa consisted of two exponentials. Both the fast and slow time constants were slightly prolonged by ISO (5 mumol/l), and by carbachol (1 mumol/l); PDB (1 mumol/l) slightly shortened the fast time constant only. The half-maximum voltages of inactivation were not significantly affected by any of the agents. 6. These results suggest that the L-type ICa current is modulated by cyclic nucleotides (cAMP and cGMP) and by PK-C stimulation, and thereby contribute to regulation of contraction of the vascular smooth muscle cells.

Animals↗

PubMed1995

Role of T-type Ca2+ channel inhibitors in the pacemaker depolarization in rabbit sino-atrial nodal cells.

1. Effects of T-type Ca2+ channel inhibitors, Ni2+ and tetramethrin, on the spontaneous action potentials in rabbit sino-atrial nodal cells were examined. 2. The firing rate of spontaneous activity was 201 +/- 11 beats/min (n = 18). Experiments were performed at 36 degrees C. 3. Ni2+ (10(-5) to 10(-4) M) and tetramethrin (10(-7) to 5 x 10(-5) M) caused a negative chronotropic effect. Both inhibitors did not affect the maximum diastolic potential, and slowed the rate of depolarization during the diastole. 4. In the presence of TTX (10(-7) M), both inhibitors caused a stronger negative chronotropic effect, and hyperpolarized the maximum diastolic potential. The maximum rate of depolarization was enhanced, and the action potential duration (at 50% repolarization) was prolonged. The action potential amplitude was unaffected. Ni2+ had more potent actions than tetramethrin. 5. T-type and other Ca2+ channel inhibitors affected only the late phase of pacemaker potential, resulting in a negative chronotropic effect. 6. These results indicate that T-type Ca2+ channel inhibitors (Ni2+ and tetramethrin) slow the pacemaker depolarization at the late phase (but not at the initial phase), resulting in a negative chronotropic effect in the sino-atrial nodal cells.

Action Potentials↗

PubMed1995

Taurine-induced hyperpolarizing shift of the reversal potential of the fast Na+ current in embryonic chick cardiomyocytes.

1. Effects of taurine on the reversal potential of Na+ channel (INa) in isolated 17-day-old embryonic chick ventricular cardiomyocytes were examined using whole-cell voltage clamp technique. Experiments were performed at room temperature (22 degrees C). 2. Test pulses were applied between -60 and +50 mV from a holding potential of -90 mV. Addition of taurine (1-20 mM) to the bath solution inhibited the INa at -30 mV in a concentration-dependent manner; by 38.8 +/- 3.7% (n = 14, P < 0.01) at 10 mM and by 49.5 +/- 4.6% (n = 12, P < 0.001) at 20 mM. 3. Simultaneously, the reversal potential was shifted in the hyperpolarizing direction by 10.6 +/- 2.9 mV (n = 10, P < 0.05) at 10 mM and by 12.6 +/- 2.2 mV (n = 9, P < 0.01) at 20 mM. The shift was also produced concentration-dependently. Even when taurine at low concentrations (1 and 5 mM) enhanced INa, the shift occurred. 4. Intracellular taurine level decreased in Langendorff perfused guinea-pig hearts with Ca(2+)- and Mg(2+)-free solution, but not with Ca(2+)-free and 20 mM Mg2+ solution. 5. These results indicate that taurine shifts the reversal potential of the INa due to Na(+)-taurine cotransport, which might play an important role for the cell functions.

Animals↗

PubMed1995

Identification of a hyperpolarization-activated inward current in uterine smooth muscle cells during pregnancy.

1. Rat uterine smooth muscle possesses spontaneous contraction and automaticity. This study was exerted to examine one of the underlying currents that may be involved in the generation of spontaneous activity, the hyperpolarization-activated inward current. 2. Whole-cell patch clamp experiments were performed on freshly-isolated single longitudinal smooth muscle cells of pregnant rat uterus (18-day gestation). The holding potential was -30 mV, and long-duration (3 sec) hyperpolarizing pulses were applied to -40 to -120 mV. Experiments were performed at room temperature (22 degrees C). 3. A hyperpolarization-activated inward current (I(f)) was produced at the larger hyperpolarizing steps. Its current density (at -120 mV) was -1.03 +/- 0.31 pA/pF (n = 5). The average cell capacitance was 64.3 +/- 12.3 pF (n = 8). The threshold potential for activation of I(f) was about -70 mV, and the reversal potential was -18.6 +/- 2.1 mV (n = 4). In the presence of Cs+ (3 mM), the I(f) current (at -120 mV) was decreased by 76.5 +/- 2.1% (n = 5, P < 0.01). 4. These results indicate that the Cs(+)-sensitive hyperpolarization-activated inward current is present in the longitudinal muscle cells of pregnant rat uterus. This I(f) current may contribute to some extent to the electrogenesis of the spontaneous activity.

Animals↗

PubMed1995

Endothelin-1 inhibition of the ATP-sensitive K+ channel in guinea-pig ventricular cardiomyocytes.

1. Effects of endothelin-1 on the ATP-sensitive K+ channel were examined in guinea-pig ventricular cardiomyocytes. 2. The ATP-sensitive K+ channel was activated outwardly with amplitude of about 2.2 pA at 0 mV. The conductance was 31 pS at 5.4 mM external K+ solution. The open probability was inhibited, and was completely blocked at 1 nM of endothelin-1. 3. In contrast, endothelin-3 (1 nM) did not cause any effects on the channels. 4. Endothelin-1 (10 nM) significantly prolonged the action potential duration. These responses were reversible. 5. These results suggest that endothelin-1 may reverse the physiological responses to the stimulation of ATP-sensitive K+ channels, indicating its regulatory mechanisms under the disease conditions.

Action Potentials↗

PubMed1995

Relation of saphenous vein graft obstruction to serum cholesterol levels.

OBJECTIVES: To determine the potential of lipid-lowering therapy to reduce saphenous vein graft obstruction, we retrospectively studied the association between graft obstruction and serum cholesterol levels. BACKGROUND: Atherosclerosis is the major cause of vein graft obstruction. Approximately 50% of grafts are occluded by 10 years after operation. It remains to be established whether lipid control affects long-term graft survival. METHODS: We carried out a retrospective review of all 284 patients who had undergone coronary artery bypass graft surgery at Juntendo University Hospital between 1976 and 1991 and met the following additional criteria: at least one saphenous vein graft, repeat coronary arteriography at some point after coronary artery bypass graft surgery and a serum cholesterol level > or = 200 mg/dl before operation. Saphenous vein graft obstruction rates were compared among three groups classified by serum cholesterol levels at follow-up arteriography: group I < 200 mg/dl; group II 200 to 239 mg/dl; group III > or = 240 mg/dl. A vein graft was considered obstructed if it was narrowed by > or = 70%. RESULTS: In group I, 88% of grafts were not obstructed 7 years after operation. The respective rates were 61% in group II and 57% in group III (p < 0.005). This relation was true for vein grafts to the left anterior descending and other coronary arteries. CONCLUSIONS: Lower serum cholesterol levels are associated with lower rates of vein graft obstruction for up to 7 years. This suggests that cholesterol-lowering therapy may improve long-term saphenous vein graft survival after coronary artery bypass surgery.

Aged↗

PubMed1995

Identification of and developmental changes in transient outward current in embryonic chick cardiomyocytes.

Identification and developmental changes in the transient outward current (I(to)) in isolated embryonic chick ventricular cells (3, 10 and 17 days old) were examined using a whole-cell voltage clamp technique. Experiments were performed at room temperature (22 degrees C). Test pulses were applied between -40 and +50 mV from a holding potential of -60 mV. The I(to) was present (but small) and increased during development; the current density of I(to) at +40 mV was 3.5 +/- 0.5 pA/pF (n = 7) in 3-day cells, 4.2 +/- 0.9 pA/pF (n = 5) in 10-day cells, and 17.1 +/- 1.6 pA/pF (n = 5) in 17-day-old cells. The average capacitances also changed with developmental age; 12.0 +/- 2.0 pF (n = 8) in 3-day cells, 10.8 +/- 2.2 pF (n = 7) in 10-day cells, and 8.6 +/- 2.3 pF (n = 7) in 17-day cells. The I(to) was not always observed in all the prepared cells, and the number of cells possessing I(to) increased during development. The threshold potential was -30 mV in 17-day cells, and appeared to be displaced to more negative potential with developmental age. The time to peak decreased during development: 10.6 +/- 1.1 ms (n = 4) in 3-day cells, 6.7 +/- 0.5 ms (n = 5) in 10-day cells, and 5.4 +/- 0.6 ms (n = 5) in 17-day cells. The time decay of the inactivation phase for the I(to) had two exponentials; the fast component was increased by about 3-fold in 17-day cells, and the slow component was decreased by about 14% in both 10- and 17-day cells, as compared to 3-day cells. Addition of 3 mM 4-aminopyridine (4-AP) inhibited I(to) at +50 mV by 81.9 +/- 2.3% (n = 4, P < 0.001). These results indicate that the I(to), voltage-dependent and 4-AP-sensitive, exists even in young embryonic cardiomyocytes (but not in all cells), and increases during development, resulting in modulation of the action potential configuration.

4-Aminopyridine↗

PubMed1995

Regulation by taurine of the spontaneous activity in young embryonic chick cardiomyocytes.

Effects of taurine on the spontaneous action potential (AP) and the ionic currents in isolated 3-day-old embryonic chick ventricular cardiomyocytes were examined at different intracellular Ca2+ concentrations ([Ca]i) by whole-cell voltage-clamp and current-clamp methods. Experiments were performed at room temperature (22 degrees C). The firing rate of spontaneous activity was 61.2 +/- 2.1 beats/min (n = 6) at pCa 10, and 68.2 +/- 1.8 beats/min (n = 6) at pCa 7. When [Ca]i was pCa 10, taurine 10 and 20 mM caused a positive chronotropic effect and enhanced the maximum rate of depolarization. In contrast, at pCa 7, taurine 10 and 20 mM had a negative chronotropic effect. In voltage-clamp experiments, addition of taurine to the bath solution at pCa 7 inhibited the L-type Ca2+ current (ICa(L)) and the delayed rectifying K+ current (IK). At pCa 10, both ICa(L) and IK currents were enhanced by taurine 10 and 20 mM. The voltage of half-maximum inactivation for ICa(L) was not modified, nor was voltage of half-maximum activation for IK. These results indicate that taurine modulates the ICa(L) and IK currents dependent on [Ca]i, resulting in regulation of spontaneous activity.

Action Potentials↗

PubMed1995

Different actions between pindolol and propranolol on the ionic currents in spontaneously beating rabbit sino-atrial node cells.

Electrophysiological effects of beta-adrenoceptor blocking drugs (pindolol and propranolol) on the action potentials (APs) and the membrane currents in spontaneously beating rabbit sino-atrial (SA) node cells were examined by the two-microelectrode voltage-clamp technique. Cumulative administrations of both blocking drugs (10(-7)-10(-6) M) prolonged the AP duration (APD) and caused a negative chronotropic effect in a concentration-dependent manner. Propranolol exhibited stronger responses than pindolol. At 10(-6) M, propranolol depolarized the maximum diastolic potential (MDP) and pindolol decreased the maximum rate of depolarization significantly, but the drugs had little or no effect on the AP amplitude (APA). In voltage-clamp experiments, both blockers (10(-7)-10(-6) M) inhibited the slow inward and the time-dependent outward currents in a concentration-dependent manner. Holding potential was -40 mV. The hyperpolarization-activated inward current was not affected by pindolol, but it was concentration-dependently inhibited by propranolol. The inactivation curve of Isi was not modified by either pindolol or propranolol. The activation curve of IK was unaffected by pindolol, but was shifted by propranolol 10(-6) M by approximately 11 mV in the depolarizing direction. These results indicate that both beta-adrenoceptor blocking drugs (pindolol and propranolol) inhibit the slow inward and the time-dependent outward currents, but produce different actions on the hyperpolarization-activated inward current and the activation kinetic of IK due to their pharmacological properties, thereby resulting in difference in decrease in the spontaneous activity of rabbit SA node cells.

Action Potentials↗

PubMed1995

Steal phenomenon in a traumatic carotid-cavernous fistula.

A patient with head injury presented with computed tomography findings of a diffuse severe infarction of the left cerebral hemisphere in which the cerebral hemodynamics can be evaluated by transcranial Doppler sonography. Serial angiograms revealed a carotid-cavernous fistula, with a complete steal phenomenon. The unusual complication of a traumatic carotidcavernous fistula is discussed.

Arteriovenous Fistula↗

PubMed1995

Growth inhibition of Ureaplasma urealyticum by the proton pump inhibitor lansoprazole: direct attribution to inhibition by lansoprazole of urease activity and urea-induced ATP synthesis in U. urealyticum.

The proton pump inhibitors (PPIs) omeprazole and lansoprazole and the acid-activated analog of lansoprazole AG-2000, which potently inhibit the urease of Helicobacter pylori (K. Nagata, H. Satoh, T. Iwahi, T. Shimoyama, and T. Tamura, Antimicrob. Agents Chemother. 37:769-774, 1993), also inhibited the urease activities of cell-free extracts as well as intact cells of Ureaplasma urealyticum. The 50% inhibitory concentrations were between 1 and 25 microM. These compounds also inhibited the ATP synthesis induced by urea in ureaplasma cells. The 50% inhibitory concentrations for ATP synthesis were close to those for urease activity, but they were lower than those of urease inhibitors, such as acetohydroxamic acid, hydroxyurea, and thiourea. In addition, one of the metabolites of lansoprazole found in human urine, M-VI, also inhibited ureaplasmal urease activity and the ATP synthesis induced by urea at almost the same concentrations as those of lansoprazole. The inhibition of PPIs against ureaplasma urease was very similar to those against H. pylori urease, suggesting that the inhibitory mechanism against these ureases was due to the blockage of the SH residues on the cysteine of the enzyme. Omeprazole, lansoprazole, AG-2000, and M-VI inhibited the growth of U. urealyticum. Since ureaplasma urease is thought to be involved in the pathogenicity of this organism in the urogenital tract, PPIs and their analogs may be useful as chemotherapeutic agents against diseases caused by U. urealyticum.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1995

Inhibitory action of lansoprazole and its analogs against Helicobacter pylori: inhibition of growth is not related to inhibition of urease.

The proton pump inhibitors omeprazole and lansoprazole and its acid-activated derivative AG-2000, which are potent and specific inhibitors of urease of Helicobacter pylori (K. Nagata, H. Satoh, T. Iwahi, T. Shimoyama, and T. Tamura, Antimicrob. Agents Chemother. 37:769-774, 1993), inhibited the growth of H. pylori. The growth was inhibited not only in urease-positive clinical isolates but also in their urease-negative derivatives which had no urease polypeptides. AG-1789, a derivative of lansoprazole with no inhibitory activity against H. pylori urease, also inhibited the growth of both strains even more strongly than the urease inhibitors lansoprazole and AG-2000. Furthermore, the antibacterial activity of omeprazole and lansoprazole was not affected by glutathione or dithiothreitol, which completely abolished the inhibitory activity of lansoprazole against H. pylori urease. These results indicated that the inhibitory action of these compounds against the growth of H. pylori was independent from the inhibitory action against urease.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1995

Na+/H+ and Na+/Ca2+ exchange in regulation of [Na+]i and [Ca2+]i during metabolic inhibition.

The relationships among intracellular Na+ and Ca2+ concentrations ([Na+]i and [Ca2+]i, respectively) and cell morphology were investigated during metabolic inhibition (MI) in isolated guinea pig myocytes. [Na+]i and [Ca2+]i were measured using the fluorescent indicators, Na(+)-binding benzofuran isophthalate and fluo 3. During the initial 20 min of MI, [Na+]i increased from 6.2 +/- 0.5 to 18.6 +/- 1.6 mM (n = 31), whereas [Ca2+]i, expressed as the percent change of fluo 3 fluorescence, remained at the low level. In the following 30 min, 94% of the cells developed contracture, and [Ca2+]i began to increase after cells had contracted (167 +/- 14% at 50 min). The level of [Ca2+]i during MI was lower than that during 500 microM strophanthidin perfusion. The increase in [Na+]i was not affected by 10 microM tetrodotoxin but was suppressed by 1 microM hexamethylene amiloride (HMA). The application of 10 mM glucose from the start of MI prevented both the increase in [Na+]i and cell contracture. However, the addition of glucose after 20 min of MI [energy repletion (ER)] led to a dramatic increase in [Ca2+]i (442 +/- 72% at 50 min, n = 31), and 84% of the cells developed contracture. The increase in [Ca2+]i and the cell contracture were suppressed by HMA or Ca(2+)-free solution. Intracellular pH decreased from 7.23 +/- 0.07 to 6.95 +/- 0.09 during MI but did not change after ER (6.90 +/- 0.11 at 35 min, n = 9). These findings suggested that during MI 1) [Na+]i increased by both the activated Na+ influx via Na+/H+ exchange and the suppressed Na+ extrusion via the Na+/K+ pump, 2) Na+/Ca2+ exchange was inhibited by energy depletion and intracellular acidosis, and 3) cell contracture was not related to Ca2+ overload but was related to rigor due to energy depletion.

Amiloride↗

PubMed1995

Mapping of rat bilirubin UDP-glucuronosyl-transferase gene (Ugt1a1) to chromosome region 9q35-->q36.

Bilirubin and phenol UDP-glucuronosyltransferases (UGTs) are located on the same chromosome and comprise the UGT1 gene complex. A 1,763-bp cDNA probe (UGT1*0) specific for rat liver bilirubin UGT was used to localize the UGT1 complex locus (Ugt1a1) to chromosome region 9q35-->q36 by fluorescence in situ hybridization. This assignment is the first report on the location of a gene of the rat UGT1 complex using high-resolution banded metaphase chromosomes.

Animals↗