Shigeyuki Yamada

University of Utah, Salt Lake City, UT, United States

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Publications (9)14.89 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Our goal was to determine if clinically relevant concentrations of aqueous extract of cigarette smoke (CSE) have direct deleterious effects on ventricular myocytes during simulated ischemia, and to investigate the mechanisms involved. CSE was prepared with a smoking chamber. Ischemia was simulated by metabolic inhibition (MI) with cyanide (CN) and 0 glucose. Adult rabbit and mouse ventricular myocyte [Ca(2+)](i) was measured by flow cytometry using fluo-3. Mitochondrial [Ca(2+)] was measured with confocal microscopy, and Rhod-2 fluorescence. The mitochondrial permeability transition (MPT) was detected by TMRM fluorescence and myocyte contracture. Myocyte oxidative stress was quantified by dichlorofluorescein (DCF) fluorescence with confocal microscopy. CSE 0.1% increased myocyte contracture caused by MI. The nicotine concentration (HPLC) in 0.1% CSE was 15 ng/ml, similar to that in humans after smoking cigarettes. CSE 0.1% increased mitochondrial Ca(2+) uptake, and increased the susceptibility of mitochondria to the MPT. CSE 0.1% increased DCF fluorescence in isolated myocytes, and increased [Ca(2+)](i) in paced myocytes exposed to 2.0 mM CN, 0 glucose (P-MI). These effects were inhibited by the superoxide scavenger Tiron. The effect of CSE on [Ca(2+)](i) during P-MI was also prevented by ranolazine. CSE in clinically relevant concentrations increases myocyte [Ca(2+)](i) during simulated ischemia, and increases myocyte susceptibility to the MPT. These effects appear to be mediated at least in part by oxidative radicals in CSE, and likely contribute to the effects of cigarette smoke to increase myocardial infarct size, and to decrease angina threshold.
    Toxicology and Applied Pharmacology 02/2009; 236(1):71-7. · 3.98 Impact Factor
  • Xiu Q Zhang, Shigeyuki Yamada, William H Barry
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    ABSTRACT: Ranolazine inhibits the late Na current and is proposed to reduce angina by decreasing [Na]i during ischemia, thereby reducing Ca influx via Na/Ca exchange (NCX). We sought to test this hypothesis and to determine whether oxidative stress during simulated-demand ischemia activates the late Na current. We measured [Ca]i and [Na]i in rabbit ventricular myocytes by flow cytometry during metabolic inhibition (MI) with 2 mM cyanide and 0 mM glucose at 37 degrees C plus pacing (P) at 0.5 Hz (P-MI), and in P-MI + 1, 10, or 50 microM ranolazine. In the clinically relevant concentration range (1-10 microM), ranolazine decreased Na and Ca loading and the development of myocyte contracture. P-MI caused an increase in fluorescence of the oxidative radical probe CM-H2DCFDA, which was inhibited by the radical scavenger Tiron 20 mM. The NCX inhibitor KB-R7943 (10 microM) and Tiron 20 mM reduced the rise in [Ca]i during P-MI and eliminated the effect of 10 microM ranolazine on [Ca]i. These results indicate that oxidative stress increases the late Na current during MI. Inhibition of the resulting increase in Na and Ca loading and contracture seems to account for the observed antiischemia effects of ranolazine.
    Journal of Cardiovascular Pharmacology 06/2008; 51(5):443-9. · 2.38 Impact Factor
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    ABSTRACT: Previously, we have reported that halothane anesthesia increases the extracellular concentrations of dopamine (DA) metabolites in the rat striatum using in vivo microdialysis techniques, and we have suggested that volatile anesthetics affect DA release and metabolism in various ways. The present investigation assesses the effect of isoflurane, widely used in clinical anesthesia, on DA release and metabolism. A microdialysis probe was implanted in the striatum of male Sprague-Dawley rats (n=5-7 per group). After recovery, the probe was perfused with modified Ringer's solution and 40 microl of dialysate were injected into a high performance liquid chromatograph every 20 min. The rats were given saline or the same volume of 10 mg kg(-1) clozapine, risperidone, fluoxetine or citalopram. After the pharmacological treatment, the rats were anesthetized with 1.0% or 2.5% isoflurane for 1h. The data were analyzed using two-way analysis of variance (ANOVA). For each drug with significant (p<0.05) drug-time interactions, the statistical analysis included one-way ANOVA and Newman-Keuls post hoc comparisons. A high concentration of isoflurane (2.5%) anesthesia increased the extracellular concentration of DA metabolites during emergence from anesthesia. The levels of DA metabolites increased in an isoflurane concentration-dependent manner. Isoflurane attenuated DA release induced by clozapine and risperidone. Fluoxetine, but not citalopram, antagonized the isoflurane-induced increase in metabolites. The results of current investigation suggest that isoflurane enhances presynaptic DA metabolism, and that the oxidation of DA might be partially modulated by the activities of the dopaminergic-serotonergic pathway at a presynaptic site in the rat striatum.
    Neurochemistry International 02/2008; 52(3):384-91. · 2.66 Impact Factor
  • Neuroscience Research - NEUROSCI RES. 01/2007; 58.
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    ABSTRACT: Pentobarbital is reported to inhibit ketamine-induced dopamine (DA) release in the rat nucleus accumbens. The accumbens is a part of the limbic dopaminergic system in the brain, and the dopaminergic neural activity of other components may also be sensitive to pentobarbital. We investigated the effect of pentobarbital administration on DA release in the striatum known as DA-rich basal ganglia, and the interaction between pentobarbital and L-DOPA, using in vivo microdialysis techniques. Male SD rats were implanted microdialysis probe into the right striatum. The probe was perfused with modified Ringer's solution and dialysate was directly injected to an HPLC. Every group of rats was consisted of six to seven animals. In the first experiment, rats were given saline, 25 and 50 mg kg(-1) pentobarbital. The second, each rat was given a local administration of 2 and 5 microg ml(-1) of L-DOPA with perfusate. Finally, other sets of rats were given 5 microg ml(-1) of L-DOPA and 25, 50, or 100 mg kg(-1) pentobarbital. Pentobarbital anaesthesia decreased the extracellular concentration of DA, and local administration of L-DOPA significantly increased DA concentration. Pretreatment with pentobarbital diminished the L-DOPA-induced DA increase. The results of the present investigation demonstrate that administration of pentobarbital might inhibit dopaminergic neural activity not only in the nucleus accumbens but also in the rat striatum. Pentobarbital anaesthesia antagonizes DA increase induced by L-DOPA and suggests the inhibition of metabolism of L-DOPA. The results of some animal experiments on dopaminergic activity under pentobarbital anaesthesia should be reconsidered.
    Brain Research Bulletin 06/2006; 69(5):593-6. · 2.94 Impact Factor
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    ABSTRACT: The effect of isoflurane anesthesia on changes in the extracellular concentrations of dopamine (DA) and its metabolites (3-methoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)) modulated by pargyline, monoamine oxidase inhibitor, was studied using in vivo microdialysis techniques. A microdialysis probe was implanted into the right striatum of male SD rats. Each rat (n=5-6) was given saline or the same volume of 30 or 75 mg kg(-1) pargyline intraperitoneally with or without 1 h isoflurane anesthesia (1 or 3%). Isoflurane anesthesia increased the extracellular concentration of DA in high dose (3%) and increased the metabolite concentrations in a dose-dependent manner. Pargyline administration increased the extracellular concentration of DA and 3-MT, and decreased that of other metabolites. After 30 mg kg(-1) pargyline treatment, 1% isoflurane-induced DA release and increasing of 3-MT were preserved, whereas high dose isoflurane (3%) decreased the concentration of metabolites (DOPAC and HVA), despite of the increase by low dose isoflurane (DOPAC). When 75 mg kg(-1) pargyline was administered, isoflurane anesthesia decreased the concentration of DA and DOPAC. The isoflurane-induced 3-MT increase was preserved in all experiments. Our results suggest that isoflurane anesthesia induced biphasic effect on DA regulation probably by the potentiation of DA release and the inhibition of DA synthesis. Isoflurane might modulate DA homeostasis presynaptically.
    Brain Research Bulletin 11/2005; 67(3):176-81. · 2.94 Impact Factor
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    ABSTRACT: A gas chromatograph-mass spectrometric assay has been developed for the quantitation of cotinine, the major metabolite of nicotine, in human urine. Extraction or condensing procedure was not required and the method reduced time involved in sample preparation. The analytes were separated on the fused-silica capillary column. The operating conditions were: injector, 250 degrees C; detector, 280 degrees C; column, 50-250 degrees C. The total gas flow-rate of helium (carrier) was 50 ml.min-1 and the pressure of column inlet was 100-200 kPa. The retention time was 18.1 min and the limit of quantitation was 5 ng.ml-1. This method provides an easy and simple assay for the detection of cotinine in clinical settings.
    Masui. The Japanese journal of anesthesiology 06/2003; 52(5):537-41.
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    ABSTRACT: To evaluate the effect of perioperative intravenous administration of flurbiprofen, a nonsteroidal anti-inflammatory drug, on the postoperative pain after minor ear, neck and nose surgery, eighty patients were randomly allocated into three groups. Control group of 40 patients, received a placebo. The second group (n = 20) received 1 mg.kg-1 flurbiprofen i.v. at the end of surgery, and the third group (n = 20) received the same dose of flurbiprofen before the start of surgery. The ratio of the patients and the time for requirement of analgesics after the operation and the serum concentration of flurbiprofen were assessed. The ratio of the patients who required analgesics was higher in control group (0.45, 0.35 and 0.10 in each group). The time without analgesics was longer in pre-treatment group. The serum concentration of flurbiprofen decreased in pre-treatment group at the end of surgery, but the effectiveness of flurbiprofen on postoperative pain might be more apparent in pre-treatment group. Administration of flurbiprofen before the start of surgery is more effective for peri-operative analgesia in minor ear, neck and nose surgery.
    Masui. The Japanese journal of anesthesiology 09/2002; 51(8):857-61.
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    ABSTRACT: The effect of the additional administration of midazolam or flumazenil on bispectral index (BIS) during propofol anesthesia was investigated in 22 scheduled surgical patients. Midazolam 10 or 30 micrograms.kg-1, or flumazenil 6 or 12 micrograms.kg-1 was injected to the patients to evaluate their effect on BIS after achieving steady state of hypnosis more than 1 hr of propofol anesthesia with 5 mg.kg-1.hr-1. The only midazolam 30 micrograms.kg-1 significantly reduced BIS value from 47.8 +/- 8.6 to 36.8 +/- 6.5. The synergistic interaction between midazolam and propofol assessed by BIS might be less clear than that assessed by hypnotic dose of propofol using psychopharmacological investigation.
    Masui. The Japanese journal of anesthesiology 08/2002; 51(7):733-6.