研究者業績

南 浩一郎

ミナミ コウイチロウ  (Kouichiro Minami)

基本情報

所属
一般財団法人救急振興財団 救急救命東京研修所 教授
自治医科大学(JMU) 医学部 麻酔科学・集中治療医学講座麻酔科学部門 講師
(兼任)救急医学講座 講師
学位
博士(医学)(1995年3月 産業医科大学)

J-GLOBAL ID
200901083310301273
researchmap会員ID
1000210218

主要な受賞

 1

主要な論文

 169
  • Kouichiro Minami, Yota Kokubo, Ichinosuke Maeda, Shingo Hibino
    The American journal of emergency medicine 34(5) 899-902 2016年5月  査読有り
    BACKGROUND: Feedback devices are used to improve the quality of chest compression (CC). However, reports have noted that accelerometers substantially overestimate depth when cardiopulmonary resuscitation (CPR) is performed on a soft surface. Here, we determined whether a flexible pressure sensor could correctly evaluate the depth CC performed on a mannequin placed on a mattress. METHODS: Chest compression was performed 100 times/min by a compression machine on the floor or a mattress, and the depth of CC was monitored using a flexible pressure sensor (Shinnosukekun) and CPRmeter(™). The depth of machine-performed CC was consistently 5cm. We compared data from the feedback sensor with the true depth of CC using dual real-time auto feedback system that incorporated an infrared camera (CPR evolution(™)). RESULTS: On the floor, the true depth of CC was 5.0±0.0cm (n=100), or identical to the depth of CC performed by the machine. The Shinnosukekun(™) measured a mean (±SD) CC depth of 5.0±0.1cm (n=100), and the CPRmeter(™) measured a depth of 5.0±0.2cm (n=100). On the mattress, the true depth of CC was 4.4±0.0cm (n=100). The Shinnosukekun(™) measured a mean CC depth of 4.4±0.0cm (n=100), and the CPRmeter(™) measured a depth of 4.7±0.1cm (n=100). The data of CPRmeter(™) were overestimated (P<.0001 between the true depth and the CPRmeter(™)-measured depth). CONCLUSION: The Shinnosukekun(™) could correctly measure the depth of CC on a mattress. According to our present results, the flexible pressure sensor could be a useful feedback system for CC performed on a soft surface.
  • Kouichiro Minami, Yota Kokubo, Ichinosuke Maeda, Shingo Hibino
    Resuscitation 99 e11-2 2016年2月  査読有り
  • Kouichiro Minami, Junichi Ogata, Yasuhito Uezono
    Naunyn-Schmiedeberg's archives of pharmacology 388(10) 999-1007 2015年10月  査読有り
    Tramadol is an analgesic that is used worldwide for pain, but its mechanisms of action have not been fully elucidated. The majority of studies to date have focused on activation of the μ-opioid receptor (μOR) and inhibition of monoamine reuptake as mechanisms of tramadol. Although it has been speculated that tramadol acts primarily through activation of the μOR, no evidence has revealed whether tramadol directly activates the μOR. During the past decade, major advances have been made in our understanding of the physiology and pharmacology of ion channels and G protein-coupled receptor (GPCR) signaling. Several studies have shown that GPCRs and ion channels are targets for tramadol. In particular, tramadol has been shown to affect GPCRs. Here, the effects of tramadol on GPCRs, monoamine transporters, and ion channels are presented with a discussion of recent research on the mechanisms of tramadol.
  • K Minami, MJ Wick, Y Stern-Bach, JE Dildy-Mayfield, SJ Brozowski, EL Gonzales, Trudell, JR, RA Harris
    JOURNAL OF BIOLOGICAL CHEMISTRY 273(14) 8248-8255 1998年4月  査読有り筆頭著者
    Molecular mechanisms of anesthetic action on neurotransmitter receptors are poorly understood. The major excitatory neurotransmitter in the central nervous system is glutamate, and recent studies found that volatile anesthetics inhibit the function of the alpha-amino-3-hydroxyisoxazolepropionic acid subtype of glutamate receptors (e.g. glutamate receptor 3 (GluR3)), but enhance kainate (GluR6) receptor function, We used this dissimilar pharmacology to identify sites of anesthetic action on the kainate GluR6 receptor by constructing chimeric GluR3/GluR6 receptors, Results with chimeric receptors implicated a transmembrane region (TM4) of GluR6 in the action of halothane. Site directed mutagenesis subsequently showed that a specific amino acid, glycine 819 in TM4, is important for enhancement of receptor function by halothane (0.2-2 mM). Mutations of Gly-819 also markedly decreased the response to isoflurane (0.2-2 mM), enflurane (0.2-2 mM), and 1-chloro-1,2,2-trifluorocyclobutane (0.2-2 mM). The nonanesthetics 1,2-dichlorohexafluorocyclobutane and 2,3-dichlorooctafluorobutane had no effect on the functions of either wild-type GluR6 or receptors mutated at Gly-819. Ethanol and pentobarbital inhibited the function of both wild-type and mutant receptors. These results suggest that a specific amino acid, Gly-819, is critical for the action of volatile anesthetics, but not of ethanol or pentobarbital, on the GluR6 receptor.
  • K MINAMI, N YANAGIHARA, Y TOYOHIRA, M TSUTSUI, A SHIGEMATSU, A WADA, F IZUMI
    NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY 349(3) 223-229 1994年3月  査読有り筆頭著者
    The effects of isoflurane on Na-22(+) influx, Ca-45(2+) influx, catecholamine secretion and cyclic GMP production induced by three kinds of secretagogue (nicotinic agonists, veratridine and a high concentration of K+) have been investigated using cultured bovine adrenal medullary cells. (1) Isoflurane (1-6%) inhibited catecholamine secretion stimulated by carbachol, nicotine and dimethyl-4-phenylpiperazinium in a concentration-dependent manner. Isoflurane suppressed carbachol-evoked Na-22(+) influx and Ca-45(2+) influx at concentrations similar to those which suppressed catecholamine secretion. The inhibition of catecholamine secretion by isoflurane was not overcome by increasing the concentration of carbachol. (2) The inhibitory effects of isoflurane on veratridine-induced Na-22(+) influx, Ca-45(2+) influx and catecholamine secretion became evident when the concentration of isoflurane was raised to 4-6%, i.e. 2-3 fold higher than the concentrations (1-2%) employed clinically. (3) High K+-evoked Ca-45(2+) influx and catecholamine secretion were not affected by isoflurane (1-6%). (4) Isoflurane (1-6%) attenuated the production of cyclic GMP caused by muscarine, but not that caused by atrial natriuretic peptide or by sodium nitroprusside. These results suggest that isoflurane, at clinical anesthetic concentrations, inhibits nicotinic acetylcholine receptor-mediated cell responses as well as muscarinic receptor-mediated cyclic GMP production in adrenal medullary cells.

MISC

 113

主要な書籍等出版物

 10

主要な共同研究・競争的資金等の研究課題

 44

主要な産業財産権

 8