start-ver=1.4 cd-journal=joma no-vol=70 cd-vols= no-issue=6 article-no= start-page=455 end-page=460 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201612 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Isoflurane Induces Transient Impairment of Retention of Spatial Working Memory in Rats en-subtitle= kn-subtitle= en-abstract= kn-abstract=Postoperative cognitive dysfunction (POCD) occurs in nearly one-third of patients after non-cardiac surgery. Many animal behavior studies have investigated the effect of general anesthesia on cognitive function. However, there have been no studies examining the effects on working memory specifically, with a focus on the retention of working memory. We demonstrate here that isoflurane anesthesia induces deficits in the retention of spatial working memory in rats, as revealed by an increase in isoflurane-induced across-phase errors in the delayed spatial win-shift (SWSh) task with a 30-min delay in an 8-arm radial arm maze on post-anesthesia days (PADs) 1,2,4, and 10. A post-hoc analysis revealed a significant increase in across-phase errors on PAD 1 and recovery on PAD 10 in the isoflurane group. In contrast, within-phase errors independent of the retention of working memory were unaffected by isoflurane. These results demonstrate that isoflurane anesthesia transiently impairs the retention of spatial working memory in rats. en-copyright= kn-copyright= en-aut-name=TaninoMasaaki en-aut-sei=Tanino en-aut-mei=Masaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KobayashiMotomu en-aut-sei=Kobayashi en-aut-mei=Motomu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SasakiToshihiro en-aut-sei=Sasaki en-aut-mei=Toshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakataKen en-aut-sei=Takata en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MizobuchiSatoshi en-aut-sei=Mizobuchi en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MoritaKiyoshi en-aut-sei=Morita en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NagaiTaku en-aut-sei=Nagai en-aut-mei=Taku kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MorimatsuHiroshi en-aut-sei=Morimatsu en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Anesthesiology and Intensive Care Medicine, Kawasaki Medical School kn-affil= affil-num=5 en-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Division of Anesthesiology, Department of Surgery Related, Kobe University Graduate School of Medicine kn-affil= affil-num=7 en-affil=Okayama University kn-affil= affil-num=8 en-affil=Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine kn-affil= affil-num=9 en-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=postoperative cognitive dysfunction kn-keyword=postoperative cognitive dysfunction en-keyword=isoflurane kn-keyword=isoflurane en-keyword=spatial working memory kn-keyword=spatial working memory en-keyword=retention kn-keyword=retention en-keyword=delayed spatial win-shift task kn-keyword=delayed spatial win-shift task END start-ver=1.4 cd-journal=joma no-vol=85 cd-vols= no-issue=12 article-no= start-page=1647 end-page=1653 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201412 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Feasibility study of immediate pharyngeal cooling initiation in cardiac arrest patients after arrival at the emergency room en-subtitle= kn-subtitle= en-abstract= kn-abstract=AIM: Cooling the pharynx and upper oesophagus would be more advantageous for rapid induction of therapeutic hypothermia since the carotid arteries run in their vicinity. The aim of this study was to determine the effects of pharyngeal cooling on brain temperature and the safety and feasibility for patients under resuscitation. METHODS: Witnessed non-traumatic cardiac arrest patients (n=108) were randomized to receive standard care with (n=53) or without pharyngeal cooling (n=55). In the emergency room, pharyngeal cooling was initiated before or shortly after return of spontaneous circulation by perfusing physiological saline (5 ‹C) into a pharyngeal cuff for 120 min. RESULTS: There was a significant decrease in tympanic temperature at 40 min after arrival (P=0.02) with a maximum difference between the groups at 120 min (32.9 } 1.2‹C, pharyngeal cooling group vs. 34.1 } 1.3‹C, control group; P<0.001). The return of spontaneous circulation (70% vs. 65%, P=0.63) and rearrest (38% vs. 47%, P=0.45) rates were not significantly different based on the initiation of pharyngeal cooling. No post-treatment mechanical or cold-related injury was observed on the pharyngeal epithelium by macroscopic observation. The thrombocytopaenia incidence was lower in the pharyngeal cooling group (P=0.001) during the 3-day period after arrival. The cumulative survival rate at 1 month was not significantly different between the two groups. CONCLUSIONS: Initiation of pharyngeal cooling before or immediately after the return of spontaneous circulation is safe and feasible. Pharyngeal cooling can rapidly decrease tympanic temperature without adverse effects on circulation or the pharyngeal epithelium. en-copyright= kn-copyright= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KawashimaTakahisa en-aut-sei=Kawashima en-aut-mei=Takahisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KiyotaKazuya en-aut-sei=Kiyota en-aut-mei=Kazuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OdaShigeto en-aut-sei=Oda en-aut-mei=Shigeto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MorimotoNaoki en-aut-sei=Morimoto en-aut-mei=Naoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KobataHitoshi en-aut-sei=Kobata en-aut-mei=Hitoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IsobeHisashi en-aut-sei=Isobe en-aut-mei=Hisashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HondaMitsuru en-aut-sei=Honda en-aut-mei=Mitsuru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=FujimiSatoshi en-aut-sei=Fujimi en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=OndaJun en-aut-sei=Onda en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=ISeishi en-aut-sei=I en-aut-mei=Seishi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=SakamotoTetsuya en-aut-sei=Sakamoto en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=IshikawaMasami en-aut-sei=Ishikawa en-aut-mei=Masami kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=NakanoHiroshi en-aut-sei=Nakano en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=SadamitsuDaikai en-aut-sei=Sadamitsu en-aut-mei=Daikai kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=KishikawaMasanobu en-aut-sei=Kishikawa en-aut-mei=Masanobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=KinoshitaKosaku en-aut-sei=Kinoshita en-aut-mei=Kosaku kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=YokoyamaTomoharu en-aut-sei=Yokoyama en-aut-mei=Tomoharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=HaradaMasahiro en-aut-sei=Harada en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=KitauraMichio en-aut-sei=Kitaura en-aut-mei=Michio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=IchiharaKiyoshi en-aut-sei=Ichihara en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=HashimotoHiroshi en-aut-sei=Hashimoto en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=TsujiHidekazu en-aut-sei=Tsuji en-aut-mei=Hidekazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= en-aut-name=YorifujiTakashi en-aut-sei=Yorifuji en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=24 ORCID= en-aut-name=NaganoOsamu en-aut-sei=Nagano en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=25 ORCID= en-aut-name=KatayamaHiroshi en-aut-sei=Katayama en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=26 ORCID= en-aut-name=UjikeYoshihito en-aut-sei=Ujike en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=27 ORCID= en-aut-name=MoritaKiyoshi en-aut-sei=Morita en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=28 ORCID= affil-num=1 en-affil= kn-affil=Department of Anesthesiology, Okayama University Medical School affil-num=2 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Iseikai Hospital affil-num=3 en-affil= kn-affil=Tertiary Emergency Medical Center, Saitama Red-Cross Hospital affil-num=4 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine affil-num=5 en-affil= kn-affil=Emergency and Critical Care Center, Tsuyama Central Hospital affil-num=6 en-affil= kn-affil=Osaka Mishima Emergency Critical Care Center affil-num=7 en-affil= kn-affil=Department of Emergency Diagnosis and Treatment, Himeji Medical Center affil-num=8 en-affil= kn-affil=Emergency and Critical Care Center, Toho University Faculty of Medicine affil-num=9 en-affil= kn-affil=Critical Care and Trauma Center, Osaka General Medical Center affil-num=10 en-affil= kn-affil=Department of Neurosurgery, Kitakyushu Yugawa Hospital affil-num=11 en-affil= kn-affil=Department of Emergency Medicine, Japanese Red Cross Kumamoto Hospital affil-num=12 en-affil= kn-affil=Trauma and Resuscitation Center, Teikyo University School of Medicine affil-num=13 en-affil= kn-affil=Emergency Department, Kure Kyosai Hospital affil-num=14 en-affil= kn-affil=Emergency Department, Okazaki City Hospital affil-num=15 en-affil= kn-affil=Emergency and Critical Care Center, Osaka Medical Center affil-num=16 en-affil= kn-affil=Emergency and Critical Care Center, Saiseikai Fukuoka General Hospital affil-num=17 en-affil= kn-affil=Emergency and Critical Care Center, Nihon University Itabashi Hospital affil-num=18 en-affil= kn-affil=Emergency and Critical Care Medicine, Tokyo Medical University Hachioji Medical Center affil-num=19 en-affil= kn-affil=Emergency and Critical Care Center, Kumamoto Medical Center affil-num=20 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Kagawa Rosai Hospital affil-num=21 en-affil= kn-affil=Department of Clinical Laboratory Science, Yamaguchi University Graduate School of Medicine affil-num=22 en-affil= kn-affil=Daiken Medical Co. affil-num=23 en-affil= kn-affil=Daiken Medical Co. affil-num=24 en-affil= kn-affil=Department of Human Ecology, Okayama University Graduate School of Environmental and Life Science affil-num=25 en-affil= kn-affil=Department of Disaster and Emergency Medicine, Kochi University Medical School affil-num=26 en-affil= kn-affil=Department of Anesthesiology and Intensive Care Medicine, Kawasaki Medical School affil-num=27 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Okayama University Medical School affil-num=28 en-affil= kn-affil=Department of Anesthesiology, Okayama University Medical School en-keyword=Brain ischaemia kn-keyword=Brain ischaemia en-keyword=Cardiac arrest kn-keyword=Cardiac arrest en-keyword=Intra-arrest cooling kn-keyword=Intra-arrest cooling en-keyword=Pharynx kn-keyword=Pharynx en-keyword=Selective cooling kn-keyword=Selective cooling en-keyword=Therapeutic hypothermia kn-keyword=Therapeutic hypothermia END start-ver=1.4 cd-journal=joma no-vol=2 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201410 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Ensuring a cool recovery from cardiac arrest en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name=•“c‹gณ kn-aut-sei=•“c kn-aut-mei=‹gณ aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Department of Anesthesiology , Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=235 cd-vols= no-issue= article-no= start-page=59 end-page=69 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130403 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=EFFECT OF LIDOCAINE ON DYNAMIC CHANGES IN CORTICAL REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE FLUORESCENCE DURING TRANSIENT FOCAL CEREBRAL ISCHEMIA IN RATS en-subtitle= kn-subtitle= en-abstract= kn-abstract=Rats were subjected to 90 min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in the formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and reduced nicotinamide adenine dinucleotide (NADH) fluorescence with ultraviolet irradiation. In the lidocaine group (n = 10), 30 min before ischemia, an intravenous bolus (1.5 mg/kg) of lidocaine was administered, followed by a continuous infusion (2 mg/kg/h) for 150 min. In the control group (n = 10), an equivalent amount of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67% of the control; P = 0.01). This was likely due to the suppression of ischemic depolarization by blockage of voltage-dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of pen-infarct depolarizations during ischemia, the high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78% of the control; P = 0.046) and 24 h later (P = 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization. en-copyright= kn-copyright= en-aut-name=NaitoH. en-aut-sei=Naito en-aut-mei=H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakedaY. en-aut-sei=Takeda en-aut-mei=Y. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=DanuraT. en-aut-sei=Danura en-aut-mei=T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KassI. S. en-aut-sei=Kass en-aut-mei=I. S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MoritaK. en-aut-sei=Morita en-aut-mei=K. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Sch Med, Dept Anesthesiol affil-num=2 en-affil= kn-affil=Okayama Univ, Sch Med, Dept Anesthesiol affil-num=3 en-affil= kn-affil=Okayama Univ, Sch Med, Dept Anesthesiol affil-num=4 en-affil= kn-affil=Suny Downstate Med Ctr, Dept Anesthesiol affil-num=5 en-affil= kn-affil=Okayama Univ, Sch Med, Dept Anesthesiol en-keyword=hypoxia kn-keyword=hypoxia en-keyword=infarction kn-keyword=infarction en-keyword=lidocaine kn-keyword=lidocaine en-keyword=NADH fluorescence kn-keyword=NADH fluorescence en-keyword=DC potential kn-keyword=DC potential en-keyword=depolarization kn-keyword=depolarization END start-ver=1.4 cd-journal=joma no-vol=25 cd-vols= no-issue=3 article-no= start-page=292 end-page=298 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201307 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Quantitative evaluation of the neuroprotective effects of a short-acting ƒภ-adrenoceptor antagonist at a clinical dose on forebrain ischemia in gerbils: effects of esmolol on ischemic depolarization and histologic outcome of hippocampal CA1. en-subtitle= kn-subtitle= en-abstract= kn-abstract=BACKGROUND: Neuroprotective effects of esmolol in laboratory and clinical settings have been reported. The present study was designed to quantitatively evaluate the neuroprotective effects of esmolol using logistic regression curves and extracellular potentials. MATERIALS AND METHODS: In 42 gerbils, bilateral occlusion of common carotid arteries was performed for 3, 5, or 7 minutes (n=7 in each group). In treated animals, esmolol (200 ?g/kg/min) was administered for 90 minutes, 30 minutes before the onset of ischemia. Direct current potentials were measured in the bilateral CA1 regions, in which histologic evaluation was performed 5 days later. Relations of neuronal damage with ischemic duration and duration of ischemic depolarization were determined using logistic regression curves. RESULTS: There was no significant difference in onset time between the 2 groups (the control group vs. the esmolol group: 1.65}0.46 vs. 1.68}0.45 min, P=0.76), and significant differences in durations of ischemic depolarization were not observed with any ischemic duration. However, logistic regression curves indicated that esmolol has a neuroprotective effect from 2.95 to 7.66 minutes of ischemic depolarization (P<0.05), and esmolol prolonged the duration of ischemic depolarization causing 50% neuronal damage from 4.97 to 6.34 minutes (P<0.05). Logistic regression curves also indicated that esmolol has a neuroprotective effect from 3.77 to 7.74 minutes of ischemic duration (P<0.05), and esmolol prolonged the ischemic duration causing 50% neuronal damage from 4.26 to 4.91 minutes (P<0.05). en-copyright= kn-copyright= en-aut-name=DanuraTetsuya en-aut-sei=Danura en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ShiraishiKensuke en-aut-sei=Shiraishi en-aut-mei=Kensuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NaitoHiromichi en-aut-sei=Naito en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MizoueRyoichi en-aut-sei=Mizoue en-aut-mei=Ryoichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SatoSachiko en-aut-sei=Sato en-aut-mei=Sachiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MoritaKiyoshi en-aut-sei=Morita en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School affil-num=2 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School affil-num=3 en-affil= kn-affil=Department of Anesthesiology, Maizuru Kyosai Hospital affil-num=4 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School affil-num=5 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School affil-num=6 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School affil-num=7 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School en-keyword=esmolol kn-keyword=esmolol en-keyword=[beta]-adrenoceptor kn-keyword=[beta]-adrenoceptor en-keyword=ischemic depolarization kn-keyword=ischemic depolarization en-keyword=neuroprotective effect kn-keyword=neuroprotective effect en-keyword=brain ischemia. kn-keyword=brain ischemia. END start-ver=1.4 cd-journal=joma no-vol=67 cd-vols= no-issue=2 article-no= start-page=87 end-page=91 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201304 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Stereoscopic Three-Dimensional Images of an Anatomical Dissection of the Eyeball and Orbit for Educational Purposes en-subtitle= kn-subtitle= en-abstract= kn-abstract=The purpose of this study was to develop a series of stereoscopic anatomical images of the eye and orbit for use in the curricula of medical schools and residency programs in ophthalmology and other specialties. Layer-by-layer dissection of the eyelid, eyeball, and orbit of a cadaver was performed by an ophthalmologist. A stereoscopic camera system was used to capture a series of anatomical views that were scanned in a panoramic three-dimensional manner around the center of the lid fissure. The images could be rotated 360 degrees in the frontal plane and the angle of views could be tilted up to 90 degrees along the anteroposterior axis perpendicular to the frontal plane around the 360 degrees. The skin, orbicularis oculi muscle, and upper and lower tarsus were sequentially observed. The upper and lower eyelids were removed to expose the bulbar conjunctiva and to insert three 25-gauge trocars for vitrectomy at the location of the pars plana. The cornea was cut at the limbus, and the lens with mature cataract was dislocated. The sclera was cut to observe the trocars from inside the eyeball. The sclera was further cut to visualize the superior oblique muscle with the trochlea and the inferior oblique muscle. The eyeball was dissected completely to observe the optic nerve and the ophthalmic artery. The thin bones of the medial and inferior orbital wall were cracked with a forceps to expose the ethmoid and maxillary sinus, respectively. In conclusion, the serial dissection images visualized aspects of the local anatomy specific to various procedures, including the levator muscle and tarsus for blepharoptosis surgery, 25-gauge trocars as viewed from inside the eye globe for vitrectomy, the oblique muscles for strabismus surgery, and the thin medial and inferior orbital bony walls for orbital bone fractures. en-copyright= kn-copyright= en-aut-name=MatsuoToshihiko en-aut-sei=Matsuo en-aut-mei=Toshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OhtsukaAiji en-aut-sei=Ohtsuka en-aut-mei=Aiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Department of Ophthalmology, Okayama University Medical School and Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Departments of Anesthesiology and Resuscitology, Okayama University Medical School and Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Human Morphology, Okayama University Medical School and Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=stereoscopic camera-captured images kn-keyword=stereoscopic camera-captured images en-keyword=education kn-keyword=education en-keyword=local anatomical dissection kn-keyword=local anatomical dissection en-keyword=orbit kn-keyword=orbit en-keyword=eye kn-keyword=eye END start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=3 article-no= start-page=163 end-page=168 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201106 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The Excitement of Multiple Noradrenergic Cell Groups in the Rat Brain Related to Hyperbaric Oxygen Seizure en-subtitle= kn-subtitle= en-abstract= kn-abstract=The mechanism of oxygen toxicity for central nervous system and hyperbaric oxygen (HBO) seizure has not been clarified. Noradrenergic cells in the brain may contribute to HBO seizure. In this study, we defined the activation of noradrenergic cells during HBO exposure by c-fos immunohistochemistry. Electroencephalogram electrodes were pre-implanted in all animals under general anesthesia. In HBO seizure animals, HBO was induced with 5 atm of 100% oxygen until manifestation of general tonic convulsion. HBO non-seizure animals were exposed to 25 min of HBO. Control animals were put in the chamber for 120 min without pressurization. All animals were processed for c-fos immunohistochemical staining. All animals in the HBO seizure group showed electrical discharge on EEG. In the immunohistochemistry, c-fos was increased in the A1, A2 and A6 cells of the HBO seizure group, and in the A2 and A6 cells of the HBO non-seizure group, yet was extremely low in all three cell types in the control group. These results suggest the participation of noradrenaline in HBO seizure, which can be explained by the early excitement of A1 cells due to their higher sensitivity to high blood pressure, hyperoxia, or by the post-seizure activation of all noradrenergic cells. en-copyright= kn-copyright= en-aut-name=AraiMinako en-aut-sei=Arai en-aut-mei=Minako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakataKen en-aut-sei=Takata en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MizobuchiSatoshi en-aut-sei=Mizobuchi en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MoritaKiyoshi en-aut-sei=Morita en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Anesthesiology and Intensive Care‡U, Kawasaki Medical School affil-num=3 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=hyperbaric oxygen kn-keyword=hyperbaric oxygen en-keyword=seizure kn-keyword=seizure en-keyword=noradrenergic cells kn-keyword=noradrenergic cells en-keyword=immunohistochemistry kn-keyword=immunohistochemistry END start-ver=1.4 cd-journal=joma no-vol=58 cd-vols= no-issue=2 article-no= start-page=91 end-page=95 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200404 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The close relationship between decreases in extracellular GABA concentrations and increases in the incidence of hyperbaric oxygen-induced electrical discharge. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

To elucidate the mechanism by which hyperbaric oxygen (HBO2) induces electrical discharge, changes in the extracellular concentrations of GABA and glutamate were measured every 5 min using a microdialysis technique in rats during a period of exposure to HBO2 (5 atm abs). Electrical discharge was observed at 28 +/- 4 min after the onset of exposure. Though the extracellular concentrations of glutamate remained unchanged, the extracellular GABA concentrations (pre-exposure level, 0.026 +/- 0.005 microM in dialysate) began to decrease 15 min after the onset of exposure and reached their lowest level (74 +/- 14%, 0.019 +/- 0.004 microM) at the time of appearance of the discharge. There was a close logistic relationship between extracellular GABA concentrations and the discharge incidence, and the extracellular concentrations of GABA causing electrical discharge in 50% of the animals were estimated to be 80% of the pre-exposure level. These results suggest a possible mechanism that HBO2 exposure-induced discharge is caused by the decrease in extracellular concentration of GABA.

en-copyright= kn-copyright= en-aut-name=ZhangShan en-aut-sei=Zhang en-aut-mei=Shan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HagiokaShingo en-aut-sei=Hagioka en-aut-mei=Shingo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=GotoKeiji en-aut-sei=Goto en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MoritaKiyoshi en-aut-sei=Morita en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=glutamic acid kn-keyword=glutamic acid en-keyword=hyperbaric oxygenation kn-keyword=hyperbaric oxygenation en-keyword=gamma-aminobutyricacid kn-keyword=gamma-aminobutyricacid en-keyword=microdialysis kn-keyword=microdialysis en-keyword=seizures kn-keyword=seizures END start-ver=1.4 cd-journal=joma no-vol=103 cd-vols= no-issue=4 article-no= start-page=257 end-page=266 dt-received= dt-revised= dt-accepted= dt-pub-year=1991 dt-pub=1991 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The effects of SMA-SOD on brain damage induced by complete global brain ischemia in dogs kn-title=ƒCƒk‚ฬŠฎ‘S‘S”]‹•ŒŒŒใ‚ฬ”]แŠQ‚ษ‹y‚ฺ‚ทSMA-SOD ‚ฬŒ๘‰ส‚ษŠึ‚ท‚้ŽภŒฑ“IŒค‹† en-subtitle= kn-subtitle= en-abstract= kn-abstract=The effects of stylene maleinic acid butyl ester superoxide dismutase (SMA-SOD) on the brain damage induced by ischemia were studied in dogs. Eighteen minutes of cerebral ischemia was produced by clamping the ascending aorta with aorta-atrial and aorta-femoral vein bypass circuit. SMA-SOD(10mg/kg) was administered just after the initiation of recirculation. Dogs were divided into, control group and SMA-SOD group. In each group, cerebral blood flow (CBF) and intracranial pressure (ICP) were measured for 7 hours after ischemia, and neurologic outcome was evaluated up to 7 days after ischemia. Furthermore, extravasation of evans blue dye (EB, 100mg/kg) were observed 30 minutes after ischemia. SMA-SOD increased CBF during the hyperemia, and improved both delayed post-ischemic hypoperfusion (DHP) and neurologic outcomes. Extravasation of EB were recognized in the control group, but not in the SMA-SOD group. In conclusion, vasogenic edema might play a role in the elevation of ICP besides the hyperemia, and SMA-SOD improved neurologic outcome by prevention of edema, and improvement of DHP. Furthermore, free radicals might play a role in the appearance of ischemic brain damage. en-copyright= kn-copyright= en-aut-name=TakedaYoshimasa en-aut-sei=Takeda en-aut-mei=Yoshimasa kn-aut-name=•“c‹gณ kn-aut-sei=•“c kn-aut-mei=‹gณ aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=‰ชŽR‘ๅŠwˆใŠw•”–ƒŒE‘hถŠw‹ณŽบ en-keyword=SMA-SOD kn-keyword=SMA-SOD en-keyword=_ŒoŠw“I—\Œใ kn-keyword=_ŒoŠw“I—\Œใ en-keyword=ŒŒ—ฌ”]Šึ–ๅ kn-keyword=ŒŒ—ฌ”]Šึ–ๅ en-keyword=’x”ญซ”]ŒŒ—ฌŒธญ kn-keyword=’x”ญซ”]ŒŒ—ฌŒธญ en-keyword=ƒCƒk kn-keyword=ƒCƒk END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1991 dt-pub=19910328 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=ƒCƒk‚ฬŠฎ‘S‘S”]‹•ŒŒŒใ‚ฬ”]แŠQ‚ษ‹y‚ฺ‚ทSMA-SOD‚ฬŒ๘‰ส‚ษŠึ‚ท‚้ŽภŒฑ“IŒค‹† en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=•“c‹gณ kn-aut-sei=•“c kn-aut-mei=‹gณ aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=‰ชŽR‘ๅŠw END