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  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>70</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2016</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Isoflurane Induces Transient Impairment of Retention of Spatial Working Memory in Rats</ArticleTitle>
    <FirstPage LZero="delete">455</FirstPage>
    <LastPage>460</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Masaaki</FirstName>
        <LastName>Tanino</LastName>
        <Affiliation>Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motomu</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshihiro</FirstName>
        <LastName>Sasaki</LastName>
        <Affiliation>Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ken</FirstName>
        <LastName>Takata</LastName>
        <Affiliation>Department of Anesthesiology and Intensive Care Medicine, Kawasaki Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshimasa</FirstName>
        <LastName>Takeda</LastName>
        <Affiliation>Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Mizobuchi</LastName>
        <Affiliation>Division of Anesthesiology, Department of Surgery Related, Kobe University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation>Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Taku</FirstName>
        <LastName>Nagai</LastName>
        <Affiliation>Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morimatsu</LastName>
        <Affiliation>Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/54808</ArticleId>
    </ArticleIdList>
    <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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">postoperative cognitive dysfunction</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">isoflurane</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">spatial working memory</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">retention</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">delayed spatial win-shift task</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier Ireland Ltd.</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0300-9572</Issn>
      <Volume>85</Volume>
      <Issue>12</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2014</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Feasibility study of immediate pharyngeal cooling initiation in cardiac arrest patients after arrival at the emergency room</ArticleTitle>
    <FirstPage LZero="delete">1647</FirstPage>
    <LastPage>1653</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yoshimasa</FirstName>
        <LastName>Takeda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takahisa</FirstName>
        <LastName>Kawashima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuya</FirstName>
        <LastName>Kiyota</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shigeto</FirstName>
        <LastName>Oda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Morimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Kobata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hisashi</FirstName>
        <LastName>Isobe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuru</FirstName>
        <LastName>Honda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Fujimi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Onda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seishi</FirstName>
        <LastName>I</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuya</FirstName>
        <LastName>Sakamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masami</FirstName>
        <LastName>Ishikawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Nakano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daikai</FirstName>
        <LastName>Sadamitsu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masanobu</FirstName>
        <LastName>Kishikawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kosaku</FirstName>
        <LastName>Kinoshita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoharu</FirstName>
        <LastName>Yokoyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Harada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Michio</FirstName>
        <LastName>Kitaura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Ichihara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Hashimoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidekazu</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Yorifuji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Osamu</FirstName>
        <LastName>Nagano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Katayama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihito</FirstName>
        <LastName>Ujike</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <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&lt;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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Brain ischaemia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Cardiac arrest</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Intra-arrest cooling</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Pharynx</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Selective cooling</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Therapeutic hypothermia</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1537-744X</Issn>
      <Volume>2012</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The Incidence and Prognostic Value of Hypochloremia in Critically Ill Patients</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Makiko</FirstName>
        <LastName>Tani</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morimatsu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumiaki</FirstName>
        <LastName>Takatsu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Little is known on the clinical effects of chloride on critically ill patients. We conducted this retrospective, observational study in 488 critically ill patients to investigate the incidence of chloride abnormalities, effects of hypochloremia in acid-base disorders, and association between chloride and clinical outcome. The study involved retrieval of arterial blood gas analyses, biochemical and demographical data from electrical records as well as quantitative acid-base analyses. For statistical analysis, the patients were stratified into three groups according to their chloride level (normal range: 98-106 mEq/L). The distribution of chloride levels was hyperchloremia 16.6%, normochloremia 74.6%, and hypochloremia 8.8%. The hypochloremic group was significantly alkalemic (P &lt; 0.0001) and has significantly higher apparent strong ion difference (SIDa) (P &lt; 0.0001) compared to the two other groups. The hypochloremic group had significantly longer stays in the ICU and hospital (P &lt; 0.0001) with higher mortality (P &lt; 0.0001). However, multiple regression analysis showed that chloride was not an independent factor of poorer outcome. In conclusion, the acid-base characteristics of the hypochloremic patients were alkalemia coexisting with higher SIDa. And although it was not an independent prognostic factor, hypochloremia was related to poorer outcome in critically ill settings.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Public Library Science</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1932-6203</Issn>
      <Volume>8</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2013</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Effects of Biliverdin Administration on Acute Lung Injury Induced by Hemorrhagic Shock and Resuscitation in Rats</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Junko</FirstName>
        <LastName>Kosaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morimatsu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toru</FirstName>
        <LastName>Takahashi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroko</FirstName>
        <LastName>Shimizu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Susumu</FirstName>
        <LastName>Kawanishi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Emiko</FirstName>
        <LastName>Omori</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasumasa</FirstName>
        <LastName>Endo</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naofumi</FirstName>
        <LastName>Tamaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Hemorrhagic shock and resuscitation induces pulmonary inflammation that leads to acute lung injury. Biliverdin, a metabolite of heme catabolism, has been shown to have potent cytoprotective, anti-inflammatory, and anti-oxidant effects. This study aimed to examine the effects of intravenous biliverdin administration on lung injury induced by hemorrhagic shock and resuscitation in rats. Biliverdin or vehicle was administered to the rats 1 h before sham or hemorrhagic shock-inducing surgery. The sham-operated rats underwent all surgical procedures except bleeding. To induce hemorrhagic shock, rats were bled to achieve a mean arterial pressure of 30 mmHg that was maintained for 60 min, followed by resuscitation with shed blood. Histopathological changes in the lungs were evaluated by histopathological scoring analysis. Inflammatory gene expression was determined by Northern blot analysis, and oxidative DNA damage was assessed by measuring 8-hydroxy-2' deoxyguanosine levels in the lungs. Hemorrhagic shock and resuscitation resulted in prominent histopathological damage, including congestion, edema, cellular infiltration, and hemorrhage. Biliverdin administration prior to hemorrhagic shock and resuscitation significantly ameliorated these lung injuries as judged by histopathological improvement. After hemorrhagic shock and resuscitation, inflammatory gene expression of tumor necrosis factor-alpha and inducible nitric oxide synthase were increased by 18- and 8-fold, respectively. Inflammatory gene expression significantly decreased when biliverdin was administered prior to hemorrhagic shock and resuscitation. Moreover, after hemorrhagic shock and resuscitation, lung 8-hydroxy-2' deoxyguanosine levels in mitochondrial DNA expressed in the pulmonary interstitium increased by 1.5-fold. Biliverdin administration prior to hemorrhagic shock and resuscitation decreased mitochondrial 8-hydroxy-2' deoxyguanosine levels to almost the same level as that in the control animals. We also confirmed that biliverdin administration after hemorrhagic shock and resuscitation had protective effects on lung injury. Our findings suggest that biliverdin has a protective role, at least in part, against hemorrhagic shock and resuscitation-induced lung injury through anti-inflammatory and anti-oxidant mechanisms.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山歯学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0913-3941</Issn>
      <Volume>28</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2009</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>岡山大学病院周術期管理センター(歯科部門)設立後5ヵ月間の活動内容および今後の展開</ArticleTitle>
    <FirstPage LZero="delete">37</FirstPage>
    <LastPage>42</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Reiko</FirstName>
        <LastName>Yamanaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshihiko</FirstName>
        <LastName>Soga</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kumiko</FirstName>
        <LastName>Nawachi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshinobu</FirstName>
        <LastName>Yanagi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Kodama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Nakata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Rumi</FirstName>
        <LastName>Miura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Misao</FirstName>
        <LastName>Hagawa</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuo</FirstName>
        <LastName>Takeuchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mieko</FirstName>
        <LastName>Yamane</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Manabu</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shogo</FirstName>
        <LastName>Takashiba</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun-ichi</FirstName>
        <LastName>Asami</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shogo</FirstName>
        <LastName>Minagi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Yoshiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tsutomu</FirstName>
        <LastName>Shimono</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuo</FirstName>
        <LastName>Kuboki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akira</FirstName>
        <LastName>Sasaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0898-4921</Issn>
      <Volume>25</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2013</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Quantitative evaluation of the neuroprotective effects of a short-acting β-adrenoceptor antagonist at a clinical dose on forebrain ischemia in gerbils: effects of esmolol on ischemic depolarization and histologic outcome of hippocampal CA1.</ArticleTitle>
    <FirstPage LZero="delete">292</FirstPage>
    <LastPage>298</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tetsuya</FirstName>
        <LastName>Danura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshimasa</FirstName>
        <LastName>Takeda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kensuke</FirstName>
        <LastName>Shiraishi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromichi</FirstName>
        <LastName>Naito</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryoichi</FirstName>
        <LastName>Mizoue</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sachiko</FirstName>
        <LastName>Sato</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <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 µg/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&lt;0.05), and esmolol prolonged the duration of ischemic depolarization causing 50% neuronal damage from 4.97 to 6.34 minutes (P&lt;0.05). Logistic regression curves also indicated that esmolol has a neuroprotective effect from 3.77 to 7.74 minutes of ischemic duration (P&lt;0.05), and esmolol prolonged the ischemic duration causing 50% neuronal damage from 4.26 to 4.91 minutes (P&lt;0.05).</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">esmolol</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">[beta]-adrenoceptor</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ischemic depolarization</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">neuroprotective effect</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">brain ischemia.</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1340-7988</Issn>
      <Volume>19</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>気管挿管における口腔内偶発症防止対策の必要性</ArticleTitle>
    <FirstPage LZero="delete">431</FirstPage>
    <LastPage>432</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
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      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">dental injury</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">perioperative management</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">complication</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>66</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Effects of Propofol on Left Ventricular Mechanoenergetics in the Excised Cross-circulated Canine Heart</ArticleTitle>
    <FirstPage LZero="delete">435</FirstPage>
    <LastPage>442</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Waso</FirstName>
        <LastName>Fujinaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Juichiro</FirstName>
        <LastName>Shimizu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Gentaro</FirstName>
        <LastName>Iribe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takeshi</FirstName>
        <LastName>Imaoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yu</FirstName>
        <LastName>Oshima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takahiko</FirstName>
        <LastName>Kiyooka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Mohria</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/49039</ArticleId>
    </ArticleIdList>
    <Abstract>Although propofol is commonly used for general anesthesia, its direct effects on left ventricular (LV) contractility and energetics remain unknown. Accordingly, we studied the effects of intracoronary propofol on excised cross-circulated canine hearts using the framework of the Emax (a contractility index)-PVA (systolic pressure-volume area, a measure of total mechanical energy)-Vo2 (myocardial oxygen consumption per beat) relationship. We obtained 1) the Vo2-PVA relationship of isovolumic contractions with varied LV volumes at a constant Emax, 2) the Vo2-PVA relationship with varied LV volumes at a constant intracoronary concentration of propofol, and 3) the Vo2-PVA relationship under increased intracoronary concentrations of either propofol or CaCl2 at a constant LV volume to assess the cardiac mechanoenergetic effects of propofol. We found that propofol decreased Emax dose-dependently. The slope of the linear Vo2-PVA relationship (oxygen cost of PVA) remained unchanged by propofol. The PVA-independent Vo2-Emax relationship (oxygen cost of Emax) was the same for propofol and Ca2＋. In conclusion, propofol showed a direct negative inotropic effect on LV. At its clinical concentrations, decreases in contractility by propofol were relatively small. Propofol shows mechanoenergetic effects on the LV that are similar to those of Ca2＋ blockers or ß-antagonists—i.e., it exerts negative inotropic effects without changing the oxygen costs of Emax and PVA.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">anesthesia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">heart</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">contractility</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">myocardial oxygen consumption</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>66</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Antinociceptive Effects of Intrathecal Landiolol Injection in a Rat Formalin Pain Model</ArticleTitle>
    <FirstPage LZero="delete">285</FirstPage>
    <LastPage>289</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Mizobuchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshikazu</FirstName>
        <LastName>Matsuoka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihiko</FirstName>
        <LastName>Obata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryuji</FirstName>
        <LastName>Kaku</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshitaro</FirstName>
        <LastName>Itano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoto</FirstName>
        <LastName>Tomotsuka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Arata</FirstName>
        <LastName>Taniguchi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Nishie</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirotaka</FirstName>
        <LastName>Kanzaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mamoru</FirstName>
        <LastName>Ouchida</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyoshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/48569</ArticleId>
    </ArticleIdList>
    <Abstract>Perioperative beta-blocker administration has recently been recommended for patients undergoing cardiac or other surgery due to the beneficial cardiovascular effects of these agents. In addition, some studies have reported that perioperatively administered beta-blockers also have analgesic effects. In this study, to investigate the antinociceptive effects and the analgesic profile of landiolol, we examined the effects of intrathecal landiolol administration on nociceptive pain behavior and c-fos mRNA expression (a neural marker of pain) in the spinal cord using a rat formalin model. We found that pain-related behavior was inhibited by intrathecal landiolol administration. Moreover, the increase in c-fos mRNA expression on the formalin-injected side was less pronounced in rats administered landiolol
than in saline administered controls. Thus, intrathecal administration of landiolol exhibited antinociceptive
effects. Further investigation of the antinociceptive mechanism of landiolol is required.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">beta-blocker</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">landiolol</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">formalin</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">pain behavior</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">c-fos</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
</ArticleSet>
