研究者詳細 - 森松　博史

MISC - 森松　博史

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岩崎達雄, 戸田雄一郎, 清水一好, 金澤伴幸, 森松博史, 森田潔

日本臨床麻酔学会誌 34 ( 2 ) 169 - 176 2014年

記述言語：日本語出版者・発行元：日本臨床麻酔学会

先天性心疾患で最もその生理が成人と異なり管理が困難な症例は,並列循環を伴う単心室症である.これらの患児は,まず第一期姑息術を受けるが,術後にも並列循環が残存するため周術期管理ではこの並列循環の管理が大切になる.理想的な並列循環を達成するために動脈血酸素飽和度のみならず体静脈血酸素飽和度をモニタリングして循環動態を正確に把握する.また体静脈血酸素飽和度は患児の予後予測,目標指向型治療の指標としても有用である.体・肺血流のバランスをとるために心拍出量,体・肺血管抵抗を調節するが,第一期姑息術後では体血管抵抗を調節する方がより効果的で,積極的な後負荷軽減療法は並列循環を安定させ,術後合併症を低減する.(著者抄録)

DOI： 10.2199/jjsca.34.169

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その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2014&ichushi_jid=J01620&link_issn=&doc_id=20140319200001&doc_link_id=%2Fci4jjsca%2F2014%2F003402%2F001%2F0169-0176%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fci4jjsca%2F2014%2F003402%2F001%2F0169-0176%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Eisenmenger症候群に対する肺移植術後の急性左心不全の病態.

清水一好, 小林求, 森松博史

日本集中治療医学会雑誌 21 ( 5 ) 481 - 484 2014年

筋弛緩モニター使用下でのスガマデクス投与にもかかわらずロクロニウムの再クラーレ化が疑われた1例

伊加真士, 清水一好, 川出健嗣, 金澤伴幸, 西谷恭子, 森松博史

日本臨床麻酔学会誌 34 ( 6 ) 2014年

Development of a Supraglottic Airway Device with the Function of Pharyngeal Cooling

Yoshimasa Takeda, Hiroshi Hashimoto, Ryoichi Mizoue, Sachiko Sato, Hiroshi Morimatsu

CIRCULATION 128 ( 22 ) 2013年11月

GAIA検索システムを用いた臨床研究の可能性

戸田雄一郎, 荒川恭佑, 森松博史, 青江尚美, 森田潔, 中塚秀輝

日本臨床麻酔学会誌 33 ( 6 ) S300 2013年10月

腹臥位胸腔鏡下食道切除術中に大量出血による心停止をきたしたが後遺症なく救命し得た1例

植村真弓, 小林求, 川西裕之, 岡原修司, 松岡義和, 森松博史

日本臨床麻酔学会誌 33 ( 6 ) S240 - S240 2013年10月

Perioperative plasma melatonin concentration in postoperative critically ill patients: Its association with delirium

Shiho Yoshitaka, Moritoki Egi, Hiroshi Morimatsu, Tomoyuki Kanazawa, Yuichiro Toda, Kiyoshi Morita

JOURNAL OF CRITICAL CARE 28 ( 3 ) 236 - 242 2013年6月

記述言語：英語出版者・発行元：W B SAUNDERS CO-ELSEVIER INC

Purpose: Delirium is a common complication in postoperative critically ill patients. Although abnormal melatonin metabolism is thought to be one of the mechanisms of delirium, there have been few studies in which the association between alteration of perioperative plasma melatonin concentration and postoperative delirium was assessed.
Materials: We conducted a prospective observational study to assess the association of perioperative alteration of plasma melatonin concentration with delirium in 40 postoperative patients who required intensive care for more than 48 hours. We diagnosed postoperative delirium using Confusion Assessment Method for the intensive care unit and measured melatonin concentration 4 times (before the operation as the preoperative value, 1 hour after the operation, postoperative day 1, and postoperative day 2).
Results: Postoperative delirium occurred in 13 (33%) of the patients. Although there was no significant difference in preoperative melatonin concentration, Delta melatonin concentration at 1 hour after the operation was significantly lower in patients with delirium than in those without delirium (-1.1 vs 0 pg/mL, P = .036). After adjustment of relevant confounders, Delta melatonin concentration was independently associated with risk of delirium (odds ratio, 0.50; P = .047).
Conclusions: Delta melatonin concentration at 1 hour after the operation has a significant independent association with risk of postoperative delirium. (c) 2013 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jcrc.2012.11.004

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Effects of Biliverdin Administration on Acute Lung Injury Induced by Hemorrhagic Shock and Resuscitation in Rats

Junko Kosaka, Hiroshi Morimatsu, Toru Takahashi, Hiroko Shimizu, Susumu Kawanishi, Emiko Omori, Yasumasa Endo, Naofumi Tamaki, Manabu Morita, Kiyoshi Morita

PLOS ONE 8 ( 5 ) e63606-e63606 2013年5月

記述言語：英語出版者・発行元：PUBLIC LIBRARY SCIENCE

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.

DOI： 10.1371/journal.pone.0063606

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Inhalation of carbon monoxide following resuscitation ameliorates hemorrhagic shock-induced lung injury

Susumu Kawanishi, Toru Takahashi, Hiroshi Morimatsu, Hiroko Shimizu, Emiko Omori, Kenji Sato, Masaki Matsumi, Shigeru Maeda, Atsunori Nakao, Kiyoshi Morita

MOLECULAR MEDICINE REPORTS 7 ( 1 ) 3 - 10 2013年1月

記述言語：英語出版者・発行元：SPANDIDOS PUBL LTD

Even after successful resuscitation, hemorrhagic shock frequently causes pulmonary inflammation that induces acute lung injury (ALI). We previously demonstrated that when CO is inhaled at a low concentration both prior to and following hemorrhagic shock and resuscitation (HSR) it ameliorates HSR-induced ALI in rats due to its anti-inflammatory effects. In the present study, we administered CO to the same model of ALI only after resuscitation and examined whether it exerted a therapeutic effect without adverse events on HSR-induced ALI, since treatment of animals with CO prior to HSR did not prevent lung injury. HSR were induced by bleeding animals to achieve a mean arterial pressure of 30 mmHg for I h followed by resuscitation with the removed blood. HSR resulted in the upregulation of inflammatory gene expression and increased the rate of apoptotic cell death in the lungs. This was determined from an observed increase in the number of cells positive for transferase-mediated dUTP-fluorescein isothiocyanate (FITC), nick-end labeling staining and activated caspase-3. HSR also resulted in prominent histopathological damage, including congestion, edema, cellular infiltration and hemorrhage. By contrast, CO inhalation for 3 h following resuscitation significantly ameliorated these inflammatory events, demonstrated by reduced histological damage, inflammatory mediators and apoptotic cell death. The protective effects of CO against lung injury were notably associated with an increase in the protein expression level of peroxisome proliferator-activated receptor (PPAR)-gamma, an anti-inflammatory transcriptional regulator in the lung. Moreover, CO inhalation did not affect the hemodynamic status or tissue oxygenation during HSR. These findings suggest that inhalation of CO at a low concentration exerts a potent therapeutic effect against HSR-induced ALI and attenuates the inflammatory cascade by increasing PPAR-gamma protein expression.

DOI： 10.3892/mmr.2012.1173

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【麻酔・全身管理で使用される薬物の基礎知識と使用法】晶質液と膠質液.

森松博史

月刊レジデント 6 ( 12 ) 90 - 95 2013年

腎代替療法における抗凝固薬としてのクエン酸.

森松博史

日本集中治療医学会雑誌(1340-7988) 20 ( 4 ) 577 - 579 2013年

生体ガスと臓器保護呼気COガスは酸化ストレスの指標か?

髙橋徹, 森松博史

Medical Gases 15 ( 1 ) 17 - 19 2013年

【エビデンスを超えたCRRT】 CRRT開始をどう考えるべきか.

塩崎恭子, 森松博史, 森田潔

医学のあゆみ(0039-2359) 245 ( 4 ) 292 - 294 2013年

重症呼吸不全に対するAirway Pressure Release Ventilationの肺酸素化能および循環動態に与える影響の検討.

岡原修司, 内藤宏道, 萩岡信吾, 森直樹, 森松博史, 森田潔

ICUとCCU(0389-1194) 37 ( 3 ) 219 - 223 2013年

Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation

Junya Matsumi, Hiroshi Morimatsu, Takashi Matsusaki, Ryuji Kaku, Hiroko Shimizu, Toru Takahashi, Takahito Yagi, Masaki Matsumi, Kiyoshi Morita

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 29 ( 2 ) 135 - 140 2012年2月

記述言語：英語出版者・発行元：SPANDIDOS PUBL LTD

Living donor liver transplantation (LDLT) requires ischemia/reperfusion (I/R), which can cause early graft injury. However, the detailed mechanism of I/R injury remains unknown. Heme oxygenase-1 (HO-1) is a rate-limiting enzyme in heme catabolism and results in the production of iron, carbon monoxide (CO), and biliverdin IX alpha. Furthermore, in animals, HO-1 has a protective effect against oxidative stress associated with I/R injury. However, in humans, the molecular mechanism and clinical significance of HO-1 remain unclear. We previously demonstrated that exhaled CO levels increase during LDLT, and postulated that this may indicate I/R injury. In this study, we elucidate the origin of increased exhaled CO levels and the role of HO-1 in I/R injury during LDLT. We studied 29 LDLT donors and recipients each. For investigation of HO-I gene expression by polymerase chain reaction and HO-I localization by immunohistological staining, liver biopsies from the grafted liver were conducted twice, once before and once after I/R. Exhaled CO levels and HO-I gene expression levels significantly increased after I/R. In addition, HO-I levels significantly increased after I/R in Kupffer cells. Furthermore, we found a significant positive correlation between exhaled CO levels and HO-I gene expression levels. These results indicated that increased heme breakdown in the grafted liver is the source of increased exhaled CO levels. We also found a significant relationship between HO-1 gene expression levels and alanine aminotransferase (ALT) levels; i.e., the higher the HO-I gene expression levels, the higher the ALT levels. These results suggest that HO-1-mediated heme breakdown is caused by I/R during LDLT, since it is associated with increased exhaled CO levels and liver damage.

DOI： 10.3892/ijmm.2011.821

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The Incidence and Prognostic Value of Hypochloremia in Critically Ill Patients

Makiko Tani, Hiroshi Morimatsu, Fumiaki Takatsu, Kiyoshi Morita

SCIENTIFIC WORLD JOURNAL 2012 Epub-Epub 2012年

記述言語：英語出版者・発行元：HINDAWI PUBLISHING CORPORATION

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 < 0.0001) and has significantly higher apparent strong ion difference (SIDa) (P < 0.0001) compared to the two other groups. The hypochloremic group had significantly longer stays in the ICU and hospital (P < 0.0001) with higher mortality (P < 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.

DOI： 10.1100/2012/474185

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Increase in exhaled CO concentration after reperfusion of the grafted liver during living donor liver transplantation

Toru Takahashi, Hiroshi Morimatsu, Takashi Matsusaki, Junya Matsumi, Hiroko Shimizu, Kiyoshi Morita

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 30 S29 - S29 2012年