研究者詳細 - 森松　博史

MISC - 森松　博史

分割表示 286 件中 181 - 200 件目／全件表示 >>

Heme oxygenase-1 is an essential cytoprotective component in oxidative tissue injury induced by hemorrhagic shock

Toru Takahashi, Hiroko Shimizu, Hiroshi Morimatsu, Kyoichiro Maeshima, Kazuyoshi Inoue, Reiko Akagi, Masaki Matsumi, Hiroshi Katayama, Kiyoshi Morita

Journal of Clinical Biochemistry and Nutrition 44 ( 1 ) 28 - 40 2009年1月

記述言語：英語掲載種別：書評論文，書評，文献紹介等

Hemorrhagic shock causes oxidative stress that leads to tissue injuries in various organs including the lung, liver, kidney and intestine. Excess amounts of free heme released from destabilized hemoproteins under oxidative conditions might constitute a major threat because it can catalyze the formation of reactive oxygen species. Cells counteract this by rapidly inducing the rate-limiting enzyme in heme breakdown, heme oxygenase-1 (HO-1), which is a low-molecular-weight stress protein. The enzymatic HO-1 reaction removes heme. As such, endogenous HO-1 induction by hemorrhagic shock protects tissues from further degeneration by oxidant stimuli. In addition, prior pharmacological induction of HO-1 ameliorates oxidative tissue injuries induced by hemorrhagic shock. In contrast, the deletion of HO-1 expression, or the chemical inhibition of increased HO activity ablated the beneficial effect of HO-1 induction, and exacerbates tissue damage. Thus, HO-1 constitutes an essential cytoprotective component in hemorrhagic shock-induced oxidative tissue injures. This article reviews recent advances in understanding of the essential role of HO-1 in experimental models of hemorrhagic shock-induced oxidative tissue injuries with emphasis on the role of its induction in tissue defense.

DOI： 10.3164/jcbn.08-210-HO

Scopus

researchmap

Impairment of leukocyte deformability in patients undergoing esophagectomy

Tomohiko Suemori, Hiroshi Morimatsu, Satoshi Mizobuchi, Kiyoshi Morita, Yuki Katanosaka, Satoshi Mohri, Keiji Naruse

CLINICAL HEMORHEOLOGY AND MICROCIRCULATION 41 ( 2 ) 127 - 136 2009年

記述言語：英語出版者・発行元：IOS PRESS

Impaired deformability might contribute to the accumulation of activated leukocytes within pulmonary microcapillaries, leading to acute lung injury. The purpose of our study was to investigate changes in leukocyte deformability during periods of inflammation after esophagectomy. The study group comprised 20 patients who underwent esophagectomy. Changes in leukocyte deformability were investigated by examining filtration through a silicon microchannel, which simulated human pulmonary microcapillaries. Changes in the neutrophil cytoskeleton were investigated by measuring neutrophil F-actin assembly. The severity of patient clinical outcome was evaluated by the lung injury score. Leukocyte filtration through the microchannel was significantly weaker in esophagectomy patients than in healthy subjects (p < 0.01). After esophagectomy, filtration was further impaired compared with preoperative values (p < 0.05). The neutrophil F-actin content was higher in patients than in controls (p < 0.01), and increased after esophagectomy compared with preoperative values (p < 0.01). We concluded that circulating leukocytes showed reduced deformability and appeared to be sequestered within microcapillaries after esophagectomy. Changes in neutrophil cytoskeleton were considered to be responsible for the reduced deformability. Leukocyte accumulation within pulmonary microcapillaries might be related to the pathogenesis of lung injury after esophagectomy.

DOI： 10.3233/CH-2009-1164

Web of Science

researchmap

血糖持続測定を用いた小児インスリノーマの麻酔経験.

真鍋素子, 森松博史, 江木盛時, 鈴木聡, 賀来隆治, 松三昌樹, 森田潔

麻酔 58 ( 6 ) 757 - 759 2009年

記述言語：日本語出版者・発行元：克誠堂出版(株)

5歳女児。出生時に持続性高インスリン血症性低血糖症と診断された。内科的治療は効果なく、膵体部切除術の適応と判断された。麻酔はミダゾラム・ベクロニウム・セボフルラン・亜酸化窒素で導入し、酸素・亜酸化窒素・セボフルランで維持した。麻酔開始時に静脈路を確保し、血糖持続測定器STG-22で測定を開始した。手術室入室時は10%ブドウ糖液点滴を行っていたが、糖の過剰負荷を危惧してブドウ糖不添加リンゲル液に変更したところ、導入前200mg・dl-1であった血糖値が99mg・dl-1まで急速に低下した。このためブドウ糖液を再開して100ml・hr-1に設定し、以後徐々に血糖は上昇し、190mg・dl-1となった時点で20ml・hr-1とした。血管処置を始めた頃から血糖値は再上昇し220mg・dl-1となったため、5ml・hr-1に減速し、速効性インスリン静注を2単位・hr-1で30分間行った。麻酔時間6時間15分、出血量150mlで、循環動態は終始落ち着いており、術後経過も良好であった。

researchmap

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2009&ichushi_jid=J01397&link_issn=&doc_id=20090611120015&doc_link_id=40016698422&url=https%3A%2F%2Fci.nii.ac.jp%2Fnaid%2F40016698422&type=CiNii&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00003_1.gif

ラット出血性ショック後腸管障害に対するHeme Oxygenase-1の保護効果.

高橋徹, 清水裕子, 井上一由, 金川文俊, 森松博史, 片山浩, 森田潔

日本Shock学会雑誌 24 ( 2 ) 28 - 32 2009年

【敗血症診療の現在 SSCG2008とその後】 SSCG2008とその後の展開について血糖コントロール.

森松博史

Progress in Medicine 29 ( 6 ) 1499 - 1503 2009年

重症敗血症の経過中に骨髄穿刺により鑑別診断が可能となった薬剤性好中球減少の1症例.

鈴木聡, 森松博史, 江木盛時, 清水一好, 松崎孝, 佐藤哲文, 片山浩, 森田潔

ICUとCCU 33 ( 9 ) 703 - 707 2009年

酸塩基平衡の新しい考え方 Stewart Approach.

森松博史

臨床麻酔 33 ( 臨増 ) 431 - 440 2009年

【急性期栄養管理の基本と実際】急性期栄養管理の施設独自の工夫岡山大学における急性期栄養管理の実際.

松崎孝, 森松博史, 溝渕知司, 片山浩

救急医学 33 ( 13 ) 1813 - 1815 2009年

【AKI】 AKIの予防、治療管理血管作動薬ドパミン、ノルアドレナリン、バソプレッシンの腎臓への影響を考える.

森松博史

Intensivist 1 ( 3 ) 523 - 529 2009年

Hemin Treatment Abrogates Monocrotaline-Induced Pulmonary Hypertension

K. Shimzu, T. Takahashi, T. Iwasaki, H. Shimizu, K. Inoue, H. Morimatsu, E. Omori, M. Matsumi, R. Akagi, K. Morita

MEDICINAL CHEMISTRY 4 ( 6 ) 572 - 576 2008年11月

記述言語：英語出版者・発行元：BENTHAM SCIENCE PUBL LTD

Treatment of rats with monocrotaline (MCT), a pyrrolizidine alkaloid plant toxin, is known to cause pulmonary hypertension (PH), and it has been used as a useful experimental model of PH. Recent findings suggested that pulmonary inflammation may play a significant role in the pathogenesis of MCT-induced PH. We also demonstrated that, following MCT administration to rats, there was a significant and sustained increase in the pulmonary expression of heme oxygenase-1 (HO-1), which is known to be induced by various oxidative stresses, including inflammation and free heme, and is thought to be essential in the protection against oxidative tissue injuries. In this study, we administered hemin (ferriprotoporphyrin chloride, 30 mol/kg b.w., subcutaneously), a potent inducer of HO-1, every 3 days to rats following subcutaneous administration of MCT (60 mg/kg) and examined its effect on MCT-induced PH and pulmonary inflammation. MCT administration caused pulmonary arterial wall thickening with marked elevation of right ventricular pressure, in association with prominent pulmonary inflammation as revealed by the increase in gene expression of tumor necrosis factor-alpha and the number of infiltrated neutrophils in the lung. In contrast, hemin treatment of MCT-administered animals, which led to a further increase in pulmonary HO-1 mRNA expression, significantly ameliorated MCT-induced PH as well as tissue inflammation. These findings suggest that hemin treatment ameliorates MCT-induced PH possibly mediated through induction of pulmonary HO-1 which leads to the attenuation of pulmonary inflammation.

DOI： 10.2174/157340608786241972

Web of Science

researchmap

意識障害で発症したII型シトルリン血症の1症例

中西統子, 松崎孝, 林真雄, 森松博史, 佐藤健治, 佐藤哲文, 中塚秀輝, 松三昌樹, 森田潔

麻酔 57 ( 10 ) 1298 2008年10月

Hypertonic lactate solutions: a new horizon for fluid resuscitation?

Florian Wagner, Peter Radermacher, Hiroshi Morimatsu

INTENSIVE CARE MEDICINE 34 ( 10 ) 1749 - 1751 2008年10月

生体肝移植術中呼気一酸化炭素濃度の動態とその意義について

松崎孝, 森松博史, 高橋徹, 林真雄, 佐藤哲文, 佐藤健治, 松三昌樹, 森田潔

Shock : 日本Shock学会雑誌 23 ( 1 ) 47 - 47 2008年4月

Acid-base balance in combined severe hepatic and renal failure: A quantitative analysis

T. Naka, R. Bellomo, H. Morimatsu, J. Rocktaschel, L. Wan, P. Gow, P. Angus

INTERNATIONAL JOURNAL OF ARTIFICIAL ORGANS 31 ( 4 ) 288 - 294 2008年4月

記述言語：英語出版者・発行元：WICHTIG EDITORE

Background: Severe hepatic failure (SHF) commonly leads to major changes in acid-base balance status. However, the direct effects of liver failure per se on acid base balance are poorly understood because this condition is usually associated with acute renal failure (ARF). Aim: To assess the effect of SHF on acid-base balance.
Design: Retrospective laboratory investigation.
Subjects: Thirty-seven critically ill patients with SHF complicated by ARF, and 42 patients with severe ARF without liver failure prior to renal replacement therapy. Intervention: Retrieval of clinical and laboratory data from prospective unit and laboratory databases.
Methods: Quantitative acid-base assessment using Stewart-Figge methodology. Comparison of findings between the two groups. Comparison of demographic and clinical features.
Results: Patients with combined SHF and ARF were younger and had significantly higher mean bilirubin, ALT and INR levels (p<0.0001). Their mean lactate concentration was higher (6.4 vs. 2.1 mmol/L; p<0.0001) leading to a greater anion gap (25.8 vs. 16.1 mmol/L; p<0.0001). The ionized calcium concentration (1.00 vs. 1.15 mmol/L; p<0.0001) was lower but the strong ion difference apparent (SIDa) was greater (42.0 vs. 38.0 mEq/L; p<0.005) due to hypochloremia. The albumin concentration was low but higher than in control patients (28 vs. 24 g/L; p<0.01) and the calculated strong ion gap (SIG) was greater (12.6 vs. 9.3 mEq/L; p<0.01). The base excess was similar to controls and the pH was preserved in the near normal range by marked hypocapnea.
Conclusions: Combined SHF and ARF is a syndrome with unique acid-base changes due mostly to lactic metabolic acidosis and, in smaller part, to the accumulation of unmeasured anions. This acidosis, like that of ARF, is attenuated by hypoalbuminemia, by a unique preservation of the SIDa due to hypochloremia, and by marked hypocapnea.

Web of Science

researchmap

Hyperglycemia and the outcome of pediatric cardiac surgery patients requiring peritoneal dialysis

M. Egi, H. Morimatsu, Y. Toda, T. Matsusaki, S. Suzuki, K. Shimizu, T. Iwasaki, M. Takeuchi, R. Bellomo, K. Morita

INTERNATIONAL JOURNAL OF ARTIFICIAL ORGANS 31 ( 4 ) 309 - 316 2008年4月

記述言語：英語出版者・発行元：WICHTIG EDITORE

Objective: To study the nature of the association between glycemia and ICU mortality in pediatric cardiac surgery patients treated with peritoneal dialysis (PD).
Materials and methods: Retrospective observational study in the ICU of a tertiary hospital involving forty pediatric cardiac surgery patients treated with PD. We selected patients requiring PD, extracted glucose measurements and nutritional intake data during ICU stay and calculated mean and maximum blood glucose values i) during ICU stay; ii) during dependence on PD; and iii) during independence from PD. We statistically assessed the relationship between glycemia-related variables and ICU mortality.
Measurements and Results: Twenty-two patients treated with PD died (mortality 55%). In the PD cohort, 9725 blood glucose measurements were performed (every 3.3 hours on average). The mean glycemia during dependence on PD was significantly higher in non-survivors than survivors (p<0.0001), but not during independence from PD (p=0.49). The area under the receiver operator characteristic curve for the mean glycemia during dependence on PD was significantly greater than that obtained during independence from PD. Even after adjustment for severity of illness using multivariate logistic analysis, the mean glycemia and calorie intake during PD were significant and independent predictors of ICU mortality.
Conclusions: A higher mean blood glucose concentration during PD, but not during PD-free periods was associated with greater ICU mortality. Mean glycemia and calorie intake during PD were significant and independent predictors of ICU mortality.

Web of Science

researchmap

Protective role of heme oxygenase 1 in the intestinal tissue injury in hemorrhagic shock in rats

Kazuyoshi Inoue, Toru Takahashi, Kenji Uehara, Hiroko Shimuzu, Kana Ido, Hiroshi Morimatsu, Emiko Omori, Hiroshi Katayama, Reiko Akagi, Kiyoshi Morita

SHOCK 29 ( 2 ) 252 - 261 2008年2月

記述言語：英語出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS

Heme oxygenase (HO) 1 is inducible by a variety of oxidative stress and is thought to play an important role in the protection of tissues from oxidative injuries. Because hemorrhagic shock (HS) is an oxidative stress that results in tissue injury, we examined in this study the role of HO-1 induction in intestinal tissue injuries in a rat model of HS. The levels of HO-1 were significantly increased after HS both at transcriptional and protein levels in mucosal epithelia[ cells in the duodenum, jejunum, and colon, whereas their expression in the ileum was hardly detectable and not increased at all by the treatment. In contrast, HS-induced mucosal inflammation and apoptotic cell death in the duodenum, jejunum, and colon were far less than those observed in ileum as judged by the levels of expression of TNF-alpha, NOS, activated caspase 3, and BcI-2. Of note, inhibition of HO activity by tin-mesoporphyrin resulted in an aggravation of HS-induced tissue inflammation and apoptotic cell death. These findings indicate that HO-1 expression in the intestine is regulated in a highly site-specific manner after HS, and that HO-1 induction plays a fundamental role in protecting mucosal cells of the intestine from oxidative damages induced by HS.

DOI： 10.1097/shk.0b013e3180cab913

Web of Science

researchmap

Increased exhaled carbon monoxide concentration during living donor liver transplantation

Takashi Matsusaki, Hiroshi Morimatsu, Toru Takahashi, Masaki Matsumi, Kenji Sato, Ryuji Kaku, Tetsufumi Sato, Takahito Yagi, Noriaki Tanaka, Kiyoshi Morita

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 21 ( 1 ) 75 - 81 2008年1月

記述言語：英語出版者・発行元：PROFESSOR D A SPANDIDOS

Exhaled carbon monoxide concentration (ExCO-C) has been reported to increase in oxidative tissue injuries such as systemic inflammation, and is thought to reflect increased heme breakdown in the affected organ. As a transplanted liver undergoes ischemia-reperfusion, we hypothesized that ExCO-C might also increase following liver transplantation and might serve as a measure of the severity of the graft tissue injury. We prospectively studied 67 living donor liver transplantation (LDLT) patients in a consecutive fashion. During anesthesia, ExCO-C was determined at 6 time points, ranging from anesthesia induction, to admission to the intensive care unit. We also measured two markers of endothelial cellular injury, i.e., serum soluble thrombomodulin (sTM) and intercellular adhesion molecule (ICAM)-1. At 5 min after reperfusion of the grafted liver, ExCO-C markedly increased from 5.69 +/- 2.34 ppm at baseline, to 9.79 +/- 4.72 ppm (p < 0.0001). There was an excellent correlation among an increase in CO concentration, arterial carboxyhemoglobin levels at the time of reperfusion (r(2)=0.19, p=0.0003), and postoperative total bilirubin levels (day 1, 2, and 3; r(2)=0. 102, 0.109 and 0.100; p=0.008, 0.007 and 0.010, respectively). Serum sTM and ICAM-1 levels were also significantly increased after reperfusion (sTM: 3.3 +/- 0.8 to 5.1 +/- 1.7 FU/ml, p=0.0001; ICAM-1: 271.9 +/- 86.3 to 515.0 +/- 157.8 FU/ml, p=0.0001). ExCO-C had a positive relationship with sTM (r(2)=0.16, p=0.035) and ICAM-1 (r(2)=0.12, p=0.08). There was, however, no correlation of ExCO-C with serum AST/ALT levels or clinical outcomes. This study demonstrated that ExCO-C significantly increased after reperfusion during LDLT. The increased ExCO-C may likely reflect increased heme breakdown and endothelial cell injury in the grafted liver.

Web of Science

researchmap

生体肝移植の麻酔（当院における術中麻酔管理）

松崎孝, 森松博史, 林真雄, 松三昌樹, 佐藤哲文, 佐藤健治, 中塚秀輝, 森田潔

Anesthesia Network 12 ( 2 ) 3 - 8 2008年

高用量フェンタニルパッチによりがん性疼痛が軽減した1症例.

松崎孝, 西江宏行, 森松博史, 石川慎一, 佐藤健治, 溝渕知司, 中塚秀輝, 松三昌樹, 横山正尚, 森田潔

日本ペインクリニック学会誌 15 ( 2 ) 150 - 152 2008年

記述言語：日本語出版者・発行元：一般社団法人日本ペインクリニック学会

がん性疼痛の軽減にフェンタニルパッチの高用量が必要であった症例を報告する．56歳の男性で，直腸癌による肛門部から仙骨部に持続的な疼痛があった．モルヒネ徐放薬150 mg/日とフェンタニルパッチ2.5 mgを使用していたが，疼痛管理が困難であったので，ペインセンターへ紹介となった．副作用の便秘が強く，フェンタニルパッチ単独に変更し，リドカインの全身投与，アミトリプチリンの内服を併用した．しかし，疼痛は軽減しなかったので，くも膜下フェノールブロックや持続硬膜外ブロックを行い，疼痛は一時的には軽減した．その後，腫瘍が増大し，痛みが増強したので，フェンタニルパッチを65 mgまで増量し，疼痛は軽減した．疼痛管理開始から7カ月後に永眠したが，意識障害や呼吸抑制はなかった．治療中にフェンタニルパッチの20 mg，50 mg，65 mgを使用していた時のフェンタニルの血中濃度は，それぞれ，9.8，21.6，22.0 ng/mlと高値であった．いずれの時期も呼吸抑制，意識障害はなかった．

DOI： 10.11321/jjspc.07-0019

CiNii Article

CiNii Books

researchmap

その他リンク： http://search.jamas.or.jp/link/ui/2008268965

生体肝移植術後に中心性橋髄鞘融解症を生じた1症例.

松﨑孝, 森松博史, 佐藤哲文, 佐藤健治, 松三昌樹, 森田潔

麻酔 57 ( 9 ) 1136 - 1138 2008年

　前のページ - 次のページ　

<森松 博史>

MISC - 森松 博史

<森松　博史>

MISC - 森松　博史