研究者詳細 - 森松　博史

MISC - 森松　博史

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Effect of tranexamic acid on blood loss in pediatric cardiac surgery: a randomized trial

Kazuyoshi Shimizu, Yuichiro Toda, Tatsuo Iwasaki, Mamoru Takeuchi, Hiroshi Morimatsu, Moritoki Egi, Tomohiko Suemori, Satoshi Suzuki, Kiyoshi Morita, Shunji Sano

JOURNAL OF ANESTHESIA 25 ( 6 ) 823 - 830 2011年12月

記述言語：英語出版者・発行元：SPRINGER TOKYO

Purpose The benefit of tranexamic acid (TXA) in pediatric cardiac surgery on postoperative bleeding has varied among studies. It is also unclear whether the effects of TXA differ between cyanotic patients and acyanotic patients. The aim of this study was to test the benefit of TXA in pediatric cardiac surgery in a well-balanced study population of cyanotic and acyanotic patients.
Methods A total of 160 pediatric patients undergoing cardiac surgery with cardiopulmonary bypass (81 cyanotic, 79 acyanotic) were included in this single-blinded, randomized trial at a tertiary care university-affiliated teaching hospital. Eighty-one children (41 cyanotic, 40 acyanotic) were randomly assigned to a TXA group, in which they received 50 mg/kg of TXA as a bolus followed by 15 mg/kg/h infusion and another 50 mg/kg into the bypass circuit. The other 79 patients were randomly assigned to a placebo group. The primary end point was the amount of 24-h blood loss.
Results The amount of 24-h blood loss was significantly less in the TXA group than in the placebo group [mean (95% confidence interval): 18.6 (15.8-21.4) vs. 23.5 (19.4-27.5) ml/kg, respectively; mean difference -4.9 (-9.7 to -0.01) ml/kg; p = 0.049]. This effect of TXA was already significant at 6 h [9.5 (7.5-11.5) vs. 13.2 (10.6-15.9) ml/kg, respectively; mean difference -3.47 (-7.0 to -0.4) ml/kg; p = 0.027]. However, there was no significant difference in the amount of blood transfusion between the groups. There was also no statistical difference in the effect of TXA in each cyanotic and acyanotic subgroup.
Conclusion TXA can reduce blood loss in pediatric cardiac surgery but not the transfusion requirement (http://ClinicalTrials.gov number NCT00994994).

DOI： 10.1007/s00540-011-1235-z

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肺高血圧を呈し心房中隔欠損症を持つ非代償性肝硬変症例に対する生体肝移植周術期管理経験

松三絢弥, 小坂順子, 賀来隆治, 森松博史, 森田潔

日本臨床麻酔学会誌 31 ( 6 ) S429 - S429 2011年10月

Two cases of variceal haemorrhage during living-donor liver transplantation

T. Matsusaki, H. Morimatsu, T. Sato, J. Matsumi, N. Okazaki, Y. Umeda, K. Morita

BRITISH JOURNAL OF ANAESTHESIA 106 ( 4 ) 537 - 539 2011年4月

記述言語：英語出版者・発行元：OXFORD UNIV PRESS

Some patients with cirrhosis experience rupture of venous varices before operation, and liver transplantation is a therapy of last resort for these patients. However, we have experienced two cases of intraoperative rupture in whom no abnormalities of the venous varices were seen on endoscopy before operation. One patient with ruptured gastrointestinal varices was treated by direct surgical ligation and the other with ruptured oesophageal gastric varices, spontaneously recovered with a Sengstaken-Blakemore tube. These cases suggest that acute variceal haemorrhage should always be considered as a possibility during living-donor liver transplantation in patients with a history of upper gastrointestinal bleeding. Careful observation of the nasogastic tube is important during clamping of the hepatic portal vein.

DOI： 10.1093/bja/aer008

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Tetrastarch for fluid resuscitation in septic shock: Good news for the kidneys?

Takashi Matsusaki, Hiroshi Morimatsu

CRITICAL CARE MEDICINE 39 ( 4 ) 905 - 906 2011年4月

Pituitary apoplexy precipitating diabetes insipidus after living donor liver transplantation

Takashi Matsusaki, Hiroshi Morimatsu, Junya Matsumi, Hiroaki Matsuda, Tetsufumi Sato, Kenji Sato, Satoshi Mizobuchi, Takahito Yagi, Kiyoshi Morita

JOURNAL OF ANESTHESIA 25 ( 1 ) 108 - 111 2011年2月

記述言語：英語出版者・発行元：SPRINGER TOKYO

Pituitary apoplexy occurring after surgery is a rare but life-threatening acute clinical condition that follows extensive hemorrhagenous necrosis within a pituitary adenoma. Pituitary apoplexy has been reported to occur spontaneously in the majority of cases or in association with various inducing factors. Reported is a case of pituitary apoplexy complicated by diabetes insipidus following living donor liver transplantation (LDLT). To the best of our knowledge, this has not been previously reported. A 56-year-old woman with nonalcoholic steatohepatitis underwent LDLT from her daughter. The patient also required dopamine support and transfusions because of massive intraoperative bleeding. Postoperatively, her coagulopathy continued, and she underwent a second laparotomy because of unknown bleeding on postoperative day 7, when she needed transfusions and dopamine support to maintain her vital signs. She complained of severe headache, excessive thirst, frequent urination, and diplopia from postoperative day 10. She also had polyuria greater than 300 ml/h and was diagnosed with pituitary apoplexy precipitating diabetes insipidus on postoperative day 13. She was treated conservatively without surgery because of the hormonally inactive status and slight mass effect of her tumor. It is important for anesthesiologists and critical care personnel in LDLT settings to take into consideration this complication as a differential diagnosis.

DOI： 10.1007/s00540-010-1070-7

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生体肝移植術後に急激な凝固異常を認めたアラジール症候群の1例

小坂順子, 森松博史, 松三絢弥, 林真雄, 賀来隆治, 佐藤哲文, 森田潔

日本集中治療医学会雑誌 18 ( Suppl. ) 360 - 360 2011年1月

生体肝移植後肝腎不全にて持続濾過透析中の高カルシウム血症の検討ケースコントロール研究

松三絢弥, 森松博史, 小坂順子, 賀来隆治, 佐藤哲文, 森田潔

日本集中治療医学会雑誌 18 ( Suppl. ) 369 - 369 2011年1月

Ⅱ.集中治療からみた薬剤とエビデンス-ステロイドを考える 2.ドパミンの在り方.

森松博史, 森田潔

Modern Physician 31 ( 5 ) 610 - 613 2011年

Rapid Response System(RRS)RRS導入5年の実態からみえてきた課題メールの限界と起動基準の重要性.

森松博史, 丸山雅道

LiSA 18 ( 7 ) 692 - 694 2011年

食道癌術後の難治性発作性心房細動に対して塩酸ランジオロールを使用した7例の検討.

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

日本集中治療医学会雑誌 18 ( 2 ) 215 - 220 2011年

記述言語：日本語出版者・発行元：(一社)日本集中治療医学会

術後の発作性心房細動の発生は、ICUや病院滞在日数、医療費の増加につながることが報告されており、その管理は重要である。我々は、食道癌術後に難治性の発作性心房細動を合併し、短時間作用型β1選択的遮断薬である塩酸ランジオロールを使用した7例を経験した。症例は51〜87歳で、いずれも男性であった。複数の抗不整脈薬が無効であり、塩酸ランジオロール投与を開始した。初期の急速投与は行わず、4.3〜33.5μg/kg/minと低用量の範囲で開始し、投与前と投与1時間後の心拍数は平均153[140、167][95%信頼区間]/minから101[88、116]/min(P<0.0001)と有意な低下を認めた。平均血圧は88[78、94]mmHgから82[74、89]mmHg(P=0.37)と有意な変化を認めず、重症な低血圧に陥る症例もなかった。6例では投与開始24時間以内に洞調律に回復した。複数の抗不整脈薬に抵抗性の食道癌術後発作性心房細動に対する低用量の塩酸ランジオロール投与は、大きな血圧の低下なく心拍数の安定をもたらした。(著者抄録)

DOI： 10.3918/jsicm.18.215

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その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2011&ichushi_jid=J02874&link_issn=&doc_id=20110422460012&doc_link_id=20110422460001%2C20111017450026&url=http%3A%2F%2Fsearch.jamas.or.jp%2Flink%2Fbc%2F20110422460001%2C20111017450026&type=jamaslink&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F99999_1.gif

特集周術期輸液・輸血管理のup-to-date アルブミン.

森松博史, 守屋佳恵, 谷真規子, 森田潔

ICUとCCU 35 ( 4 ) 285 - 289 2011年

医療ガスと中枢神経系毒ときどき薬一酸化炭素.

高橋徹, 森松博史, 川西進, 清水裕子, 森田潔

Medical Gases 13 ( 1 ) 24 - 26 2011年

低濃度一酸化炭素吸入は自然免疫系の活性を抑制してラット出血性ショック後の急性肺障害を軽減する.

川西進, 高橋徹, 清水裕子, 小坂順子, 森松博史, 松三昌樹, 森田潔

エンドトキシン・自然免疫研究 14 70 - 74 2011年

急性腎障害（AKI）の診療３．集中治療領域におけるAKI.

森松博史, 森田潔

Modern Physician 31 ( 1 ) 13 - 16 2011年

An increase in exhaled CO concentration in systemic inflammation/sepsis

Hiroshi Morimatsu, Toru Takahashi, Takashi Matsusaki, Masao Hayashi, Jyunya Matsumi, Hiroko Shimizu, Masaki Matsumi, Kiyoshi Morita

JOURNAL OF BREATH RESEARCH 4 ( 4 ) 47103 - 47103 2010年12月

記述言語：英語出版者・発行元：IOP PUBLISHING LTD

Despite recent progress in Critical Care Medicine, sepsis is still a major medical problem with a high rate of mortality and morbidity especially in intensive care units. Oxidative stress induced by inflammation associated with sepsis causes degradation of heme protein, increases microsomal free heme content, promotes further oxidative stress and results in cellular and organ damage. Heme-oxygenase-1 (HO-1) is a rate-limiting enzyme for heme breakdown. HO-1 breaks down heme to yield CO, iron and biliverdin. Measurement of CO in exhaled air may potentially be useful in monitoring changes in HO enzyme activity in vivo, which might reflect the degree of inflammation or oxidative stress in patients with systemic inflammation. The increased exhaled CO concentrations were observed after anesthesia/surgery, in critically ill patients and also in systemic inflammation/sepsis. Some reports also showed that exhaled CO concentration is related to mortality. Further studies are needed to elucidate whether increased endogenous CO production may predict a patient's morbidity and mortality. Techniques for monitoring CO are continuously being refined and this technique may find its way into the office of clinicians.

DOI： 10.1088/1752-7155/4/4/047103

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LONG TERM OUTOCOME IN CHILDREN WITH CONGENITAL HEART DISEASE WHO SUFFERED FROM ACUTE KIDNEY INJURY DURING POSTOPERATIVE ICU STAY

Yuichiro Toda, Tatsuo Iwasaki, Kazuyoshi Shimizu, Tomohiko Suemori, Noriko Ishii, Hirokazu Kawase, Kentaro Sugimoto, Moritoki Egi, Hiroshi Morimatsu, Kiyoshi Morita

CRITICAL CARE MEDICINE 38 ( 12 ) U188 - U188 2010年12月

Responses to surgical stress after esophagectomy Gene expression of heat shock protein 70, toll-like receptor 4, tumor necrosis factor-α and inducible nitric oxide synthase

Suzuki S, Morimatsu H, Omori E, Shimizu H, Takahashi H, Yamatsuji T, Naomoto Y, Morita K

Mol Med Rep 3 ( 5 ) 765 - 769 2010年9月

Thrombotic microangiopathy after living-donor liver re-transplantation

Takashi Matsusaki, Hiroshi Morimatsu, Tetsufumi Sato, Kenji Sato, Satoshi Mizobuchi, Kiyoshi Morita

JOURNAL OF ANESTHESIA 24 ( 4 ) 614 - 617 2010年8月

記述言語：英語出版者・発行元：SPRINGER TOKYO

Thrombotic microangiopathy (TMA) is a rare but potentially lethal complication encountered in solid organ and bone marrow transplant recipients that requires rapid recognition, diagnosis, and initiation of therapy. Several causes have been identified, including viral infections and various medications. We report a case of TMA after living-donor liver transplantation (LDLT). A 60-year-old man underwent LDLT for end-stage liver disease secondary to hepatitis C virus. After 6 months, he required re-transplantation because graft failure was caused by a small-for-size graft. The immunosuppressive regimen for the second transplantation consisted of tacrolimus and prednisolone; cyclosporine (CsA), mycophenolate mofetil, and prednisolone had been used for the first transplantation. Despite multiple transfusions of packed red blood cells and concentrated platelets, his hemoglobin and platelets decreased and lactate dehydrogenase increased following re-transplantation. Hematological evaluation revealed findings consistent with TMA. As soon as TMA was diagnosed, the calcineurin inhibitor (CNI) was changed from tacrolimus to CsA, and fresh frozen plasma (FFP) was given. The patient's platelets gradually increased after the CNI was changed, and no transfusions were needed. Therefore, tacrolimus was suspected as the cause of the patient's TMA. Early diagnosis, switching CNIs, and FFP supplementation allowed the TMA to resolve without the need for plasma exchange.

DOI： 10.1007/s00540-010-0953-y

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Protective Effect of Carbon Monoxide Inhalation on Lung Injury After Hemorrhagic Shock/Resuscitation in Rats

Fumitoshi Kanagawa, Toru Takahashi, Kazuyoshi Inoue, Hiroko Shimizu, Emiko Omori, Hiroshi Morimatsu, Shigeru Maeda, Hiroshi Katayama, Atsunori Nakao, Kiyoshi Morita

JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE 69 ( 1 ) 185 - 194 2010年7月

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

Background: Hemorrhagic shock and resuscitation (HSR) induces pulmonary inflammation that leads to acute lung injury. Carbon monoxide (CO), a by-product of heme catalysis, was shown to have potent cytoprotective and anti-inflammatory effects. The aim of this study was to examine the effects of CO inhalation at low concentration on lung injury induced by HSR in rats.
Methods: Rats were subjected to HSR by bleeding to achieve mean arterial pressure of 30 mm Hg for 60 minutes followed by resuscitation with shed blood and saline as needed to restore blood pressure. HSR animals were either maintained in room air or were exposed to CO at 250 ppm for 1 hour before and 3 hours after HSR.
Results: HSR caused an increase in the DNA binding activity of nuclear factor-kappa B and activator protein-1 in the lung followed by the up-regulation of pulmonary gene expression of tumor necrosis factor-alpha, inducible nitric oxide synthase, and interleukin (IL)-10. HSR also resulted in an increase in myeloperoxidase activity and wet weight to dry weight ratio in the lung, and more prominent histopathologic changes including congestion, edema, cellular infiltration, and hemorrhage. In contrast, CO inhalation significantly ameliorated these inflammatory events as judged by fewer histologic changes, less up-regulation of inflammatory mediators, and less activation of nuclear factor-kappa B and activator protein-1. Interestingly, the protective effects against lung injury afforded by CO were associated with further increases in mRNA expression of IL-10 in the lung.
Conclusions: These findings suggest that inhaled CO at a low concentration ameliorated HSR-induced lung injury and attenuated inflammatory cascades by up-regulation of anti-inflammatory IL-10.

DOI： 10.1097/TA.0b013e3181bbd516

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Role of heme oxygenase-1 in protection of the kidney after hemorrhagic shock

Yutaka Arimori, Toru Takahashi, Hiroyuki Nishie, Kazuyoshi Inoue, Hiroko Shimizu, Emiko Omori, Susumu Kawanishi, Yuichiro Toda, Hiroshi Morimatsu, Kiyoshi Morita

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 26 ( 1 ) 27 - 32 2010年7月

記述言語：英語出版者・発行元：SPANDIDOS PUBL LTD

Hemorrhagic shock followed by resuscitation (HSR) causes oxidative stress, which results in multiple organ damage. The kidney is one of the target organs of HSR-mediated oxidative tissue injury. Heme oxygenase (HO)-1, the rate-limiting enzyme in heme catabolism, is induced by oxidative stress; it protects against oxidative tissue injuries. The aim of the present study was to examine the role of renal HO-1 induction after HSR. Rats were subjected to hemorrhagic shock to achieve a mean arterial pressure of 30 mmHg for 60 min, followed by resuscitation with the shed blood. HSR resulted in a significant increase in functional HO-1 protein in the tubular epithelial cells of the kidney, whereas HSR resulted in only a slight increase in gene expression of tumor necrosis factor (TNE)-alpha and inducible nitric oxide synthase (iNOS), and in protein expression of activated caspase-3 solely in renal cells where HO-1 expression was absent. HSR also resulted in a significant increase in Bcl-2 gene expression. Pretreatment of HSR animals with tin-mesoporphyrin (0.5 mu mol/kg), a specific competitive inhibitor of HO activity, resulted in a significant decrease in HO activity and exacerbated tissue inflammation and apoptotic cell death as judged by the marked increase in expression of TNF-alpha and iNOS, and in activated caspase-3-positive cells, and the significant reduction in Bcl-2 expression, respectively. These findings indicate that HO-1 induction is an adaptive response to HSR-induced oxidative stress and is essential for protecting tubular epithelial cells from oxidative damage through its anti-inflammatory and anti-apoptotic properties.

DOI： 10.3892/ijmm_00000430

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