Department of Anesthesiology and Resuscitology

望月 利昭

モチヅキ トシアキ  (Toshiaki Mochizuki)

基本情報

所属
藤田医科大学医学部 麻酔・蘇生学講座(岡崎医療センター) 教授
学位
博士(医学)(1999年7月 浜松医科大学)

研究者番号
40293641
ORCID ID
 https://orcid.org/0000-0001-8645-5775
J-GLOBAL ID
200901056991259388
Researcher ID
B-5432-2012
researchmap会員ID
6000004476

外部リンク

麻酔科医/集中治療医/救急科医です。

主要な委員歴

 5

主要な論文

 15
  • Manzo Suzuki, Junpei Shibata, Toshiaki Mochizuki, Hiroyasu Bito
    Langenbeck's Archives of Surgery 408(1) 337 2023年8月26日  査読有り
  • Yoshiaki Takahashi, Takeji Saitoh, Misaki Okada, Hiroshi Satoh, Toshiya Akai, Toshiaki Mochizuki, Hironao Hozumi, Masao Saotome, Tsuyoshi Urushida, Hideki Katoh, Hideharu Hayashi, Atsuto Yoshino
    Hong Kong Journal of Emergency Medicine 26(2) 106-110 2018年  査読有り
  • Shuchun Yu, Toshiaki Mochizuki, Takasumi Katoh, Hiroshi Makino, Yuya Kawashima, Soichiro Mimuro, Shigehito Sato
    SPRINGERPLUS 3 371 2014年7月  査読有り責任著者
    Background: Hypocapnia induced following the accidental intravenous infusion of a local anesthetic can mitigate anesthetic toxicity, but the effects of hypocapnia induced prior to local anesthetic infusion are unknown. In this study, we examined the effects of prior hypocapnia on bupivacaine-induced cardiotoxicity in rats. Methods: Eighteen Sprague-Dawley rats were randomly divided into two groups: one receiving sevoflurane with normal ventilation (Control Group) and the other receiving sevoflurane with hyperventilation to induce hypocapnia (Hypocapnia Group). After 30 min, both groups received continuous intravenous infusions of 0.25% bupivacaine at 2 mg . kg(-1) . min(-1). The time taken to reach 25% and 50% reductions in heart rate (HR; HR-25%, HR-50%) and mean arterial pressure (MAP; MAP-25%, MAP-50%) from the start of bupivacaine infusion were recorded. The difference between HR-25% and MAP-25% was calculated. The times of the first ventricular premature beat (VPB) and final systole were also recorded. Results: In the Hypocapnia Group, HR-50%, MAP-25%, and MAP-50% were prolonged compared with the Control Group (P < 0.001). Furthermore, the interval between HR-25% and MAP-25% and the times between the first VPB and final systole were prolonged in the Hypocapnia Group (P < 0.001). Conclusion: In rats under sevoflurane anesthesia, prior hypocapnia delayed the onset of bupivacaine-induced cardiotoxicity. Prior hypocapnia should be avoided during continuous bupivacaine nerve block under general anesthesia, because it may delay the detection of cardiotoxicity.
  • Toshiaki Mochizuki, Qiliang Jiang, Takasumi Katoh, Katsunori Aoki, Shigehito Sato
    Shock 39(6) 527-532 2013年6月  査読有り責任著者
  • Toshiaki Mochizuki, Yoshinori Kamio, Seiji Hosokawa, Tetsuro Kimura, Atsuto Yoshino
    American Journal of Emergency Medicine 31(2) 463.e3-5 2013年  査読有り責任著者
  • Toshiaki Mochizuki, Shuchun Yu, Takasumi Katoh, Katsunori Aoki, Shigehito Sato
    Resuscitation 83(2) 238-242 2012年2月  査読有り責任著者
  • Toshiaki Mochizuki, Shigehito Sato
    CANADIAN JOURNAL OF ANAESTHESIA-JOURNAL CANADIEN D ANESTHESIE 55(12) 836-846 2008年12月  査読有り責任著者
    Purpose: Systemic alkalinization is recommended for resuscitation from local anesthetic-induced cardiotoxicity. It has been suggested that inducing hypocapnic alkalosis, prior to exposure to toxic concentrations of local anesthetics, may minimize cardiotoxicity. However, it remains unclear whether inducing severe hypocapnic alkalosis after administration of local anesthetics will minimize the duration of bradycardia. We used isolated rat hearts to investigate the effects of hypocapnic alkalosis on heart rate (HR) recovery from bupivacaine or levobupivacaine-induced bradycardia. Methods: We measured the time required for the HR in 24 isolated rat hearts, respectively, to attain 90% of the baseline HR (recovery time) following bradycardia induced by 1 mu g.mL(-1) and 10 mu g.mL(-1) concentrations of either bupivacaine or levobupivacaine. Normal pH perfusate (bupivacaine or levobupivacaine with normal pH washout groups) or severe hypocapnic alkalosis perfusate (bupivacaine or levobupivacaine with hypocapnic alkalosis washout groups) were reperfused after exposure to the local anesthetics. Results: Severe hypocapnic alkalosis prolonged the recovery time from 273 coproduct 122 sec, at the 1 mu g.mL(-1) bupivacaine concentration with normal pH washout, to 1203 coproduct 540 sec, in the bupivacaine with hypocapnic alkalosis washout (P = 0.029). Severe hypocapnic alkalosis also prolonged the recovery time from 1153 +/- 644 sec, at a 10 mu g.mL(-1) bupivacaine concentration in the normal pH washout group, to 2065 +/- 617 sec, in the bupivacaine with hypocapnic alkalosis washout group (P = 0.032). With levobupivacaine 10 mu g.mL(-1) in the normal pH washout group, HR recovery time increased from 863 +/- 186 sec to 1565 +/- 567 sec, compared to the hypocapnic alkalosis washout group (P = 0.045). Conclusions: Severe hypocapnic alkalosis prolonged the recovery time from bupivacaine or levobupivacaine-induced bradycardia in isolated rat hearts. When bradycardia occurs after intravascular bupivacaine or levobupivacaine administration, maintenance of normocapnia may minimize the duration of bradycardia.
  • Yue Hui, Toshiaki Mochizuki, Kazunao Kondo, Kazuo Umemura, Shigehito Sato
    JOURNAL OF ANESTHESIA 22(3) 229-235 2008年8月  査読有り責任著者
    Purpose. Our purpose was to investigate whether the NO donor, 3-(2-hydroxy-1-methyl-2-nitroso-hydrazino)-N-methyl-1-propanamine (NOC7), restored cardiac function following global ischemia in an isolated rat heart model and whether intracellular messengers were involved in its effect. Methods. Isolated rat hearts (n = 36) were randomly divided into six groups. The sham control group was perfused with modified Krebs-Henseleit bicarbonate buffer (KHB) alone. The ischemic control group and the NOC7 groups were subjected to 35 min of global ischemia, followed by 30 min of reperfusion with KHB alone, or reperfusion with KHB including NOC7 at 0.2, 2, 20, or 200 mu M, respectively. Left ventricular developed pressure (LVDP), the maximum and the minimal rate of rise in LVP (+/- dP/dt), and coronary flow were measured continuously. Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) levels were measured in myocardium homogenate, using enzyme immunoassay (EIA) methods. Results. NOC7 at 2 and 20 mu M rescued myocardial performance (LVDP, 111.9 +/- 10.5% and 124.3 +/- 12.5% of baseline, respectively; P < 0.05 vs ischemic control) at 30 min after reperfusion. However, NOC7 at 200 mu M reduced the LVDP to 55.3 +/- 6.0% of baseline. Coronary flows remain unchanged. The cAMP levels increased significantly from 0.83 +/- 0.44 pmol.mg(-1) protein in the ischemic control group to 1.79 +/- 0.39, 1.86 +/- 0.25, and 2.63 +/- 0.24 pmol.mg(-1) protein, in the groups with NOC7 at 2, 20, and 200 mu M, respectively (P < 0.05). The cGMP level increased from 1.49 +/- 0.61 pmol.mg(-1) protein in the ischemic control group to 3.92 +/- 0.66 pmol.mg(-1) protein in the group with NOC7 at 200 mu M alone (P < 0.05). Conclusion. NOC7 appeared to exert a biphasic effect on the contractile force of the isolated rat heart after 35-min global ischemia. The balance between intracellular cAMP and cGMP levels seemed to be involved in its mechanism.
  • T Mochizuki, PJ Olson, F Szlam, JG Ramsay, JH Levy
    ANESTHESIA AND ANALGESIA 87(4) 781-785 1998年10月  査読有り
    Bleeding after cardiopulmonary bypass (CPB) is related to multiple factors. Excess protamine weakens clot structure and decreases platelet function; therefore, an increased activated clotting time (ACT) after protamine reversal of heparin may be misinterpreted as residual heparin anticoagulation. We evaluated the effects of protamine, recombinant platelet factor 4 (rPF4), and hexadimethrine on ACT in blood obtained after CPB. Ln addition, we examined the effect of protamine on in vitro platelet aggregation. Incremental doses of protamine, rPF4, and hexadimethrine were added to heparinized blood from CPB, and ACTs were performed. Incremental concentrations of protamine were added to heparinized platelet-rich plasma, and aggregometry was induced by adenosine diphosphate (ADP) and collagen. The mean heparin concentration at the end of CPB was 3.3 U/mL. Protamine to heparin ratios >1.3:1 produced a significant prolongation of the ACT that was not seen with rPF4 and was observed only with 5:1 hexadimethrine to heparin ratios. ADP-induced platelet aggregation was reduced with protamine administration greater than or equal to 1.3:1. Excessive protamine reversal of heparin prolongs ACT and alters ADP-induced platelet aggregation in a dose-dependent manner in vitro. Additional protamine administered to treat a prolonged ACT may further increase clotting time, reduce platelet aggregation, and potentially contribute to excess bleeding after CPB. Implications: We found that excess protamine prolonged the activated clotting time and altered platelet function after cardiopulmonary bypass, whereas heparin antagonists, such as recombinant platelet factor 4 and hexadimethrine, exhibited a wider therapeutic range without adversely affecting the activated clotting time. Approaches to avoid excess protamine or use of alternative heparin antagonists after cardiopulmonary bypass may be beneficial.
  • BE Miller, T Mochizuki, JH Levy, JM Bailey, Tosone, SR, VKH Tam, KR Kanter
    ANESTHESIA AND ANALGESIA 85(6) 1196-1202 1997年12月  査読有り
    Coagulopathies in children after cardiopulmonary bypass (CPB) are complex. There are very limited data correlating coagulation tests with postoperative bleeding. We evaluated coagulation changes after CPB and after the administration of coagulation products to 75 children. Baseline coagulation tests were obtained and repeated after protamine administration, after transfusion of individual coagulation products, and on arrival in the intensive care unit (ICU). Regression analysis demonstrated no baseline coagulation test to predict postoperative chest tube drainage. Weight and duration of CPB were determined to be the only predictors of bleeding. Further analyses demonstrated that children <8 kg had more bleeding and required more coagulation products than children >8 kg. Postprotamine platelet count and fibrinogen level correlated independently with 24-h chest tube drainage in children <8 kg, whereas postprotamine platelet count and thrombelastographic values did so in patients weighing >8 kg. Platelet administration alone was found to restore effective hemostasis in many patients. With ongoing bleeding, cryoprecipitate improved coagulation parameters and limited blood loss. Fresh-frozen plasma administration after platelets worsened coagulation parameters and was associated with greater chest tube drainage and more coagulation product transfusions in the ICU. Objective data to guide post-CPB component therapy transfusion in children are suggested. Implications: Children <8 kg can be expected to have more severe coagulopathies, require more coagulation product transfusions, and bleed more after cardiopulmonary bypass. Correlations between coagulation tests and postoperative chest tube drainage are defined. Platelets and, if necessary, cryoprecipitate optimally restore hemostasis. Fresh-frozen plasma offers no benefits in correcting postcardiopulmonary bypass coagulopathies in children.

MISC

 81

書籍等出版物

 12
  • 望月 利昭 (担当:分担執筆, 範囲:心肺蘇生と脳保護)
    総合医学社 2017年1月 (ISBN: 9784883786497)
  • 望月 利昭 (担当:分担執筆, 範囲:心肺蘇生と脳保護(心停止後体温管理を中心に))
    総合医学社 2016年 (ISBN: 9784883786251)
  • 望月 利昭 (担当:分担執筆, 範囲:心肺蘇生と脳保護)
    総合医学社 2015年2月 (ISBN: 9784883788880)
  • 望月 利昭 (担当:分担執筆, 範囲:心肺蘇生と脳保護)
    総合医学社 2014年 (ISBN: 9784883788668)
  • 望月 利昭 (担当:分担執筆, 範囲:心肺蘇生と脳保護)
    総合医学社 2013年 (ISBN: 9784883788545)

講演・口頭発表等

 17

担当経験のある科目(授業)

 6

共同研究・競争的資金等の研究課題

 5