記述言語：英語   掲載種別：研究論文（学術雑誌）  

STUDY OBJECTIVE: It remains unclear whether it is the hypotension prediction index itself or goal-directed haemodynamic therapy that mitigates intraoperative hypotension. DESIGN: A single centre randomised controlled trial. SETTING: Sapporo Medical University Hospital. PATIENTS: A total of 64 adults patients undergoing major non-cardiac surgery under general anaesthesia. INTERVENTIONS: Patients were randomly assigned to either group receiving conventional goal-directed therapy (FloTrac group) or combination of the hypotension prediction index and conventional goal-directed therapy (HPI group). To investigate the independent utility of the index, the peak rates of arterial pressure and dynamic arterial elastance were not included in the treatment algorithm for the HPI group. MEASUREMENTS: The primary outcome was the time-weighted average of the areas under the threshold. Secondary outcomes were area under the threshold, the number of hypotension events, total duration of hypotension events, mean mean arterial pressure during the hypotension period, number of hypotension events with mean arterial pressure < 50 mmHg, amounts of fluids, blood products, blood loss, and urine output, frequency and amount of vasoactive agents, concentration of haemoglobin during the monitoring period, and 30-day mortality. MAIN RESULTS: The time-weighted average of the area below the threshold was lower in the HPI group than in the control group; 0.19 mmHg (interquartile range, 0.06-0.80 mmHg) vs. 0.66 mmHg (0.28-1.67 mmHg), with a median difference of -0.41 mmHg (95% confidence interval, -0.69 to -0.10 mmHg), p = 0.005. Norepinephrine was administered to 12 (40%) and 5 (17%) patients in the HPI and FloTrac groups, respectively (p = 0.045). No significant differences were observed in the volumes of fluid and blood products between the study groups. CONCLUSIONS: The current randomised controlled trial results suggest that using the hypotension prediction index independently lowered the cumulative amount of intraoperative hypotension during major non-cardiac surgery.

DOI： 10.1016/j.jclinane.2023.111348

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Remimazolam is a newly developed ultra-short-acting benzodiazepine that exerts sedative effects. This study aimed to clarify the effects of remimazolam on cardiac contractility. In a randomised-parallel group trial, haemodynamic parameters were compared between propofol (n = 11) and remimazolam (n = 12) groups during the induction of general anaesthesia in patients undergoing non-cardiac surgery. In a preclinical study, the direct effects of remimazolam on cardiac contractility were also evaluated using isolated rat hearts. RNA sequence data obtained from rat and human hearts were analysed to assess the expression patterns of the cardiac γ-aminobutyric acid type A (GABAA ) receptor subunits. In a clinical study, the proportional change of the maximum rate of arterial pressure rise was milder during the study period in the remimazolam group (propofol: -52.6 [10.2] (mean [standard deviation])% vs. remimazolam: -39.7% [10.5%], p = 0.007). In a preclinical study, remimazolam did not exert a negative effect on left ventricle developed pressure, whereas propofol did exert a negative effect after bolus administration of a high dose (propofol: -26.9% [3.5%] vs. remimazolam: -1.1 [6.9%], p < 0.001). Analysis of the RNA sequence revealed a lack of γ subunits, which are part of the major benzodiazepine binding site of the GABAA receptor, in rat and human hearts. These results indicate that remimazolam does not have a direct negative effect on cardiac contractility, which might contribute to its milder effect on cardiac contractility during the induction of general anaesthesia. The expression patterns of cardiac GABAA receptor subunits might be associated with the unique pharmacokinetics of benzodiazepines in the heart.

DOI： 10.1111/1440-1681.13840

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

INTRODUCTION: Myocardial ischemia/reperfusion (I/R) injury can cause additional damage to an ischemic myocardium, even after successful reperfusion therapy. Inflammation is a mechanism that exacerbates myocardial damage after I/R injury. Rikkunshito (RKT) is a traditional Japanese herbal medicine widely used to treat gastrointestinal symptoms. It attenuates inflammation and fibrosis in some diseases of the heart; however, it remains unclear whether RKT exerts cardioprotective effects against myocardial I/R injury. To elucidate this, we evaluated the effects of RKT pre-treatment by oral administration on the myocardium in a mouse model of in vivo I/R injury. METHODS: Mice were randomly assigned to a group receiving distilled water (DW) or one receiving RKT (1000 mg/kg/day) for 14 days orally. For each of the RKT and DW groups, a sham group, an I/R 2 h group, and an I/R 24 h group were created. On day 15, myocardial I/R surgery was performed. The left anterior descending coronary artery (LAD) was ligated for 30 min, and reperfusion time was set at 2 h or 24 h. The myocardial infarct size (IS) was measured after 2 h of reperfusion, and cardiac cytokine mRNA expression levels were evaluated by quantitative reverse transcription polymerase chain reaction (RT-PCR) after 2 h and 24 h of reperfusion. RESULTS: RKT pre-treatment significantly suppressed the cardiac mRNA expression level of interleukin-1β in the RKT-I/R 2 h group compared to the DW-I/R 2 h group (P < 0.05). Additionally, RKT significantly suppressed the mRNA expression levels of transforming growth factor-β compared to DW; the same result was obtained for the expression levels of interleukin-6. However, RKT did not reduce the IS or mRNA expression levels of the cardiac congestive markers natriuretic peptide a (NPPA) and natriuretic peptide b (NPPB). In addition, RKT did not alter the plasma concentration of ghrelin and sirtuin 1 (Sirt1), which have been reported to be stimulated by RKT. CONCLUSION: This study showed that pre-treatment of RKT for myocardial I/R injury partially suppressed inflammation-related cytokines. However, further studies are needed on the effect of RKT on the reduction of myocardial infarction size.

DOI： 10.7759/cureus.54485

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Dexmedetomidine (DEX), a highly selective alpha2-adrenoceptors agonist, is not only a sedative drug used during mechanical ventilation in the intensive care unit but also a cardio-protective drug against ischemia-reperfusion injury (IRI). Numerous preclinical in vivo and ex vivo studies, mostly evaluating the effect of DEX pretreatment in healthy rodents, have shown the efficacy of DEX in protecting the hearts from IRI. However, whether DEX can maintain its cardio-protective effect in hearts with comorbidities such as diabetes has not been fully elucidated. Multiple clinical trials have reported promising results, showing that pretreatment with DEX can attenuate cardiac damage in patients undergoing cardiac surgery. However, evidence of the post-treatment effects of DEX in clinical practice remains limited. In this narrative review, we summarize the previously reported evidence of DEX-induced cardio-protection against IRI and clarify the condition of the hearts and the timing of DEX administration that has not been tested. With further investigations evaluating these knowledge gaps, the use of DEX as a cardio-protective drug could be further facilitated in the management of patients undergoing cardiac surgery and might be considered in a broader area of clinical settings beyond cardiac surgery, including patients with acute myocardial infarction.

DOI： 10.1007/s00540-023-03261-w

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Background The aim of this retrospective observational study was to explore the early predictive parameters for maximum amplitudein the kaolin with heparinase (HKH) assay (MAHKH) of TEG6s Platelet Mapping in cardiovascular surgery including cardiopulmonary bypass (CPB) period. The relationship between each parameter of the assay and laboratory data was also assessed. Methods We included the patients who underwent TEG6s Platelet Mapping during cardiovascular surgery under CPB between November 2021 and May 2022. The correlation between MAHKH and the early parameters was assessed. The association between each parameter of Platelet Mapping and a combination of fibrinogen concentration > 150 mg/dL and platelet count > 100,000µL was also evaluated by the receiver operating characteristic (ROC) curve. Results In 23 patients who underwent TEG6s Platelet Mapping during the study period, 62 HKH assay data including 59 pairs of data (HKH assay and laboratory data) were analyzed. K and angle, but not R, were significantly correlated with MAHKH (r [95% CI]: -0.90 [-0.94, -0.83], p < 0.0001 for K, and 0.87 [0.79, 0.92], p < 0.0001 for angle). Furthermore, ROC curves suggested that these parameters predicted a combination of fibrinogen concentration > 150 mg/dL and platelet count > 100,000/µL with high accuracy. Similar results were confirmed in the heparinized blood samples obtained during CPB. Conclusion These findings suggest that not only MAKHK but also K and angle, which are early parameters in the HKH assay, provide clinically significant information that will facilitate rapid decision-making regarding coagulation strategies during cardiovascular surgery including the CPB period.

DOI： 10.7759/cureus.38044

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記述言語：英語  

WATCHMAN is a percutaneous left atrial appendage closure device that is implanted in patients who are unsuitable for anticoagulation therapy for atrial fibrillation. During WATCHMAN implantation, inducing apnea in the patient is preferable to allow stable deployment. We present three cases in which apneic oxygenation was employed to maintain oxygenation during apnea, and oxygen reserve index (ORiTM) was measured to evaluate its safety and efficacy. Oxygen was administered continuously via the endotracheal tube during apnea. During all four apneic events in three patients (mean duration of 356 seconds), the ORi values maintained above 0.24, which is generally considered the threshold of partial pressure of arterial oxygen (PaO2) > 100 mmHg. Transcutaneous oxygen saturation and PaO2 remained above 99% and 300 mmHg, respectively. There were no respiratory or circulatory complications during or after the surgery.

DOI： 10.4103/aca.aca_11_23

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

PURPOSE: The effects of remimazolam on autonomic nervous activity have not been elucidated. We investigated the differential effects of remimazolam and propofol on autonomic nervous activity during anesthesia induction. METHODS: Thirty patients were randomly divided into a remimazolam group or a propofol group for anesthesia induction. Hemodynamics and indices of heart rate variability were recorded before and after anesthesia. Low frequency power (LF; 0.04-0.15 Hz, ms2) and high frequency power (HF; 0.15-0.4 Hz, ms2) were calculated from power spectral density of heart rate variability. LF reflects both sympathetic and parasympathetic activities and HF reflects parasympathetic activity. To investigate the balance between sympathetic and parasympathetic activities, the normalized unit (%) of LF (LF nu) and that of HF (HF nu) were calculated. Changes in LF nu (ΔLF nu) before and after anesthesia (ΔLF nu = LF nu at awake-LF nu after anesthesia) were compared between the groups. RESULTS: Remimazolam and propofol decreased blood pressure and power spectral density of heart rate variability. Remimazolam did not change LF nu and HF nu, while propofol increased LF nu and decreased HF nu (P = 0.020). ΔLF nu in the remimazolam group (1.4 ± 23.6%) were less than that in the propofol group (19.3 ± 22.4%, P = 0.0415). CONCLUSION: Remimazolam and propofol decreased autonomic nervous activity during anesthesia induction. Remimazolam preserved the balance of sympathetic and parasympathetic activities, while propofol modulated it to sympathetic dominance.

DOI： 10.1007/s00540-022-03037-8

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Traumatic brain injury (TBI) initiates immune responses involving infiltration of monocyte-derived macrophages (MDMs) in the injured brain tissue. These MDMs play a key role in perioperative neurocognitive disorders (PNDs). We tested the hypothesis that preanesthetic treatment with dexmedetomidine (DEX) could suppress infiltration of MDMs into the hippocampus of TBI model mice, ameliorating PND. METHODS: We first performed bone marrow transplantation from green fluorescent protein-transgenic mice to C57BL/6 mice to identify MDMs. We used only male mice for homogeneity. Four weeks after transplantation, a controlled cortical impact model of TBI was created using recipient mice. Four weeks after TBI, mice received pretreatment with DEX before general anesthesia (GA). Mice performed the Barnes maze test (8-12 mice/group) 2 weeks after GA and were euthanized for immunohistochemistry (4-5 mice/group) or immunoblotting (7 mice/group) 4 weeks after GA. RESULTS: In Barnes maze tests, TBI model mice showed longer primary latency (mean difference, 76.5 [95% confidence interval, 41.4-111.6], P < .0001 versus Naïve), primary path length (431.2 [98.5-763.9], P = .001 versus Naïve), and more primary errors (5.7 [0.62-10.7], P = .017 versus Naïve) than Naïve mice on experimental day 3. Expression of MDMs in the hippocampus was significantly increased in TBI mice compared to Naïve mice (2.1 [0.6-3.7], P = .003 versus Naïve). Expression of monocyte chemotactic protein-1 (MCP1)-positive areas in the hippocampus was significantly increased in TBI mice compared to Naïve mice (0.38 [0.09-0.68], P = .007 versus Naïve). Immunoblotting indicated significantly increased expression of interleukin-1β in the hippocampus in TBI mice compared to Naïve mice (1.59 [0.08-3.1], P = .035 versus Naïve). In contrast, TBI mice pretreated with DEX were rescued from these changes and showed no significant difference from Naïve mice. Yohimbine, an α2 receptor antagonist, mitigated the effects of DEX (primary latency: 68.3 [36.5-100.1], P < .0001 versus TBI-DEX; primary path length: 414.9 [120.0-709.9], P = .0002 versus DEX; primary errors: 6.6 [2.1-11.2], P = .0005 versus TBI-DEX; expression of MDMs: 2.9 [1.4-4.4], P = .0001 versus TBI-DEX; expression of MCP1: 0.4 [0.05-0.67], P = .017 versus TBI-DEX; expression of interleukin-1β: 1.8 [0.34-3.35], P = .01 versus TBI-DEX). CONCLUSIONS: Preanesthetic treatment with DEX suppressed infiltration of MDMs in the hippocampus and ameliorated PND in TBI model mice. Preanesthetic treatment with DEX appears to suppress infiltration of MDMs in the hippocampus and may lead to new treatments for PND in patients with a history of TBI.

DOI： 10.1213/ANE.0000000000005699

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Background: Ischemia-reperfusion injury (IRI) is one of the major risk factors implicated in morbidity and mortality associated with cardiovascular disease. During cardiac ischemia, the build-up of acidic metabolites results in decreased intracellular and extracellular pH that can reach as low as 6.0-6.5. The resulting tissue acidosis exacerbates ischemic injury and significantly impacts cardiac function. Methods: We used genetic and pharmacological methods to investigate the role of acid sensing ion channel 1a (ASIC1a) in cardiac IRI at the cellular and whole organ level. Human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) as well as ex vivo and in vivo models of IRI were used to test the efficacy of ASIC1a inhibitors as pre- and post-conditioning therapeutic agents. Results: Analysis of human complex trait genetics indicate that variants in the ASIC1 genetic locus are significantly associated with cardiac and cerebrovascular ischemic injuries. Using hiPSC-CMs in vitro and murine ex vivo heart models, we demonstrate that genetic ablation of ASIC1a improves cardiomyocyte viability after acute IRI. Therapeutic blockade of ASIC1a using specific and potent pharmacological inhibitors recapitulates this cardioprotective effect. We used an in vivo model of myocardial infarction (MI) and two models of ex vivo donor heart procurement and storage as clinical models to show that ASIC1a inhibition improves post-IRI cardiac viability. Use of ASIC1a inhibitors as pre- or post-conditioning agents provided equivalent cardioprotection to benchmark drugs, including the sodium-hydrogen exchange inhibitor zoniporide. At the cellular and whole organ level, we show that acute exposure to ASIC1a inhibitors has no impact on cardiac ion channels regulating baseline electromechanical coupling and physiological performance. Conclusions: Collectively, our data provide compelling evidence for a novel pharmacological strategy involving ASIC1a blockade as a cardioprotective therapy to improve the viability of hearts subjected to IRI.

DOI： 10.1161/CIRCULATIONAHA.121.054360

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

OBJECTIVES: The association of preoperative RV function with hemodynamics during OPCAB or emergency conversion is not clear. The aim of this study was to investigate the association of vasoactive-inotropic score with tricuspid annular plane systolic excursion and tricuspid regurgitation in off-pump coronary artery bypass grafting, and to calculate the optimal cut-off value of tricuspid annular plane systolic excursion to predict emergency conversion to cardiopulmonary bypass. METHODS: Patients over 20 years of age who had undergone off-pump coronary artery bypass grafting between April 2015 and March 2020 were enrolled in this study. We retrospectively assessed the association of intraoperative maximum "vasoactive-inotropic score", a weighted sum of various inotropes and vasoconstrictors, with tricuspid annular plane systolic excursion and tricuspid regurgitation. A receiver operating characteristic curve of conversion on tricuspid annular plane systolic excursion was also constructed. RESULTS: 135 patients were included in final analysis. Conversion was performed in 10 cases. Multiple regression analysis showed that tricuspid annular plane systolic excursion, mild or more tricuspid regurgitation and experienced surgeon were significantly related to vasoactive-inotropic score. The receiver operating characteristic curve to predict conversion by tricuspid annular plane systolic excursion showed an optimal cut-off value of 15.0 mm and area under the curve of 0.808. CONCLUSIONS: Tricuspid annular plane systolic excursion and tricuspid regurgitation were associated with vasoactive-inotropic score in off-pump coronary artery bypass grafting. The optimal cut-off value of tricuspid annular plane systolic excursion to predict emergency conversion was 15 mm.

DOI： 10.1007/s11748-020-01557-2

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1097/EJA.0000000000001358

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Cerebrospinal fluid drainage (CSFD) is recommended as a spinal cord protective strategy in open and endovascular thoracic aortic repair. Although small studies support the use of CSFD, systematic reviews have not suggested definite conclusion and a large-scale study is needed. Therefore, we reviewed medical records of patients who had undergone descending and thoracoabdominal aortic repair (both open and endovascular repair) at multiple institutions to assess the association between CSFD and postoperative motor deficits. METHODS: Patients included in this study underwent descending or thoracoabdominal aortic repair between 2000 and 2013 at 12 hospitals belonging to the Japanese Association of Spinal Cord Protection in Aortic Surgery. We conducted a retrospective study to investigate whether motor-evoked potential monitoring is effective in reducing motor deficits in thoracic aortic aneurysm repair. We use the same dataset to examine whether CSFD reduces motor deficits after propensity score matching. RESULTS: We reviewed data from 1214 patients [open surgery, 601 (49.5%); endovascular repair, 613 (50.5%)]. CSFD was performed in 417 patients and not performed in the remaining 797 patients. Postoperative motor deficits were observed in 75 (6.2%) patients at discharge. After propensity score matching (n = 700), mixed-effects logistic regression performed revealed that CSFD is associated with postoperative motor deficits at discharge [adjusted odds ratio (OR), 3.87; 95% confidence interval (CI), 2.30-6.51]. CONCLUSION: CSFD may not be effective for postoperative motor deficits at discharge.

DOI： 10.1007/s00540-020-02857-w

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Background: Chronic and/or intermittent exposure to hypobaric hypoxia reportedly exerts cardioprotective effects against ischemia-reperfusion injury. However, few studies have focused on the cardioprotective effects of acute and/or short-term hypobaric and hypoxic exposures. This study investigated the effects of acute hypobaric hypoxia on myocardial ischemia-reperfusion injury. Materials and Methods: Rats were assigned to groups receiving normobaric normoxia (NN group), hypobaric hypoxia (HH group), or normobaric hypoxia (NH group). HH group rats were exposed to 60.8 kPa and 12.6% fraction of inspired oxygen in a hypobaric chamber for 6 h. NH group rats were exposed to hypoxic conditions under normal pressure. After each exposure, 30 min of myocardial ischemia was followed by 60 min of reperfusion. Cardiac function and infarct size were determined after reperfusion. Expression of hypoxia-inducible factor 1 alpha (HIF1α) was also measured. Results: Cardiac function was better preserved in the HH and NH groups than in the NN group (p < 0.01 each). Median infarct size/area at risk was significantly lower in the HH group (50%, interquartile range [IQR] 48-54%; p < 0.01 vs. NN group) and NH group (45%, IQR 36-50%; p < 0.01 vs. NN group) than in the NN group (72%, IQR 69-75%). HIF1α expression was significantly higher in the HH group (p < 0.05 vs. NN group) and NH group (p < 0.01 vs. NN group) than in the NN group. Conclusions: Exposure to acute and/or short-term hypobaric and hypoxic conditions might exert cardioprotective effects against myocardial ischemia-reperfusion injury via HIF1α modulation.

DOI： 10.1155/2021/6617374

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Wolters Kluwer Medknow Publications  

DOI： 10.4103/aca.ACA_69_19

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Inflationary noninvasive blood pressure (iNIBP) monitoring can determine BP in a shorter time compared to conventional deflationary NIBP (dNIBP) monitoring. We assessed the efficacy of iNIBP monitoring during induction of general anaesthesia and tracheal intubation, which can cause rapid changes in haemodynamics. Our study included 14 surgery patients receiving tracheal intubation under general anaesthesia. Blood pressure was continuously measured using iNIBP monitoring. We recorded the percentage of successful iNIBP monitoring (measurements made without switching to dNIBP mode) during anaesthesia induction. We obtained 326 BP-measurements from 14 patients. The iNIPB mode was able to perform 90.9% of the measurements during the induction of general anaesthesia. iNIBP could determine BP even during periods of high blood pressure variability (31.6% [interquartile range; 22-40]). Our results validate the utility of iNIBP monitoring during the induction period of general anaesthesia, despite the rapid haemodynamic changes.

DOI： 10.1177/1750458920957917

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Remote ischemic preconditioning (RIPC) offers cardioprotection against myocardial ischemia-reperfusion injury. The humoral factors involved in RIPC that are released from parasympathetically innervated organs have not been identified. Previous studies showed that ghrelin, a hormone released from the stomach, is associated with cardioprotection. However, it is unknown whether or not ghrelin is involved in the mechanism of RIPC. This study aimed to determine whether ghrelin serves as one of the humoral factors in RIPC. RIPC group rats were subjected to three cycles of ischemia and reperfusion for 5 min in two limbs before left anterior descending (LAD) coronary artery ligation. Unacylated ghrelin (UAG) group rats were given 0.5 mcg/kg UAG intravenously 30 min before LAD ligation. Plasma levels of UAG in all groups were measured before and after RIPC procedures and UAG administration. Additionally, JAK2/STAT3 pathway inhibitor (AG490) was injected in RIPC and UAG groups to investigate abolishment of the cardioprotection of RIPC and UAG. Plasma levels of UAG, infarct size and phosphorylation of STAT3 were compared in all groups. Infarct size was significantly reduced in RIPC and UAG groups, compared to the other groups. Plasma levels of UAG in RIPC and UAG groups were significantly increased after RIPC and UAG administration, respectively. The cardioprotective effects of RIPC and UAG were accompanied by an increase in phosphorylation of STAT3 and abolished by AG490. This study indicated that RIPC reduces myocardial ischemia and reperfusion injury through UAG-induced activation of JAK/STAT pathway. UAG may be one of the humoral factors involved in the cardioprotective effects of RIPC.

DOI： 10.1007/s00395-020-0809-z

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

PURPOSE: Preoperative anxiety in children is challenging for anesthesia providers and nurses. The use of video glasses (VG), an immersive head mount display, helps conceal the unfamiliar operating room environment from the patient's visual field. The aim of this study was to determine the anxiolytic effect of VG compared with that of a portable multimedia player (PMP) during the preoperative period in children. DESIGN: Prospective randomized trial. METHODS: Participants were randomized into VG or PMP groups. Patients watched their favorite animation videos using the allocated device from the time of entering the preanesthetic holding area to the end of anesthetic induction. We evaluated modified Yale Preoperative Anxiety Scale scores during anesthetic induction. FINDINGS: The modified Yale Preoperative Anxiety Scale score in the VG group was significantly lower than that in the PMP group (P = .001). CONCLUSIONS: In children, the anxiolytic effect of VG during the preoperative period is larger than that of PMP.

DOI： 10.1016/j.jopan.2019.10.001

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

PURPOSE: Prolonged propofol infusion induces skeletal muscle damage. However, it is well known that the lipid emulsion that is the solvent of propofol causes various types of tissue damage via lipid peroxidation, and that propofol, conversely, has an anti-lipid peroxidative effect. The purpose of this study was to determine whether propofol or the lipid emulsion is the cause of muscle damage following prolonged administration. METHODS: Rats were divided into four groups: NI group (no intervention), Cath group (venous catheter insertion only), Prop group (1% propofol (Maruishi) intravenous infusion at 10 mg/kg/h), and Lipid group (10% Lipofundin® intravenous infusion at 100 mg/kg/h) (n = 10, each group). 1% Propofol (Maruishi) or Lipofundin was infused at 1 mL/kg/h for 72 h. The solvent of 1% propofol (Maruishi) is a 10% lipid emulsion. Lipofundin consists of 50% long-chain triacylglycerols and 50% medium-chain triacylglycerols, similar to the propofol solvent. Plasma concentrations of creatine kinase and myoglobin, superoxide production level, and 4-hydroxynonenal and malondialdehyde expression in the gastrocnemius muscle were evaluated 72 h after the interventions. RESULTS: Plasma concentrations of creatine kinase and myoglobin in the Lipid group were significantly higher than those in the other three groups. The superoxide production level, and 4-hydroxynonenal and malondialdehyde expression in the Lipid group were also significantly higher than in the other three groups. CONCLUSION: Lipofundin induces skeletal muscle damage via lipid peroxidation, and 1% propofol (Maruishi) conversely suppresses the muscle damage via antioxidant effects.

DOI： 10.1007/s00540-019-02676-8

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

OBJECTIVES: The authors investigated the association between intraoperative motor-evoked potential (MEP) changes and the severity of spinal cord infarction diagnosed with magnetic resonance imaging (MRI) to clarify the discrepancy between them, which was observed in patients with postoperative motor deficits after thoracic and thoracoabdominal aortic surgery. DESIGN: A multicenter retrospective study. SETTING: Motor-evoked potential <25% of control values was deemed positive for spinal cord ischemia. The severity of spinal cord infarction was categorized into grades A to D based on previous studies using the most severe axial MRI slices. The associations between MRI grade, MEP changes, and motor deficits were examined using logistic regression. PARTICIPANTS: Twenty-three of 1,245 patients (from 1999 to 2013, at 12 hospitals in Japan) were extracted from medical records of patients who underwent thoracic and thoracoabdominal aortic repair, with intraoperative MEP examinations and postoperative spinal MRI. INTERVENTIONS: No intervention (observational study). MEASUREMENTS AND MAIN RESULTS: Motor-evoked potential <25% of control value was associated significantly with motor deficits at discharge (adjusted odds ratio [OR], 130.0; p = 0.041), but not with severity of spinal cord infarction (adjusted OR, 0.917; p = 0.931). Motor deficit at discharge was associated with severe spinal cord infarction (adjusted OR, 4.83; p = 0.043), MEP <25% (adjusted OR, 13.95; p = 0.031), and combined deficits (motor and sensory, motor and bowel or bladder, or sensory and bowel or bladder deficits; adjusted OR, 31.03; p = 0.072) in stepwise logistic regression analysis. CONCLUSION: Motor-evoked potential <25% was associated significantly with motor deficits at discharge, but not with the severity of spinal cord infarction.

DOI： 10.1053/j.jvca.2018.12.004

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Dexmedetomidine (DEX), a highly selective alpha2 adrenergic receptor agonist, directly protects hearts against ischemia/reperfusion (I/R) injury. However, the detailed mechanism has not been fully elucidated. We studied differentially expressed mRNAs and miRNAs after DEX administration in rat hearts by comprehensive analysis. Additionally, bioinformatics analysis was applied to explore candidate genes and pathways that might play important roles in DEX-induced cardioprotection. The results of microarray analysis showed that 165 mRNAs and 6 miRNAs were differentially expressed after DEX administration. Through bioinformatics analysis using differentially expressed mRNAs, gene ontology (GO) terms including MAP kinase tyrosine/serine/threonine phosphatase activity and pathways including the p53 pathway were significantly enriched in the down-regulated mRNAs. Dusp1 and Atm were associated with the GO term of MAP kinase tyrosine/serine/threonine phosphatase activity and the p53 pathway, respectively. On the other hand, no significant pathway was found in the target mRNAs of deregulated miRNAs. The results indicated some possible key genes and pathways that seem to be of significance in DEX-induced cardioprotection, although miRNAs seem to be unlikely to contribute to cardioprotection induced by DEX.

DOI： 10.3390/ijms20071614

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記述言語：英語  

DOI： 10.1111/pan.13546

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記述言語：英語  

The anesthetic management of myasthenia gravis patients undergoing cardiac or aortic surgery under cardiopulmonary bypass, especially with deep hypothermic circulatory arrest, is challenging. We describe a case of successful anesthetic management of a myasthenia gravis patient undergoing total arch replacement with deep hypothermic circulatory arrest under neuromuscular monitoring and complete reversal of the action of neuromuscular blocking drugs by sugammadex. The present case suggests that patients with well-controlled myasthenia gravis might be safely managed in cardiac or aortic surgery under cardiopulmonary bypass with deep hypothermic circulatory arrest.

DOI： 10.1155/2019/3278147

PubMed

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記述言語：英語  

DOI： 10.1053/j.jvca.2018.06.018

PubMed

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記述言語：日本語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Kokuseido Publishing Co. Ltd  

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記述言語：英語  

DOI： 10.1007/s00540-018-2487-7

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Spinal cord ischemic injury is the most devastating sequela of descending and thoracoabdominal aortic surgery. Motor-evoked potentials (MEPs) have been used to intraoperatively assess motor tract function, but it remains unclear whether MEP monitoring can decrease the incidence of postoperative motor deficits. Therefore, we reviewed multicenter medical records of patients who had undergone descending and thoracoabdominal aortic repair (both open surgery and endovascular repair) to assess the association of MEP monitoring with postoperative motor deficits. METHODS: Patients included in the study underwent descending or thoracoabdominal aortic repair at 12 hospitals belonging to the Japanese Association of Spinal Cord Protection in Aortic Surgery between 2000 and 2013. Using multivariable mixed-effects logistic regression analysis, we investigated whether intraoperative MEP monitoring was associated with postoperative motor deficits at discharge after open and endovascular aortic repair. RESULTS: We reviewed data from 1214 patients (open surgery, 601 [49.5%]; endovascular repair, 613 [50.5%]). MEP monitoring was performed in 631 patients and not performed in the remaining 583 patients. Postoperative motor deficits were observed in 75 (6.2%) patients at discharge. Multivariable logistic regression analysis revealed that postoperative motor deficits at discharge did not have a significant association with MEP monitoring (adjusted odds ratio [OR], 1.13; 95% confidence interval [CI], 0.69-1.88; P = .624), but with other factors: history of neural deficits (adjusted OR, 6.08; 95% CI, 3.10-11.91; P < .001), spinal drainage (adjusted OR, 2.14; 95% CI, 1.32-3.47; P = .002), and endovascular procedure (adjusted OR, 0.45; 95% CI, 0.27-0.76; P = .003). The sensitivity and specificity of MEP <25% of control value for motor deficits at discharge were 37.8% (95% CI, 26.5%-49.5%) and 95.5% (95% CI, 94.7%-96.4%), respectively. CONCLUSIONS: MEP monitoring was not significantly associated with motor deficits at discharge.

DOI： 10.1213/ANE.0000000000002749

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Dexmedetomidine (DEX) has a direct cardioprotective effect against ischemia/reperfusion injury through endothelial nitric oxide synthase (eNOS) phosphorylation via α2-adrenoreceptor (α2-AR). By using spontaneously hypertensive rat (SHR) and Wistar-Kyoto (WKY) rat models, the cardioprotective effect of DEX in hypertrophied myocardium and the differential characteristics of cardiac α2-AR and the I1 imidazoline receptor (I1R) were examined. METHODS: Langendorff-perfused rat hearts underwent 40 minutes of global ischemia followed by 120 minutes of reperfusion in the presence or absence of DEX before ischemia. Infarct size was measured, and eNOS phosphorylation was assessed by Western blotting. The presence and expression of the receptors were assessed by immunohistochemistry, real-time reverse transcriptase polymerase chain reaction, and Western blotting. RESULTS: In WKY, DEX significantly decreased infarct size and increased phosphorylated-eNOS/eNOS. These effects were counteracted by yohimbine (α2-AR antagonist) and efaroxan (α2-AR and I1R antagonist). In SHR, DEX significantly decreased infarct size, and the effect was counteracted by efaroxan but not yohimbine. DEX did not alter phosphorylated-eNOS/eNOS in SHR. α2-AR and I1R were observed in WKY and SHR hearts. Although alpha2A-AR and alpha2B-AR messenger RNA and protein levels were upregulated in SHR, I1R expression was comparable between the 2 species. CONCLUSIONS: In the hypertrophied heart, DEX maintains its direct cardioprotective effect against ischemia/reperfusion injury via I1R in an eNOS-nondependent manner despite upregulation of α2-AR.

DOI： 10.1213/ANE.0000000000002452

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Acute kidney injury (AKI) after cardiopulmonary bypass (CPB) is a well-known postoperative complication. Remifentanil, which is a commonly used ultra-short-acting opioid, has antiinflammatory and sympatholytic effects with improvement of microcirculation. METHODS: A retrospective study was conducted to clarify the effect of the use of remifentanil during CPB on the incidence of postoperative AKI. Patients who underwent valve surgery while under cardiopulmonary bypass between January 2012 and December 2014 in our hospital were enrolled in this study. The incidences of postoperative AKI were compared in patients who received remifentanil during CPB (group R) and those who did not (group N). Univariate and multivariate regression analyses were performed to determine risk factors for AKI. RESULTS: Eighty patients received remifentanil (group R) and 50 patients did not (group N). The incidences of AKI were not significantly different in group R and group N (51% vs. 36%, P = 0.10). In multivariate regression analysis, age [adjusted odds ratio (OR) 1.048, 95% CI 1.008-1.089, P = 0.017], male gender (adjusted OR 3.101, 95% CI 1.303-7.378, P = 0.011), and use of preoperative calcium channel blockers (adjusted OR 3.240, 95% CI 1.302-8.063, P = 0.011) and diuretics (adjusted OR 2.673, 95% CI 1.178-6.066, P = 0.019) were associated with the incidence of AKI. The use of remifentanil was not associated with AKI (adjusted OR 2.321, 95% CI 0.997-5.402, P = 0.051). CONCLUSION: The use of remifentanil during CPB did not decrease the incidence of postoperative AKI after cardiac surgery.

DOI： 10.1007/s00540-017-2419-y

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Background: Glycosylation is one of the major posttranslational modifications of proteins and it is essential for proteins to obtain normal biological functions. Congenital disorders of glycosylation (CDGs) are very rare genetic disorders that lack enzymes needed for glycosylation. Phosphomannomutase-2 (PMM2)-CDG is the most common type of CDG. CDGs can cause a wide variety of clinical symptoms in almost every organ system. Muscular hypotonia is often present in patients with CDGs and is one of the most notable problems for anesthetic management because the susceptibility to nondepolarizing neuromuscular blocking agents (NMBAs) in patients with CDGs is unknown. Case presentation: The patient was a 17-month-old boy who weighed 6.5 kg and was 71 cm tall. He presented for strabismus surgery. He had muscular hypotonia, mental retardation, hepatic dysfunction, mild cerebellar hypoplasia, and some dysmorphic features including inverted nipples and abnormal subcutaneous fat distribution of the hips. Gene analysis revealed a compound heterozygous mutation in the gene encoding PMM2 and the patient was diagnosed as having PMM2-CDG. General anesthesia was performed with sevoflurane, nitrous oxide, and rocuronium. Neuromuscular monitoring was performed during anesthesia using train-of-four (TOF)-Watch® (MSD, Japan). As postoperative analgesia, the surgeon performed sub-Tenon's anesthesia. We did not use any intravenous analgesic. After completion of the operation, residual rocuronium was competed by administration of sugammadex. The patient gained consciousness and spontaneous breathing was established shortly thereafter, and the trachea was smoothly extubated. He was transported to an inpatient ward and was discharged to his home the next day without any complication. Conclusions: We performed safe anesthetic management in a 17-month-old boy with PMM2-CDG using rocuronium under neuromuscular monitoring.A patient with PMM2-CDG may show nearly normal susceptibility to nondepolarizing NMBAs.

DOI： 10.1186/s40981-017-0080-y

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：W.B. Saunders  

DOI： 10.1053/j.jvca.2012.11.006

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：麻酔科学サマーセミナー事務局  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：麻酔科学サマーセミナー事務局  

医中誌

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J-GLOBAL

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記述言語：日本語   出版者・発行元：克誠堂出版  

その他リンク:： http://search.jamas.or.jp/link/ui/2016401821

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：麻酔科学サマーセミナー事務局  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本集中治療医学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：日本小児麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：日本小児麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本Shock学会  

医中誌

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記述言語：日本語   出版者・発行元：日本蘇生学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本心臓血管麻酔学会  

医中誌

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記述言語：日本語   出版者・発行元：克誠堂出版(株)  

その他リンク:： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2012&ichushi_jid=J01397&link_issn=&doc_id=20120413220002&doc_link_id=40019256093&url=http%3A%2F%2Fci.nii.ac.jp%2Fnaid%2F40019256093&type=CiNii&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00003_1.gif

医中誌

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