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Purpose: We investigated the impact of surgical masks (SM) during oxygen therapy using oxygen masks in volunteer- and simulation-based studies. Methods: Fifteen volunteers wore the Hudson RCI® or Open-Face Mask® with/without an SM. The fraction of inspired oxygen concentration (FIO2), end-tidal CO2 (EtCO2), partial pressure of inspired CO2 (PICO2), and respiratory rate (RR) were measured. The oxygen flow rate increased from 0 to 10 L/min. In the simulation-based study, FIO2 was measured using a simulator that reproduced spontaneous breathing. RR was 12 or 24 bpm, and the tidal volume (Tv) was 300, 500, or 700 mL. The effect of oxygen mask fitting conditions were also examined. The primary outcome measure was FIO2 at 6 L/min. Results: In the volunteer-based study, FIO2 was reduced when the SM was used with the Hudson RCI® or Open-Face Mask®. The FIO2 drop was larger with the Open-Face Mask® than with the Hudson RCI®. The RR, EtCO2, and PICO2 significantly changed with the SM, but the differences were not clinically meaningful. In the simulation-based study, the SM with the Hudson RCI® did not reduce FIO2, but the SM with the Open-Face Mask® significantly decreased FIO2 under several conditions. However, the SM with the Hudson Mask® reduced FIO2 when the fit of the mask was inadequate. With the Open-Face Mask®, lower RR and Tv resulted in larger differences in FIO2. Conclusions: The SM decreased FIO2 during oxygen therapy with oxygen masks. The impact of SM depended on the type of the oxygen mask, mask fitting, and respiratory condition.

Objectives: Takotsubo cardiomyopathy (TCM) is a life-threatening complication of electroconvulsive therapy (ECT). We report the case of a 66-year-old woman who was re-challenged with ECT after ECT-induced TCM. Moreover, we have made a systematic review to assess the safety of and strategies for re-initiating ECT after TCM. Methods: We searched for published reports on ECT-induced TCM since 1990 in MEDLINE (PubMed), Scopus, Cochrane Library, ICHUSHI, and CiNii Research. Results: A total of 24 ECT-induced TCM cases were identified. Patients who developed ECT-induced TCM were predominantly middle-aged and older women. There was no specific trend in anesthetic agents used. Seventeen (70.8%) cases developed TCM by the third session in the acute ECT course. Eight (33.3%) cases developed ECT-induced TCM despite the use of β-blockers. Ten (41.7%) cases developed cardiogenic shock or abnormal vital signs related to cardiogenic shock. All cases recovered from TCM. Eight (33.3%) cases tried to receive ECT retrial. The duration until ECT retrial was between 3 weeks and 9 months. The most common preventive measures during ECT retrial were related to β-blockers; however, the type, dose, and route of administration of β-blockers varied. In all cases, ECT could be re-performed without TCM recurrence. Conclusions: ECT-induced TCM is more likely to cause cardiogenic shock than non-perioperative cases; nevertheless, it has good prognosis. Cautious re-initiation of ECT after TCM recovery is possible. Further studies are required to determine preventive measures for ECT-induced TCM.

Purpose: Although it is important to recognize gender disparities in publishing to achieve gender diversity, women's authorship in Japan remains unclear. Therefore, this study aimed to investigate the percentage and analyze the trends of articles authored and published in anesthesiology journals by Japanese female authors. Methods: The genders of the first and last authors affiliated with Japanese institutions were surveyed in the Journal of Anesthesia (JA) (1990, 1995, and 2000–2022) and 11 international anesthesiology journals (2010–2022). Results: We included 845 and 819 original research articles from JA in the analyses of the first and last authors, respectively. The proportion of female first authors significantly increased from 41 (11.7%) out of 351 before 2009 to 119 (24.1%) out of 494 after 2010 (p < 0.001). The proportion of female last authors was 11 (3.3%) out of 335 before 2009 and 22 (4.5%) out of 484 after 2010, respectively, with no significant difference (p = 0.470). We included 624 and 572 original research articles from international anesthesiology journals in the analyses of first and last authors, respectively. Among these, there were 134 (21.5%) and 23 (4.0%) female first and last authors, respectively. These proportions in international anesthesiology journals did not significantly differ from those in JA (p = 0.334, p = 0.789, respectively). Conclusion: The percentage of female first authors has increased, commensurate with the percentage of female anesthesiologists. However, the percentage of female last authors has not increased and remains low in Japan.

Neuronal intranuclear inclusion disease (NIID) is a progressive neurodegenerative disease with diverse clinical manifestations, including dementia and muscle weakness. We summarize anesthetic considerations in reporting general anesthesia for a 58-year-old man with bladder dysfunction and cerebellar ataxia who was diagnosed with NIID. The patient developed postinduction hypotension relevant to autonomic neuropathy. The potential risks, such as prolonged reaction to neuromuscular blocking agent, postoperative delirium, and worsening of NIID-related symptoms, were also considered. The responsiveness to anesthetics may vary widely from case t case. As the number of NIID cases increases, a better understanding of NIID is needed.

Background Remimazolam confers a lower risk of hypotension than propofol. However, no studies have compared the efficacy of remimazolam and propofol administered using target-controlled infusion (TCI). This study aimed to investigate hemodynamic effects of remimazolam and target-controlled propofol in middle-aged and elderly patients during the induction of anesthesia. Methods Forty adults aged 45–80 years with the American Society of Anesthesiologists Physical Status 1–2 were randomly assigned to remimazolam or propofol group (n = 20 each). Patients received either remimazolam (12 mg/kg/h) or propofol (3 μg/mL, TCI), along with remifentanil for inducing anesthesia. We recorded the blood pressure, heart rate (HR), and estimated continuous cardiac output (esCCO) using the pulse wave transit time. The primary outcome was the maximum change in mean arterial pressure (MAP) after induction. Secondary outcomes included changes in HR, cardiac output (CO), and stroke volume (SV). Results MAP decreased after induction of anesthesia in both groups, without significant differences between the groups (− 41.1 [16.4] mmHg and − 42.8 [10.8] mmHg in remimazolam and propofol groups, respectively; mean difference: 1.7 [95% confidence interval: − 8.2 to 4.9]; p = 0.613). Furthermore, HR, CO, and SV decreased after induction in both groups, without significant differences between the groups. Remimazolam group had significantly shorter time until loss of consciousness than propofol group (1.7 [0.7] min and 3.5 [1.7] min, respectively; p p = 0.341). Conclusions Hemodynamics were not significantly different between remimazolam and target-controlled propofol groups during induction of anesthesia. Thus, not only the choice but also the dose and usage of anesthetics are important for hemodynamic stability while inducing anesthesia. Clinicians should monitor hypotension while inducing anesthesia with remimazolam as well as propofol. Trial registration UMIN-CTR (UMIN000045612).

Objectives To compare the effects of nicorandil and nitroglycerin on arterial oxygenation during two-lung ventilation (TLV) and one-lung ventilation (OLV) in patients with risk factors for myocardial ischemia. Design A prospective, randomized, double-blind study. Setting A tertiary care hospital. Participants Fifty-six patients scheduled for elective video-assisted thoracic surgery were assigned randomly to either the nicorandil group or the nitroglycerin group. Interventions Patients in the nicorandil group received a bolus dose of nicorandil, 0.08 mg/kg during induction of anesthesia, followed by a continuous infusion at a rate of 0.08 mg/kg/h. Patients in the nitroglycerin group received a continuous infusion of nitroglycerin at a rate of 1 µg/kg/min from the induction of anesthesia. Measurements and Main Results Arterial blood gas analysis was performed at the following points: before induction of anesthesia; during TLV; at 5, 10, 20, and 30 minutes after the initiation of OLV. PaO2 at TLV (479.7 ± 57.1 v 408.2 ± 70.9 mmHg, p Conclusion This study demonstrated that oxygenation during TLV and OLV was significantly higher in patients receiving nicorandil than in those receiving nitroglycerin.

Background: We investigated the effects of a novel method of anesthesia combining propofol and volatile anesthesia on the incidence of postoperative nausea and vomiting in patients undergoing laparoscopic gynecological surgery. Methods: Patients were randomly divided into three groups: those maintained with sevoflurane (Group S, n = 42), propofol (Group P, n = 42), or combined propofol and sevoflurane (Group PS, n = 42). We assessed complete response (no postoperative nausea and vomiting and no rescue antiemetic use), incidence of nausea and vomiting, nausea severity score, vomiting frequency, rescue antiemetic use, and postoperative pain at 2 and 24 h after surgery. Results: The number of patients who exhibited a complete response was greater in Groups P and PS than in Group S at 0–2 h (74%, 76% and 43%, respectively, p = 0.001) and 0–24 h (71%, 76% and 38%, respectively, p

Purpose : Activation of the mitochondrial calcium-activated potassium (mKCa) channel reportedly confers resistance to myocardial ischemic stress. However, the role of the mKCa channel in postconditioning induced by volatile anesthetic remains unclear. Methods :Male Japanese white rabbits underwent coronary artery occlusion for 30 min followed by reperfusion for 3 h. Volatile anesthetic, isoflurane, was administered at 3min prior to reperfusion for 5 min. Rabbits were injected with the mKCa channel blocker, iberiotoxin, or the mKCa channel opener, NS1619, at 8 min prior to reperfusion. Myocardial infarct size and the area at risk (AAR) were measured at the end of the experiment. Results : Isoflurane significantly reduced infarct size (23.0±9.8% of the AAR, P

Takotsubo cardiomyopathy, also known as stress-induced cardiomyopathy, is a disease in which the patient exhibits transient, reversible left ventricular dysfunction that is triggered by physical or emotional stress. Prolongation of QT interval, a risk factor for arrhythmia and sudden death, has been reported to be prevalent among patients with Takotsubo cardiomyopathy and is also observed in those with severe anorexia nervosa. In this report, we describe the rare case of a 30-year-old female patient with anorexia nervosa who developed Torsades de Pointes associated with Takotsubo cardiomyopathy during emergence from general anesthesia for emergency exploratory laparotomy.

Peutz–Jeghers syndrome (PJS) is a dominantly inherited human disorder characterized by gastrointestinal hamartomatous polyposis and mucocutaneous melanin pigmentation. LKB1 (STK11) serine/threonine kinase is the product of the causative gene of PJS, which has been mapped to chromosome 19p13.3. However, several studies have produced results that are not consistent with a link between LKB1 gene mutation and PJS. We constructed a knockout gene mutation of Lkb1 to determine whether it is the causative gene of PJS and to examine the biological role of the Lkb1 gene. Lkb1 −/− mice died in utero between 8.5 and 9.5 days postcoitum. At 9.0 days postcoitum, Lkb1 −/− embryos were generally smaller than their age-matched littermates, showed developmental retardation, and did not undergo embryonic turning. Multiple gastric adenomatous polyps were observed in 10- to 14-month-old Lkb1 +/− mice. Our results indicate that functional Lkb1 is required for normal embryogenesis and that it is related to tumor development. The Lkb1 +/− mouse is suitable for studying molecular mechanism underlying the development of inherited gastric tumors in PJS.

We have previously prepared monoclonal antibodies (MAbs) against tumor vasculature using cultured rat tumor endothelial cells (TECs) isolated from solid KMT-17 tumors and identified 40 and 80 kDa antigens recognized by TES-17 and TES-23 MAbs, respectively. To clarify the nature of antigens on tumor vasculature, molecular cloning was conducted by screening the rat TEC cDNA library. Two antigens were detected: a 40 kDa OTS-8 antigen, which had been defined as a differentiation marker for osteoblastic lineage, and an 80 kDa CD44H antigen. Northern blots showed that OTS-8 mRNA was expressed exclusively in the lung, in addition to TECs, while CD44H mRNA was detected in the lung, intestine, spleen, thymus and peripheral blood cells, in addition to TECs. Immuno-histochemistry of KMT-17 tumors revealed that OTS-8 and CD44 were expressed on sprouting TECs. In addition, TES-23 MAb stained TECs of tubular vessels as well as sprouting TECs, but anti-rat CD44 MAbs stained only sprouting TECs. PCR showed that CD44 cDNA with a splice in exon 6 (CD44ex6) was present in rat TECs at low levels. Our results indicate that OTS-8 and CD44 are expressed on rat sprouting TECs and that TES-23 MAb recognizes CD44H on sprouting TECs as well as an unknown epitope on TECs of tubular vessels that could not be recognized by anti-rat CD44 MAbs.

We have isolated a serine protease, halystase, from Agkistrodon halys blomhoffii venom by chromatography on DEAE-Sepharose, heparin-Sepharose and Q-Sepharose columns, and have determined the complete amino acid sequence by Edman degradation and by mass spectral analysis of peptides generated by enzymatic and chemical cleavage. The 238-residue sequence of halystase, containing N-linked carbohydrates (about 13%) at two sites showed significant similarity to other thrombin-like snake venom serine proteases (66-72%), mammalian tissue kallikrein (42%) and thrombin (26%). Halystase contained the tentative catalytic triad of His43, Asp88 and Ser184 common to all serine proteases and Asp178 in the primary substrate-binding site. Although halystase contained an RGD sequence at residues 181-183, it did not inhibit platelet aggregation induced by ADP or collagen. It hydrolyzed most efficiently a tissue-kallikrein substrate, prolylphenylalanylarginyl-4-methyl-coumaryl-7-amide, and released bradykinin from bovine kininogen. Halystase did not coagulate human plasma, but it cleaved the fibrinogen B beta chain at the carboxyl side of Arg42 and cleaved slowly the fibrogen A alpha chain. Fibrinogen thus treated gradually became insensitive to thrombin. The proteolytic activity was inhibited with diisopropyl fluorophosphate, phenylmethylsulfonyl fluoride or leupeptin. These results indicate that halystase is a serine protease structurally similar to coagulating thrombin-like snake venom proteases, but it specifically cleaves fibrinogen at sites different from thrombin without inducing fibrin clotting, and hydrolyzes kininogen to produce bradykinin, resulting in the reduction of blood pressure.

Background Cardiac protection by volatile anesthetic-induced preconditioning and ischemic preconditioning have similar signaling pathways. Recently, it was reported that augmentation of protein modified with O-linked β-N-acetylglucosamine (O-GlcNAc) contributes to cardiac protection. This study investigated the role of O-GlcNAc in cardiac protection induced by anesthetic-induced preconditioning. Methods O-GlcNAc-modified proteins were visualized by immunoblotting. Tolerance against ischemia or reperfusion was tested in vivo (n = 8) and in vitro (n = 6). The opening of the mitochondrial permeability transition pore (mPTP) upon oxidative stress was examined in myocytes treated with calcein AM (n = 5). Coimmunoprecipitation and enzymatic labeling were performed to detect the mitochondrial protein responsible for the mPTP opening. Results Isoflurane treatment and the consequent augmentation of O-GlcNAc concentrations reduced the infarct size (26 ± 5% [mean ± SD], P < 0.001) compared with the control. The protective effect of O-GlcNAc was eliminated in the group pretreated with the O-GlcNAc transferase inhibitor alloxan (39 ± 5%, P < 0.001). Myocyte survival also showed the same result in vitro. Formation of the mPTP was abrogated in the isoflurane-treated cells (86 ± 4%, P < 0.001) compared with the control and alloxan-plus-isoflurane-treated cells (57 ± 7%, P < 0.001). Coimmunoprecipitation and enzymatic labeling studies revealed that the O-GlcNAc-modified, voltage-dependent anion channel restained the mPTP opening. Conclusions Isoflurane induced O-GlcNAc modification of mitochondrial voltage-dependent anion channel. This modification inhibited the opening of the mPTP and conferred resistance to ischemia-reperfusion stress.

Aims Compound K (C-K; 20-O- d -glucopyranosyl-20(S)-protopanaxadiol) is a novel ginsenoside metabolite formed by intestinal bacteria and does not occur naturally in ginseng. In this study, we investigated whether administration of C-K has protective effects on myocardial ischemia-reperfusion injury and its potential mechanisms. Main methods We used in vivo mouse models of ischemia-reperfusion injury and performed biochemical assays in excised hearts. Key findings C-K reduced infarct size compared with the control group after ischemia-reperfusion. Immunoblot analysis showed that C-K significantly enhanced protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS) activity. Wortmannin, a phosphoinositide 3-kinase (PI3K) inhibitor, blocked cardiac protection in vivo and attenuated phosphorylation of Akt and eNOS. Additionally, the hearts of C-K pretreated mice showed inhibition of mitochondrial swelling induced by Ca 2+ . Significance This study showed that Compound K pretreatment has protective effects on myocardial ischemia-reperfusion injury, partly by mediating the activation of PI3K pathway and phosphorylation of Akt and eNOS.

article i nfo Article history: Received 15 June 2010 Accepted 27 October 2010 Aims: Volatile anesthetics, such as isoflurane, reverse glucose-induced inhibition of pancreatic adenosine triphosphate-sensitive potassium (KATP) channel activity, resulting in reduced insulin secretion and impaired glucose tolerance. No previous studies have investigated the effects of intravenous anesthetics, such as propofol, on pancreatic KATP channels. We investigated the cellular mechanisms underlying the effects of isoflurane and propofol on pancreatic KATP channels and insulin secretion. Main methods: Intravenous glucose tolerance tests (IVGTT) were performed on male rabbits. Pancreatic islets were isolated from male rats and used for a perifusion study, measurement of intracellular ATP concentration ((ATP)i), and patch clamp experiments. Key findings: Glucose stimulus significantly increased insulin secretion during propofol anesthesia, but not isoflurane anesthesia, in IVGTT study. In perifusion experiments, both islets exposed to propofol and control islets not exposed to anesthetic had a biphasic insulin secretory response to a high dose of glucose. However, isoflurane markedly inhibited glucose-induced insulin secretion. In a patch clamp study, the relationship between ATP concentration and channel activity could be fitted by the Hill equation with a half-maximal inhibition of 22.4, 15.8, and 218.8 μM in the absence of anesthetic, and with propofol, and isoflurane, respectively. (ATP)i and single KATP channel conductance did not differ in islets exposed to isoflurane or propofol. Significance: Our results indicate that isoflurane, but not propofol, decreases the ATP sensitivity of KATP channels and impairs glucose-stimulated insulin release. These differential actions of isoflurane and propofol on ATP sensitivity may explain the differential effects of isoflurane and propofol on insulin release.

ResumoJustificativaInvestigamos os efeitos de um novo método de anestesia, que combina propofol e anestesia volátil, sobre a incidência de náusea e vômito no período pós‐operatório de pacientes submetidas à laparoscopia ginecológica.MétodosAs pacientes foram randomicamente divididas em três grupos: manutenção com sevoflurano (Grupo S, n = 42), com propofol (Grupo P, n = 42) ou com a combinação de propofol e sevoflurano (Grupo PS, n = 42). Avaliamos as respostas completas (sem náusea e vômito no pós‐operatório e sem uso de antiemético de resgate), incidência de náusea e vômito, escore de gravidade da náusea, frequência de vômitos, uso de antiemético de resgate e dor no pós‐operatório em duas e 24horas após a cirurgia.ResultadosO número de doentes que apresentou uma resposta completa foi maior nos grupos P e PS do que no Grupo S em 0‐duashoras (74%, 76% e 43%m respectivamente, p = 0,001) e 0‐24horas (71%, 76% e 38%, respectivamente, p < 0,0005). A incidência de náusea em 0‐duashoras (Grupo S = 57%, Grupo P = 26% e Grupo PS = 21%, p = 0,001) e 0‐24horas (Grupo S = 62%; Grupo P = 29% e grupo PS = 21%, p < 0,0005) também foi significativamente diferente entre os grupos. Porém, não houve diferença significativa entre os grupos em relação à incidência ou frequência de vômitos ou uso de antiemético de resgate em 0‐24horas.ConclusãoA combinação de propofol e anestesia volátil durante a laparoscopia ginecológica efetivamente diminui a incidência de náusea no pós‐operatório.AbstractBackgroundWe investigated the effects of a novel method of anesthesia combining propofol and volatile anesthesia on the incidence of postoperative nausea and vomiting in patients undergoing laparoscopic gynecological surgery.MethodsPatients were randomly divided into three groups: those maintained with sevoflurane (Group S; n = 42), propofol (Group P; n = 42), or combined propofol and sevoflurane (Group PS; n = 42). We assessed complete response (no postoperative nausea and vomiting and no rescue antiemetic use), incidence of nausea and vomiting, nausea severity score, vomiting frequency, rescue antiemetic use, and postoperative pain at 2 and 24h after surgery.ResultsThe number of patients who exhibited a complete response was greater in Groups P and PS than in Group S at 0‐2h (74%; 76% and 43%; respectively, p = 0.001) and 0‐24h (71%; 76%, and 38%; respectively, p < 0.0005). The incidence of nausea at 0‐2h (Group S = 57%; Group P = 26% and Group PS = 21%; p = 0.001) and 0‐24h (Group S = 62%; Group P = 29% and Group PS = 21%; p < 0.0005) was also significantly different among groups. However, there were no significant differences among groups in the incidence or frequency of vomiting or rescue antiemetic use at 0‐24h.ConclusionCombined propofol and volatile anesthesia during laparoscopic gynecological surgery effectively decreases the incidence of postoperative nausea.

Background Remifentanil enhances intraoperative hemodynamic stability, suggesting that it may decrease intraoperative blood loss when included as an adjuvant to general anesthesia. This retrospective study compared intraoperative blood loss during spinal surgery in patients administered either remifentanil or fentanyl as an opioid adjuvant. Methods We reviewed clinical and surgical data from 64 consecutive laminoplasty or laminectomy patients treated at National Hospital Organization Zentsuji Hospital between April 2010 and March 2011. Patients received either remifentanil (n = 35) or fentanyl (n = 29) as an opioid analgesic during general anesthesia. In addition to intraoperative blood loss, indices of hemodynamic stability, including heart rate as well as systolic, mean, and diastolic blood pressure (BP), were compared over the entire perioperative period between remifentanil and fentanyl groups. Results The remifentanil group exhibited significantly lower intraoperative arterial BP than the fentanyl group. Intraoperative blood loss was also significantly lower in the remifentanil group (125 ± 67 mL vs. 165 ± 82 mL, P = 0.035). Conclusions Intraoperative blood loss during spinal surgery was decreased in patients who received remifentanil as an opioid adjuvant, possibly because of lower intraoperative BP. A larger-scale prospective randomized controlled trial is warranted to confirm our results and to test whether remifentanil can decrease intraoperative blood loss during other surgical procedures.

Purpose : Post-operative nausea and vomiting (PONV) remains the most fre- quently reported patient complaint after anesthesia. Aprepitant is the first neurokinin- 1(NK1) receptor antagonism available for use as an antiemetic. We investigated whether aprepitant can effectively decrease PONV in patients undergoing laparoscopic gyneco- logical surgery. Methods : Sixty four patients receiving general anesthesia for laparoscopic gynecological surgery were randomly assigned to either receive a preoperative dose of 80 mg aprepitant or no drug. Efficacy was assessed in 2 and 24 hours after surgery. Primary and secondary endpoints were analyzed for the time intervals 0-2 hours (acute phase) and 2-24 hours (delayed phase). Vomiting, nausea, use of rescue anti-emetic, and visual analog scale (VAS) were assessed. Nausea was assessed on a 4-point scale, from 0 to 3. Results : Sixty patients participated in the study. At acute phase, PONV was present in both control and NK1 group and were 63% nd 43% respectively. The severity of nausea was much less in the NK1 group. PONV prevalence at delayed phase was present in control but absent in NK1 group 27% s. 0% respectively. The amount of pain medication used by patients in the NK1 group was significantly less for diclofenac and pentazocine sug- gesting increase pain tolerance. Conclusions : Neurokinin-1 receptor antagonism effec- tively lowered PONV increased pain tolerance, and expedited recovery in patients under- going laparoscopic gynecological surgery. J. Med. Invest. 58 : 246-251, August, 2011