Sevoflurane Does Not Promote the Colony-Forming Ability of Human Mesenchymal Glioblastoma Stem Cells In Vitro.

Background and Objectives: Clinically used concentrations of sevoflurane, an inhaled anesthetic, have been reported to significantly inhibit tumor growth. We investigated the effects of sevoflurane on sphere formation and the proliferation of human glioblastoma stem cells (GSCs) to determine whether sevoflurane exerts short- and long-term effects on human tumor cells. Materials and Methods: High-grade patient-derived GSCs (MD13 and Me83) were exposed to 2% sevoflurane. To evaluate the effect of sevoflurane on viability, proliferation, and stemness, we performed a caspase-3/7 essay, cell proliferation assay, and limiting dilution sphere formation assays. The expression of CD44, a cell surface marker of cancer stem-like cells in epithelial tumors, was evaluated using quantitative reverse transcription PCR. Differences between groups were evaluated with a one-way analysis of variance (ANOVA). Results: Sevoflurane exposure for 4 days did not significantly promote caspase 3/7 activity in MD13 and Me83, and cell proliferation was not observed after 5 days of exposure. Furthermore, prolonged exposure to sevoflurane for 6 days did not promote the sphere-forming and proliferative potential of MD13 and Me83 cells. These results suggest that sevoflurane does not promote either apoptosis, proliferative capacity, or the colony-forming ability of human mesenchymal glioblastoma stem cells in vitro. Conclusions: Sevoflurane at clinically used concentrations does not promote the colony-forming ability of human mesenchymal glioblastoma stem cells in vitro. It is very important for neurosurgeons and anesthesiologists to know that sevoflurane, a volatile anesthetic used in surgical anesthesia, would not exacerbate the disease course of GSCs.

Polysulfide inhibits hypoxia-elicited hypoxia-inducible factor activation in a mitochondria-dependent manner.

In cellular signaling, the diverse physiological actions of biological gases, including O2, CO, NO, and H2S, have attracted much interest. Hypoxia-inducible factors (HIFs), including HIF-1 and HIF-2, are transcription factors that respond to reduced intracellular O2 availability. Polysulfides are substances containing varying numbers of sulfur atoms (H2Sn) that are generated endogenously from H2S by 3-mercaptopyruvate sulfurtransferase in the presence of O2, and regulate ion channels, specific tumor suppressors, and protein kinases. However, the effect of polysulfides on HIF activation in hypoxic mammalian cells is largely unknown. Here, we have investigated the effect of polysulfide on cells in vitro. In established cell lines, polysulfide donors reversibly reduced cellular O2 consumption and inhibited hypoxia-induced HIF-1α protein accumulation and the expression of genes downstream of HIFs; however, these effects were not observed in anoxia. In Von Hippel-Lindau tumor suppressor (VHL)- and mitochondria-deficient cells, polysulfides did not affect HIF-1α protein synthesis but destabilized it in a VHL- and mitochondria-dependent manner. For the first time, we show that polysulfides modulate intracellular O2 homeostasis and regulate HIF activation and subsequent hypoxia-induced gene expression in a VHL- and mitochondria-dependent manner.

A rare case of atropine-resistant bradycardia following sugammadex administration.

BACKGROUND: Profound bradycardia caused by sugammadex has been reported, although its mechanism is unclear. Herein, we suggest a possible culprit for this phenomenon. CASE PRESENTATION: A 50-year-old woman without comorbidity except mild obesity underwent a transabdominal hysterectomy and right salpingo-oophorectomy. After surgery, sugammadex 200 mg was intravenously administered. Approximately 4 min later, her heart rate decreased to 36 bpm accompanied by hypotension (41/20 mmHg) and ST depression in limb lead electrocardiogram (ECG). Atropine 0.5 mg was injected intravenously without improving the hemodynamics. Intravenous adrenaline 0.5 mg was added despite the lack of signs suggesting allergic reactions. Her heart rate and blood pressure quickly recovered and remained stable thereafter, although 12-lead ECG taken 1 h later still showed ST depression. CONCLUSIONS: In this case, the significant bradycardia appeared attributable to coronary vasospasm (Kounis syndrome) induced by sugammadex, considering the ECG findings and high incidence of anaphylaxis due to sugammadex.

Pharmacological polysulfide suppresses glucose-stimulated insulin secretion in an ATP-sensitive potassium channel-dependent manner.

Hydrogen sulfide (H2S) is an endogenous gaseous transmitter synthesized in various cell types. It is well established that H2S functions in many physiological processes, including the relaxation of vascular smooth muscle, mediation of neurotransmission, regulation of inflammation, and modulation of insulin signaling. In recent years, it has been revealed that polysulfides, substances with a varying number of sulfur atoms (H2Sn), are generated endogenously from H2S in the presence of oxygen. A series of studies describes that sulfane sulfur has the unique ability to bind reversibly to other sulfur atoms to form hydropersulfides and polysulfides, and that polysulfides activate ion channels and promote calcium influx. Furthermore, polysulfides regulate tumor suppressor activity, promote the activation of transcription factors targeting antioxidant genes and regulate blood pressure by vascular smooth muscle relaxation. Insulin secretion from pancreatic ß cells plays a critical role in response to increased blood glucose concentration. H2S has emerged as an important regulator of glycemic control and exhibits characteristic regulation of glucose homeostasis. However, the effects of polysulfides on glucose-stimulated insulin secretion (GSIS) are largely unknown. In this study, we demonstrated that pharmacological polysulfide salts including Na2S2, Na2S3, and Na2S4 considerably inhibit GSIS in mouse and rat pancreatic ß-cell-derived MIN6 and INS-1 cell lines, and that the effect is dependent on the activation of ATP-sensitive potassium channels. In addition, we demonstrated that a mixture of Na2S and diethylamine NONOate inhibits GSIS in a similar way to the pharmacological administration of polysulfide salts.

Propofol inhibits stromatoxin-1-sensitive voltage-dependent K+ channels in pancreatic ß-cells and enhances insulin secretion.

BACKGROUND: Proper glycemic control is an important goal of critical care medicine, including perioperative patient care that can influence patients' prognosis. Insulin secretion from pancreatic ß-cells is generally assumed to play a critical role in glycemic control in response to an elevated blood glucose concentration. Many animal and human studies have demonstrated that perioperative drugs, including volatile anesthetics, have an impact on glucose-stimulated insulin secretion (GSIS). However, the effects of the intravenous anesthetic propofol on glucose metabolism and insulin sensitivity are largely unknown at present. METHODS: The effect of propofol on insulin secretion under low glucose or high glucose was examined in mouse MIN6 cells, rat INS-1 cells, and mouse pancreatic ß-cells/islets. Cellular oxygen or energy metabolism was measured by Extracellular Flux Analyzer. Expression of glucose transporter 2 (GLUT2), potassium channels, and insulin mRNA was assessed by qRT-PCR. Protein expression of voltage-dependent potassium channels (Kv2) was also assessed by immunoblot. Propofol's effects on potassium channels including stromatoxin-1-sensitive Kv channels and cellular oxygen and energy metabolisms were also examined. RESULTS: We showed that propofol, at clinically relevant doses, facilitates insulin secretion under low glucose conditions and GSIS in MIN6, INS-1 cells, and pancreatic ß-cells/islets. Propofol did not affect intracellular ATP or ADP concentrations and cellular oxygen or energy metabolism. The mRNA expression of GLUT2 and channels including the voltage-dependent calcium channels Cav1.2, Kir6.2, and SUR1 subunit of KATP, and Kv2 were not affected by glucose or propofol. Finally, we demonstrated that propofol specifically blocks Kv currents in ß-cells, resulting in insulin secretion in the presence of glucose. CONCLUSIONS: Our data support the hypothesis that glucose induces membrane depolarization at the distal site, leading to KATP channel closure, and that the closure of Kv channels by propofol depolarization in ß-cells enhances Ca2+ entry, leading to insulin secretion. Because its activity is dependent on GSIS, propofol and its derivatives are potential compounds that enhance and initiate ß-cell electrical activity.

Cancerous phenotypes associated with hypoxia-inducible factors are not influenced by the volatile anesthetic isoflurane in renal cell carcinoma.

The possibility that anesthesia during cancer surgery may affect cancer recurrence, metastasis, and patient prognosis has become one of the most important topics of interest in cancer treatment. For example, the volatile anesthetic isoflurane was reported in several studies to induce hypoxia-inducible factors, and thereby enhance malignant phenotypes in vitro. Indeed, these transcription factors are considered critical regulators of cancer-related hallmarks, including "sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, replicative immortality, angiogenesis, invasion, and metastasis." This study aimed to investigate the impact of isoflurane on the growth and migration of derivatives of the renal cell line RCC4. We indicated that isoflurane treatment did not positively influence cancer cell phenotypes, and that hypoxia-inducible factors (HIFs) maintain hallmark cancer cell phenotypes including gene expressions signature, metabolism, cell proliferation and cell motility. The present results indicate that HIF activity is not influenced by the volatile anesthetic isoflurane.

Bromocriptine use for sudden peripartum cardiomyopathy in a patient with preeclampsia: a case report.

BACKGROUND: Peripartum cardiomyopathy is an uncommon form of heart failure that occurs in otherwise healthy women during pregnancy or until 5 months postpartum. Here, we report a rare case where a female patient underwent cesarean section after the occurrence of preeclampsia and intrauterine fetal death, and developed peripartum cardiomyopathy following postsurgical respiratory distress. The prompt initiation of inotropic drug and bromocriptine therapy quickly restored cardiac function. CASE PRESENTATION: The patient was a 36-year-old woman who underwent emergency cesarean section for a previous preeclampsia and an intrauterine fetal death that occurred after 24 weeks of pregnancy. In addition, the patient had an extremely low platelet count of 5000/µL on admission. She had been diagnosed as idiopathic thrombocytopenic purpura at the age of 29 years old and treated with prednisolone at 15 mg/day. Therefore, the cesarean section was performed under general anesthesia. The patient did not exhibit respiratory or hemodynamic dysfunction during surgery. However, she developed respiratory distress with sinus tachycardia after extubation and was transferred to the intensive care unit. A chest radiograph showed butterfly shadows, and transthoracic echocardiogram confirmed the reduction of left ventricle contractility (ejection fraction 20%). She was diagnosed with peripartum cardiomyopathy and treated immediately with intravenous milrinone, oral bromocriptine, and angiotensin-converting enzyme inhibitor. Respiratory and hemodynamic function improved rapidly, and the patient was moved to the general ward 2 days after surgery. Fourteen days after surgery, the patient had an ejection fraction of 57%. The patient recovered without any further complications and was discharged 24 days after surgery. CONCLUSION: A sudden case of peripartum cardiomyopathy was successfully managed by a prompt diagnosis and treatment with inotropic agents and bromocriptine.

Suppression of mitochondrial oxygen metabolism mediated by the transcription factor HIF-1 alleviates propofol-induced cell toxicity.

A line of studies strongly suggest that the intravenous anesthetic, propofol, suppresses mitochondrial oxygen metabolism. It is also indicated that propofol induces the cell death in a reactive oxygen species (ROS)-dependent manner. Because hypoxia-inducible factor 1 (HIF-1) is a transcription factor which is involved in cellular metabolic reprogramming by modulating gene expressions of enzymes including glycolysis pathway and oxygen utilization of mitochondria, we examined the functional role of HIF-1 activity in propofol-induced cell death. The role of HIF-1 activity on oxygen and energy metabolisms and propofol-induced cell death and caspase activity was examined in renal cell-derived RCC4 cells: RCC4-EV cells which lack von Hippel-Lindau protein (VHL) protein expression and RCC4-VHL cells, which express exogenous VHL, and in neuronal SH-SY5Y cells. It was demonstrated that HIF-1 is involved in suppressing oxygen consumption and facilitating glycolysis in cells and that the resistance to propofol-induced cell death was established in a HIF-1 activation-dependent manner. It was also demonstrated that HIF-1 activation by treatment with HIFα-hydroxylase inhibitors such as n-propyl gallate and dimethyloxaloylglycine, alleviated the toxic effects of propofol. Thus, the resistance to propofol toxicity was conferred by HIF-1 activation by not only genetic deletion of VHL but also exposure to HIFα-hydroxylase inhibitors.

Propofol induces a metabolic switch to glycolysis and cell death in a mitochondrial electron transport chain-dependent manner.

The intravenous anesthetic propofol (2,6-diisopropylphenol) has been used for the induction and maintenance of anesthesia and sedation in critical patient care. However, the rare but severe complication propofol infusion syndrome (PRIS) can occur, especially in patients receiving high doses of propofol for prolonged periods. In vivo and in vitro evidence suggests that the propofol toxicity is related to the impaired mitochondrial function. However, underlying molecular mechanisms remain unknown. Therefore, we investigated effects of propofol on cell metabolism and death using a series of established cell lines of various origins, including neurons, myocytes, and trans-mitochondrial cybrids, with defined mitochondrial DNA deficits. We demonstrated that supraclinical concentrations of propofol in not less than 50 µM disturbed the mitochondrial function and induced a metabolic switch, from oxidative phosphorylation to glycolysis, by targeting mitochondrial complexes I, II and III. This disturbance in mitochondrial electron transport caused the generation of reactive oxygen species, resulting in apoptosis. We also found that a predisposition to mitochondrial dysfunction, caused by a genetic mutation or pharmacological suppression of the electron transport chain by biguanides such as metformin and phenformin, promoted propofol-induced caspase activation and cell death induced by clinical relevant concentrations of propofol in not more than 25 µM. With further experiments with appropriate in vivo model, it is possible that the processes to constitute the molecular basis of PRIS are identified.

HIF-1-mediated suppression of mitochondria electron transport chain function confers resistance to lidocaine-induced cell death.

The local anesthetic lidocaine induces cell death by altering reactive oxygen species (ROS) generation and mitochondrial electron transport chain function. Because hypoxia-inducible factor 1 (HIF-1) is involved in determining oxygen metabolism and mitochondria function, we investigated the involvement of HIF-1 activity in lidocaine-induced cell death. We investigated the role of HIF activation on lidocaine-induced caspase activation and cell death in renal cell-derived RCC4 cells lacking functional von Hippel-Lindau (VHL) protein. We demonstrate that HIF-1 suppressed oxygen consumption and facilitated glycolysis in a pyruvate dehydrogenase kinase-1-dependent manner and that activation of HIF-1 conferred resistance to lidocaine-induced cell death. We also demonstrated that exogenous HIF-1 activation, through HIFα-hydroxylase inhibition or exposure to hypoxic conditions, alleviates lidocaine toxicity by suppressing mitochondria function and generating ROS, not only in RCC4 cells, but also in the neuronal SH-SY5Y cells. In conclusion, we demonstrate that HIF-1 activation due to VHL deletion, treatment with small molecule HIFα-hydroxylase inhibitors, and exposure to hypoxic conditions suppresses mitochondrial respiratory chain function and confers resistance to lidocaine toxicity.

Mitigation of inflammation using the intravenous anesthetic dexmedetomidine in the mouse air pouch model.

Dexmedetomidine, an α2-adrenergic/imidazoline receptor agonist, is a widely used intravenous anesthetic. Its primary current usage is for sedation of patients in the intensive care unit. The mouse air pouch model is versatile in studying the anti-inflammatory effect of a drug on a local inflammation, which is induced by a variety of substances. In the present study, using the carrageenan-induced air pouch inflammation model, we tested whether dexmedetomidine mitigates inflammation occurring locally in the mouse air pouch. We found that dexmedetomidine dose-dependently inhibited the production of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the pouch and decreased the number of white blood cells (WBC) recruited into the pouch. Dexmedetomidine also dose-dependently inhibited the production of neutrophil chemokines, cxcl1 and cxcl2. Furthermore, the dexmedetomidine-induced decreased recruitment of WBC into the pouch was successfully reversed with intra-pouch administration of cxcl1/cxcl2, but not TNF-α or IL-6. Lastly, the inhibition of the production of the cytokines and chemokines with dexmedetomidine was reversed by the treatment of yohimbine, suggesting that dexmedetomidine's anti-inflammatory effect is primarily via the stimulation of the α2-adrenergic receptor. We conclude that dexmedetomidine has an anti-inflammatory property in the carrageenan-induced mouse air pouch inflammation model, and that the dexmedetomidine-induced inhibition of production of the neutrophil chemokines, cxcl1 and cxcl2, may be related, at least in part, to the inhibition of WBC intra-pouch recruitment.

Impact of hydroxyethyl starch 70/0.5 on acute kidney injury after gastroenterological surgery.

BACKGROUND: Previous studies reported a higher mortality risk and a greater need for renal replacement therapy in patients administered hydroxyethyl starch (HES) rather than other fluid resuscitation preparations. In this study, we investigated the association between 6% HES 70/0.5 use and postoperative acute kidney injury (AKI) in gastroenterological surgery patients. METHODS: We conducted retrospective full-cohort and propensity-score-based analyses of patients who underwent gastroenterological surgery between June 2011 and August 2013 in a Japanese university hospital. The study sample comprised 66 AKI and 2,152 non-AKI patients in the full-cohort analysis and 35 AKI and 1,269 non-AKI patients in the propensity-score-based analysis. Propensity scores were calculated using an ordered logistic regression model in which the dependent variable comprised three groups based on HES infusion volumes (0, 1-999, and ≥ 1,000 ml). The association between HES groups and postoperative AKI incidence was analyzed using multiple logistic regression models. Other candidate independent variables included patient characteristics and intraoperative measures. RESULTS: In the full-cohort analysis, 40 (60.6%) AKI patients were diagnosed as "risk", 15 (22.7%) as "injury," and 11 (16.7%) as "failure". In the propensity-score-based analysis, the corresponding values were 22 (62.9%), 8 (22.9%), and 5 (14.3%). There was no significant association between total infused HES and postoperative AKI incidence in either the full-cohort or the propensity-score-based analysis (P = 0.168 and P = 0.42, respectively). CONCLUSIONS: AKI incidence was not associated with clinical 6% HES 70/0.5 administration in gastroenterological surgery patients treated at a single center.

The antioxidant N-acetyl cysteine suppresses lidocaine-induced intracellular reactive oxygen species production and cell death in neuronal SH-SY5Y cells.

BACKGROUND: The local anesthetic lidocaine can affect intra- and extra-cellular signaling pathways in both neuronal and non-neuronal cells, resulting in long-term modulation of biological functions, including cell growth and death. Indeed, lidocaine was shown to induce necrosis and apoptosis in vitro. While several studies have suggested that lidocaine-induced apoptosis is mitochondrial pathway-dependent, it remains unclear whether reactive oxygen species (ROS) are involved in this process and whether the observed cell death can be prevented by antioxidant treatment. METHODS: The effects of lidocaine and antioxidants on cell viability and death were evaluated using SH-SY5Y cells, HeLa cells, and HeLa cell derivatives. Cell viability was examined via MTS/PES ([3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt]/phenazine ethosulfate) assay. Meanwhile, cell apoptosis and necrosis were evaluated using a cell death detection assay with Annexin V-FITC and PI staining, as well as by assaying for caspase-3/7 and caspase-9 activity, and by measuring the release of lactate dehydrogenase, respectively. Mitochondrial transmembrane potential (ΔΨm) was assessed using the fluorescent probe tetramethylrhodamine ethyl ester. RESULTS: Lidocaine treatment resulted in suppression of the mitochondrial electron transport chain and subsequent attenuation of mitochondrial membrane potential, as well as enhanced ROS production, activation of caspase-3/7 and caspase-9, and induction of apoptosis and necrosis in SH-SY5Y cells in a dose- and time-dependent manner. Likewise, the anesthetics mepivacaine and bupivacaine also induced apoptosis in SH-SY5Y cells. Notably, the antioxidants N-acetyl cysteine (NAC) and Trolox successfully scavenged the mitochondria-derived ROS and suppressed local lidocaine-induced cell death. CONCLUSIONS: Our findings demonstrate that the local anesthetics lidocaine, mepivacaine, and bupivacaine inhibited the activity of mitochondria and induced apoptosis and necrosis in a dose-dependent manner. Furthermore, they demonstrate that treatment with the antioxidants NAC, Trolox, and GGA resulted in preservation of mitochondrial voltage and inhibition of apoptosis via suppression of caspase activation.

[Combined use of continuous epidural anesthesia nand transversus abdominis plane block for postoperative management of cesarean delivery in a patient whose previous cesarean deliveries were not properly controlled].

We report the successful combined use of continuous epidural anesthesia and transversus abdominis plane block for the management of postoperative pain following a cesarean delivery in a patient whose paralysis and pain were not well controlled after two previous cesarean deliveries. A 28-year-old female patient with no remarkable medical history was scheduled to undergo cesarean delivery at 38 weeks and 3 days of pregnancy. She had undergone cesarean deliveries twice previously, at 23 and 25 years of age. Both of these procedures were concluded using combined spinal-epidural anesthesia. However, in both procedures, the continuous epidural catheter could not be removed within 12 hours because of paralysis of the right leg and sharp pain. Therefore, during the third operation, the concentration of the continuous epidural anesthesia infusion was decreased to prevent complications, and a transversus abdominis plane block was added. The patient experienced no postoperative pain and fewer complications. We think that the combined use of these blocks provided good postoperative pain control with fewer complications.

Successful treatment of fulminant community-acquired Pseudomonas aeruginosa necrotizing pneumonia in a previously healthy young man.

This report presents a case of fulminant community-acquired Pseudomonas aeruginosa necrotizing pneumonia in a previously healthy young man, including an analysis of the virulence of the P.aeruginosa isolated from the patient. The patient was successfully treated with intensive care and antibiotic treatment. This study analyzed the pathogenicity of the isolated strain both in vivo (using a mouse pneumonia model) and in vitro (using biofilm production), but could not explain how an otherwise healthy young man developed such severe community-acquired P.aeruginosa pneumonia. Although rare in community-acquired pneumonia, P.aeruginosa infection should be considered in patients with severe rapidly progressive pneumonia.

Sevoflurane causes greater QTc interval prolongation in elderly patients than in younger patients.

BACKGROUND: Sevoflurane and droperidol prolong the QT interval, and advancing age is not only associated with a prolongation of the QT interval but is also a risk factor for drug-induced QT interval prolongation. In this study, we compared the effect of sevoflurane and droperidol on the corrected QT (QTc) interval and the dispersion of ventricular repolarization (time interval from the peak to the end of the T wave [Tp-e]) in elderly patients with those in younger patients. METHODS: Under sevoflurane anesthesia (1.5%-2.5%) with an antiemetic dose of droperidol (1.25 mg), the QT interval and the Tp-e interval, which indicates transmural dispersion of repolarization across the myocardial wall, were measured in 30 elderly patients (70 years and older) and in 30 younger patients (20-69 years) for 2 hours. The QT interval was normalized for heart rate (QTc) using 3 different formulas: Bazett, Matsunaga, and Van de Water. Data are presented as mean +/- sd. RESULTS: The elderly group was 24.4 years older (P < 0.05) than the younger group. The QTc intervals in the 2 groups before anesthesia were not significantly different. Using all 3 formulas, the QTc interval in the elderly patient group was significantly prolonged by sevoflurane (the QTc intervals at preanesthesia and 60, 75, 90, and 120 minutes after sevoflurane exposure were 0.434 +/- 0.028 seconds, 0.450 +/- 0.037 seconds, 0.463 +/- 0.037 seconds, 0.461 +/- 0.037 seconds, and 0.461 +/- 0.038 seconds, respectively, with the Bazett formula). The sevoflurane-induced QTc interval prolongation in the elderly patient group was significantly greater than that in the younger patient group (0.450 +/- 0.037 seconds vs 0.432 +/- 0.034 seconds, 60 minutes after sevoflurane exposure; 0.463 +/- 0.037 seconds vs 0.441 +/- 0.037 seconds, 75 minutes after sevoflurane exposure; and 0.461 +/- 0.038 seconds vs 0.436 +/- 0.030 seconds, 120 minutes after sevoflurane exposure with the Bazett formula), but the sevoflurane-induced QTc interval prolongation was neither further enhanced with time nor by droperidol. The Tp-e interval was not affected in either group. CONCLUSION: Sevoflurane causes greater QTc interval prolongation in elderly patients than in younger patients. Although sevoflurane does not affect the transmural dispersion of repolarization and sevoflurane-induced QTc prolongation does not advance with time and by droperidol administration, QT interval prolongation and its associated arrhythmias should be carefully monitored during sevoflurane anesthesia in elderly patients.

Airway management in an infant with double aortic arch.

A 2-month old male was admitted due to repeated cyanotic attacks. He had suffered from stridor and retractive breathing since birth. Double aortic arch was diagnosed and the vascular ring formed by the double aortic arch was compressing the trachea. Multirow detector computed tomography showed that he had a right-dominant double aortic arch with left ductus arteriosus and an aberrant left subclavian artery, and that the narrowest part of the trachea, where the diameter was 2.0 mm, was located 9.0 mm above the carina. Airway management in patients with extreme narrowing of the trachea is challenging for anesthesiologists. He was scheduled for ligation and division of the left aortic arch and ductus arteriosus. In the operating theater, anesthesia was slowly induced with sevoflurane (0-4%) in oxygen. After mask ventilation was confirmed to be adequate, a 4.0 mm internal diameter endotracheal tube (ETT) was inserted and advanced smoothly beyond the tracheal stenosis. The tip of the ETT was placed just above the carina using a fiber optic bronchoscope (fiberscope) that was passed through the ETT. Since mechanical ventilation was adequate, vecuronium was administered. Surgery was conducted in the right lateral position and using a left thoracotomy approach. Anesthesia was maintained with sevoflurane (2-3%). After positioning, right one-lung ventilation was performed unexpectedly. However, anesthetic management was achieved without difficult ventilation during surgery. The tip of the ETT was pulled past the stenotic part before transfer to the intensive care unit (ICU). A patent trachea during spontaneous breathing under CPAP (5 and 2 cmH(2)O) was confirmed with a bronchofiberscope in the ICU. After weaning from mechanical ventilation, he had the persistence of mild stridor despite improvement of respiratory symptoms.

[Gas leakage from an anesthetic circuit caused by mis-installation of a canister].

We report a case of gas leakage from an anesthetic circuit, due to mis-installation of a different but very similar canister. A 56-year-old woman was scheduled for a pylogastrectomy. We planned to use a Mera MD757XLV anesthesia machine. At preoperative checking of the anesthetic machine, there was a gas leak from the anesthesia circuit without apparent reasons. We therefore had to use another anesthetic machine, MD705XL, which showed no gas leakage and was used without problems during anesthesia. Closed examination after the operation showed that the gas leakage from the MD757XLV machine occurred, because one of two canisters was wrongly replaced by a canister of MD705XL. The shapes of canisters of these two anesthesia machines look very similar, but there are crucial differences in their specifications, but even the manufacturer did not notice. These unnoticeable differences led to mis-installation of canisters, and one machine provided an airtight seal whereas the other did not. Both manufacturer and users should be aware of this danger.