Publications by authors named "Maiko Satomoto"

48 Publications

Preoperative heart rate variability analysis is as a potential simple and easy measure for predicting perioperative delirium in esophageal surgery.

Ann Med Surg (Lond) 2021 Oct 13;70:102856. Epub 2021 Sep 13.

Department of Psychosomatic and Palliative Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

Background: Delirium is one of the most common but severe perioperative complications. Autonomic activity evaluated by heart rate variability (HRV) has been recently reported as a useful tool for prediction and for early detection of delirium in acute care medicine, especially in postoperative intensive care unit (ICU) patients. We hypothesized that HRV, by 3-lead electrocardiogram (ECG), one day prior to surgery might correlate with the presence of postoperative delirium.

Materials And Methods: This study was cohort prospective pilot study. We measured preoperative HRV and postoperative delirium in patients who underwent surgery for elective esophageal cancer. ECG of the participants was performed for 10 min 6-12 h preceding surgery. Postoperatively, patients were admitted to the ICU or critical care unit and stayed for at least 3 days. Delirium was diagnosed by psychiatrist rounds twice a day.

Results: Delirium was assessed for 3 days after surgery and 30 patients performed the study. Seven patients developed delirium during their ICU stay, while the remaining twenty-three did not. After HRV analysis, the preoperative high frequency power in delirium patients was significantly lower than that in non-delirium patient. Other parameters of HRV, including lower frequency power, total power and the ratio showed no statistically significant difference between the groups.

Conclusion: The results of current study demonstrated that preoperative measurement of HRV may be a useful predictor of delirium. Further investigation could pave the way to a non-invasive, minimally stressful method of predicting postoperative delirium.
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http://dx.doi.org/10.1016/j.amsu.2021.102856DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8452778PMC
October 2021

Erector spinae plane block for back surgery.

J Anesth 2021 Sep 17. Epub 2021 Sep 17.

Department of Emergency Medicine, Shizuoka Saiseikai General Hospital, 1-1-1 Oshika, Suruga-ku, Shizuoka, 4228527, Japan.

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http://dx.doi.org/10.1007/s00540-021-03001-yDOI Listing
September 2021

Pregabalin-induced hypoglycemia in a dialysis patient.

Korean J Anesthesiol 2021 Feb 18;74(1):87. Epub 2021 Jan 18.

Department of Anesthesiology, Ohmori Medical Center, Toho University, Tokyo, Japan.

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http://dx.doi.org/10.4097/kja.20368.e1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7862940PMC
February 2021

JM-1232(-) and propofol, a new combination of hypnotics with short-acting and non-cumulative preferable properties.

Exp Anim 2021 Feb 16;70(1):101-107. Epub 2020 Oct 16.

Department of Anesthesiology, Aichi Gakuin University School of Dentistry, 2-11 Suemori-dori, Chikusa-ku, Nagoya, Aichi 4658651, Japan.

Drug interactions are significant in anesthesiology because drug combinations can potentially possess novel properties. The pharmacological advantages of a new combination of the benzodiazepine receptor agonist JM-1232(-) and propofol were investigated in mice. Male adult mice were administered JM-1232(-) or propofol or combinations of the two drugs intravenously. Loss of the righting reflex was evaluated as achieving hypnosis, and the time until recovery of the reflex was measured as hypnosis time. After determining the ED, doses double and triple the ED of propofol were injected with JM-1232(-) to compare hypnosis time. The injections were repeated four times, and the hypnosis times were compared. Flumazenil was administered separately immediately after the last dose was injected. The ED values ([95% confidence interval]) for hypnosis were 3.76 [3.36-4.10] for JM-1232(-) and 9.88 [8.03-11.58] mg kg for propofol. Co-administration of 0.5 and 1 mg kg JM-1232(-) reduced the ED values of propofol to 1.76 [1.21-2.51] and 1.00 [0.46-1.86] mg kg, respectively. The drug combination for hypnosis produced a supra-additive interaction. Hypnosis time was significantly shorter in the groups given the mixtures compared to each hypnotic administered alone. After repeated injections, hypnosis time with the mixtures showed smaller prolongation than that with the hypnotic alone. Flumazenil completely restored the recovery time after anesthesia. The combination of JM-1232(-) and propofol showed a supra-additive interaction, and the reduced hypnotic dose contributed to a faster recovery even after multiple injections.
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http://dx.doi.org/10.1538/expanim.20-0071DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7887627PMC
February 2021

Aspiration of massive free air from a large bore intravenous catheter sheath: A case report.

Radiol Case Rep 2020 Oct 4;15(10):1777-1780. Epub 2020 Aug 4.

Department of Anesthesiology, Ohmori Medical Center, Toho University, Tokyo, Japan.

We firstly experienced a rare case demonstrating that massive volume of free air was aspirated from a large bore intravenous catheter sheath of the pulmonary arterial catheter during placement. A 44-year-old male patient underwent the emergency induction of anesthesia for transplantation of liver donated by the brain death subject. After the induction, the central venous and pulmonary artery catheter placement was conducted. The aspiration of venous blood confirmed the intravascular insertion, but massive free air was aspirated when we advanced the sheath proximally. A perforation of subclavian vein and subsequent pneumothorax was strongly suspected. The emergency computed tomography revealed no sign of pneumothorax, pneumomediastinum nor extravasation. The operation was undergone with intensive monitoring and no further adverse complication was observed. The postoperative medical inquiry concluded that the massive free air was not aspirated from extravascular space, for example, thorax or mediastinum through the tip of the sheath, but from the proximal main port of the sheath. When the tip of sheath is occluded by the migration into small vessels, the large negative pressure through side port might easily aspirate the air through the 1-way valve of the main proximal port. Physicians should keep in mind of the structure of the catheter sheath.
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http://dx.doi.org/10.1016/j.radcr.2020.07.023DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406973PMC
October 2020

Pregabalin-induced hypoglycemia in a dialysis patient.

Korean J Anesthesiol 2020 12 29;73(6):570-571. Epub 2020 Jul 29.

Department of Anesthesiology, Ohmori Medical Center, Toho University, Tokyo, Japan.

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http://dx.doi.org/10.4097/kja.20368DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7714625PMC
December 2020

Blood-brain barrier disruption caused by neonatal sevoflurane-induced depends on exposure time and is reversible in mice.

Korean J Anesthesiol 2019 08 12;72(4):389-391. Epub 2019 Feb 12.

Department of Anesthesiology, Sasaki Foundation Kyoundo Hospital, Tokyo, Japan.

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http://dx.doi.org/10.4097/kja.d.19.00029DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676031PMC
August 2019

Sevoflurane preconditioning ameliorates lipopolysaccharide-induced cognitive impairment in mice.

Exp Anim 2018 May 29;67(2):193-200. Epub 2017 Nov 29.

Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.

Systemic inflammation induces brain neuronal inflammation, in turn causing acute cognitive disorders. Furthermore, neuronal inflammation is one cause of postoperative cognitive disorder (POCD) and delirium. However, no sufficiently established pharmacological treatment is available for neurocognitive inflammation. This study evaluated the possible neuroprotective effects of preconditioning with sevoflurane anesthesia on cognition and neuroinflammatory changes in an animal model of lipopolysaccharide (LPS)-induced systemic inflammation. Adult mice were randomly divided into (1) control, (2) 2% sevoflurane preconditioning for 1 h, (3) intraperitoneal 5 mg/kg LPS injection, and (4) 2% sevoflurane preconditioning for 1 h + LPS injection groups. At 24 h after 5 mg/kg LPS injection, microglial activation based on ionized calcium-binding adapter molecule 1 (Iba-1) expression in the hippocampus was determined using immunostaining and immunoblotting. IL-1β and IL-6 immunoblotting were used as inflammation markers, and β-site of amyloid precursor protein cleaving enzyme 1 (BACE1) immunoblotting was performed to evaluate amyloid β-protein (Aβ) accumulation. Long-term cognitive impairment was evaluated using fear conditioning tests. Intraperitoneal LPS increased levels of Iba-1 (150%), inflammation markers (160%), and Aβ accumulation (350%), and sevoflurane preconditioning suppressed these increases. Systemic LPS caused learning deficits. Sevoflurane also maintained long-term memory in mice receiving LPS injection. Sevoflurane preconditioning prevented long-term memory impairment in the mouse model administered systemic LPS by decreasing excessive microglial activation, inflammation, and Aβ accumulation. This study supports the hypothesis that sevoflurane preconditioning might also be beneficial for neuronal inflammation. Sevoflurane might be beneficial for reducing delirium and POCD.
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http://dx.doi.org/10.1538/expanim.17-0102DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5955751PMC
May 2018

Corrigendum to "Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice".

Anesthesiol Res Pract 2017 17;2017:1368514. Epub 2017 Oct 17.

Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 1138519, Japan.

[This corrects the article DOI: 10.1155/2016/9682703.].
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http://dx.doi.org/10.1155/2017/1368514DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664264PMC
October 2017

Smaller effect of propofol than sevoflurane anesthesia on dopamine turnover induced by methamphetamine and nomifensine in the rat striatum: an in vivo microdialysis study.

Exp Anim 2018 May 23;67(2):147-153. Epub 2017 Nov 23.

Departemnt of Surgical Intensive Care Medicine, Nagoya University Hospital, 65 Tsurumai-cho, Showaku, Nagoya-shi, Aichi 466-8550, Japan.

Volatile anesthetics accelerate dopamine turnover in the brain, especially when used in conjunction with psychotropic agents such as methamphetamine and nomifensine. The effect of intravenous propofol anesthesia on the extracellular dopamine concentrations is unclear. The aim of this study was to compare the effect of two anesthetics on the extracellular concentrations of dopamine and metabolites using an in vivo microdialysis model. Male Sprague Dawley rats were implanted with a microdialysis probe into the right striatum. The probe was perfused with modified Ringer's solution, and the dialysate was directly injected into a high-performance liquid chromatography system every 20 min. The rats were intraperitoneally administered saline, methamphetamine at 2 mg/kg, or nomifensine at 10 mg/kg. After treatment, the rats were anesthetized with intravenous propofol (20 mg/kg followed by 25 or 50 mg/kg/h) or inhalational sevoflurane (2.5%) for 1 h. Propofol showed no effect on the extracellular concentration of dopamine during anesthesia; however, propofol decreased the dopamine concentration after anesthesia in the high-dose group. Sevoflurane anesthesia increased the concentration of metabolites. Systemic administration of methamphetamine and nomifensine increased the extracellular concentration of dopamine. Sevoflurane anesthesia significantly enhanced the increase in the dopamine concentration induced by both methamphetamine and nomifensine, whereas propofol anesthesia showed no effect on the methamphetamine- and nomifensine-induced dopamine increase during anesthesia. The enhancing effect of psychotropic agent-induced acceleration of dopamine turnover was smaller for propofol anesthesia than for sevoflurane anesthesia.
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http://dx.doi.org/10.1538/expanim.17-0092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5955746PMC
May 2018

Perioperative airway management of a 16-year-old boy with progressive airway obstruction due to juvenile nasopharyngeal angiofibroma.

Clin Case Rep 2017 08 23;5(8):1274-1276. Epub 2017 Jun 23.

Department of Anesthesiology Sasaki Foundation Kyoundo Hospital Tokyo Japan.

Juvenile nasopharyngeal angiofibroma (JNA) involves difficult anesthetic management because of the risk of massive bleeding, while airway management is rarely a problem in JNA. This report presents an unusual case of JNA causing airway obstruction.
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http://dx.doi.org/10.1002/ccr3.1056DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5538053PMC
August 2017

Apocynin preserves glutamatergic neurons in the basolateral amygdala in mice with neonatal sevoflurane exposure.

Korean J Anesthesiol 2017 Jun 21;70(3):335-340. Epub 2017 Apr 21.

Department of Anesthesiology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan.

Background: Neonatal exposure to anesthetics induces neuronal apoptosis and long-term cognitive dysfunction in rodents. We showed that the nicotinamide adenine dinucleotide phosphate-oxidase inhibitor apocynin not only reduces neurotoxicity by decreasing superoxide levels and preventing mitochondrial dysfunction but also improves long-term memory impairment in neonatal mice exposed to sevoflurane. We also found that after the contextual fear conditioning test, glutamatergic neurons expressed c-Fos (neural activation) regardless of previous exposure to sevoflurane. Moreover, there were fewer c-Fos-expressing glutamatergic neurons in the basolateral amygdala (BLA) after exposure to sevoflurane than after exposure to carrier gas. In this study, we investigated whether the administration of apocynin prior to sevoflurane exposure would preserve glutamatergic neurons in the BLA.

Methods: Apocynin (50 mg/kg) was injected intraperitoneally into six-day-old male mice 30 min before 6 h of exposure to 3% sevoflurane or carrier gas only. The mice were allowed to mature and then were subjected to the contextual fear conditioning test. The neural activation and neuron population in the BLA were investigated 2 h later.

Results: Administration of apocynin prior to neonatal sevoflurane exposure not only prevented learning deficits but also preserved c-Fos-expressing glutamatergic neurons in the BLA.

Conclusions: Apocynin mitigates the cognitive impairment induced by neonatal sevoflurane exposure and preserves c-Fos-expressing glutamatergic neurons in the basolateral amygdala.
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http://dx.doi.org/10.4097/kjae.2017.70.3.335DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5453896PMC
June 2017

Rapid Fluid Infusion and Depth of Anesthesia.

Anesthesiology 2017 05;126(5):985-986

Nagoya University Graduate School of Medicine, Nagoya, Japan (Y.U.A.).

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http://dx.doi.org/10.1097/ALN.0000000000001577DOI Listing
May 2017

A low dose of droperidol decreases the desflurane concentration needed during breast cancer surgery: a randomized double-blinded study.

Korean J Anesthesiol 2017 Feb 25;70(1):27-32. Epub 2016 Oct 25.

Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.

Background: Droperidol (DHB) reportedly reduces the dose of propofol needed to achieve hypnosis when anesthesia is induced and decreases the bispectral index (BIS) in propofol-sedated patients during spinal anesthesia. We reported previously that supplemental DHB decreased the BIS after the administration of sevoflurane and remifentanil. This study investigated the effect of DHB on desflurane (DES) consumption in a clinical setting.

Methods: We conducted a prospective, randomized double-blinded study of 35 women with American Society of Anesthesiologist physical status I or II who underwent a mastectomy. Either DHB (20 µg/kg) or a saline placebo was administered to patients 30 min after the induction of anesthesia. A blinded anesthesiologist maintained a BIS value of 50 during anesthesia by modulating inhaled DES concentrations that changed 0.5% at 2.5 min intervals and maintained analgesia via the constant administration of remifentanil by referring to vital signs. The primary endpoint was the effect of DHB on DES consumption. The secondary endpoints included blood circulatory parameters, the time from the end of surgery to extubation, and discharge time between the groups.

Results: The characteristics of the patients did not differ between the groups. The DHB group used a mean of 27.2 ± 6.0 ml of DES compared with 41.4 ± 9.5 ml by the placebo group (P < 0.05).

Conclusions: A small dose of DHB reduced the DES concentration needed to maintain a BIS of 50. Our results show that DHB reduced the consumption of DES without adverse effects.
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http://dx.doi.org/10.4097/kjae.2017.70.1.27DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5296383PMC
February 2017

Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice.

Anesthesiol Res Pract 2016 8;2016:9682703. Epub 2016 Nov 8.

Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 1138519, Japan.

In rodents, neonatal sevoflurane exposure induces neonatal apoptosis in the brain and results in learning deficits. Sugammadex is a new selective neuromuscular blockade (NMB) binding agent that anesthesiologists can use to achieve immediate reversal of an NMB with few side effects. Given its molecular weight of 2178, sugammadex is thought to be unable to pass through the blood brain barrier (BBB). Volatile anesthetics can influence BBB opening and integrity. Therefore, we investigated whether the intraperitoneal administration of sugammadex could exacerbate neuronal damage following neonatal 2% sevoflurane exposure via changes in BBB integrity. Cleaved caspase-3 immunoblotting was used to detect apoptosis, and the ultrastructure of the BBB was examined by transmission electron microscopy. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice. Sugammadex alone without sevoflurane did not induce apoptosis. The coadministration of sugammadex with sevoflurane to neonatal mice caused a significant increase (150%) in neuroapoptosis in the brain compared with 2% sevoflurane. In neonatal anesthesia, sugammadex could influence neurotoxicity together with sevoflurane. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice.
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http://dx.doi.org/10.1155/2016/9682703DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5118529PMC
November 2016

Anesthesia-induced neurotoxicity in an animal model of the developing brain: mechanism and therapies.

Neural Regen Res 2016 Sep;11(9):1407-1408

Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.

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http://dx.doi.org/10.4103/1673-5374.191207DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5090835PMC
September 2016

Neonatal Sevoflurane Exposure Induces Adulthood Fear-induced Learning Disability and Decreases Glutamatergic Neurons in the Basolateral Amygdala.

J Neurosurg Anesthesiol 2018 Jan;30(1):59-64

Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.

Background: Neonatal mice exposed to sevoflurane show certain cognitive and behavioral impairments in adulthood. However, the mechanisms underlying long-term cognitive deficits induced by sevoflurane exposure remain unknown. The present study was performed to investigate whether there is differential neuronal activation between naive mice and sevoflurane-exposed neonates in fear-conditioning tests based on immediate early gene (c-Fos) expression.

Methods: Male mice were exposed to 3% sevoflurane (SEVO group) or carrier gas alone (no anesthesia, NA group) for 6 hours on postnatal day 6. The mice were allowed to mature before performing the contextual fear-conditioning test. A reduced freezing response was confirmed in the SEVO group. Neural activation in the regions of the medial prefrontal cortex, hippocampus, and amygdala was investigated using c-Fos immunostaining 2 hours after the test. The types of neurons activated were also identified.

Results: The number of c-Fos-positive cells decreased by 27% in the basolateral amygdala in the SEVO group, while no significant changes were observed in other regions. Furthermore, glutamatergic, but not γ-aminobutyric acid (GABA)ergic, neurons expressed c-Fos after the contextual fear-conditioning test in both groups. The number of glutamatergic neurons in the basolateral amygdala in the SEVO group was reduced by 27%.

Conclusions: Decreased neural activation in the basolateral amygdala may be associated with reduced freezing time in neonatal sevoflurane-exposed mice. Fewer glutamatergic neurons responding to fear stimuli in the basolateral amygdala may contribute to decreased neural activation and learning deficits in mice exposed to sevoflurane as neonates.
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http://dx.doi.org/10.1097/ANA.0000000000000387DOI Listing
January 2018

Sevoflurane Inhalation Accelerates the Long-Term Memory Consolidation via Small GTPase Overexpression in the Hippocampus of Mice in Adolescence.

PLoS One 2016 15;11(9):e0163151. Epub 2016 Sep 15.

Department of Anesthesiology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.

Sevoflurane exposure impairs the long-term memory in neonates. Whether the exposure to animals in adolescence affects the memory, however, has been unclear. A small hydrolase enzyme of guanosine triphosphate (GTPase) rac1 plays a role in the F-actin dynamics related to the synaptic plasticity, as well as superoxide production via reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation. The current study was designed to examine whether sevoflurane exposure to mice in early adolescence modifies the long-term learning ability concomitantly with the changes in F-actin constitution as well as superoxide production in the hippocampus according to the levels of rac1 protein expression. Four-week-old mice were subjected to the evaluation of long-term learning ability for three days. On day one, each mouse was allowed to enter a dark chamber for five min to acclimatization. On day two, the procedure was repeated with the addition of an electric shock as soon as a mouse entered the dark chamber. All mice subsequently inhaled 2 L/min air with (Sevoflurane group) and without (Control group) 2.5% sevoflurane for three hours. On day three, each mouse was placed on the platform and retention time, which is the latency to enter the dark chamber, was examined. The brain removed after the behavior test, was used for analyses of immunofluorescence, Western immunoblotting and intracellular levels of superoxide. Sevoflurane exposure significantly prolonged retention time, indicating the enhanced long-term memory. Sevoflurane inhalation augmented F-actin constitution coexisting with the rac1 protein overexpression in the hippocampus whereas it did not alter the levels of superoxide. Sevoflurane exposure to 4-week-old mice accelerates the long-term memory concomitantly with the enhanced F-actin constitution coexisting with the small GTPase rac1 overexpression in the hippocampus. These results suggest that sevoflurane inhalation may amplify long-term memory consolidation via the increased cytoskeleton constitution in the hippocampus of animals in early adolescence.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0163151PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5025001PMC
August 2017

The Influence of Differences in Solvents and Concentration on the Efficacy of Propofol at Induction of Anesthesia.

Anesthesiol Res Pract 2016 21;2016:9178523. Epub 2016 Jan 21.

Department of Intensive Care Unit, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka 4313192, Japan.

Background. Propofol is a popular intravenous anesthetic and varieties of formulations were produced from different laboratories. The present study compared efficacy of propofol of different laboratories and different concentrations (1 and 2%) during induction of anesthesia. Methods. Seventy-five scheduled surgical patients were randomly allocated into three groups. The patients of group D1 received AstraZeneca Diprivan 1% (Osaka, Japan) at a rate of 40 mg kg(-1) h(-1). Group M1 was given 1% Maruishi (Maruishi Pharmaceutical, Osaka, Japan) and group M2 was given 2% formulation at the same rate of propofol. Achieving hypnosis was defined as failure to open their eyes in response to a verbal command and the venous blood sample was withdrawn. Results. The hypnotic doses of M2 were significantly larger (D1: 91.4 ± 30.9, M1: 90.7 ± 26.7, and M2: 118.4 ± 40.2 mg, resp. (mean ± SD). p < 0.005). Age and gender were selected as statistically significant covariates using general linear model-ANOVA. The blood concentration showed no significant difference among the groups (3.73 ± 2.34, 4.10 ± 3.04, and 4.70 ± 2.12 μg mL(-1), resp.). Conclusion. The required dose of propofol was different among the formulations; however, the serum concentration showed no significant difference. This trial is registered with UMIN Clinical Trial Registry: UMIN000019925.
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http://dx.doi.org/10.1155/2016/9178523DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4745982PMC
February 2016

Therapeutic effects of intravenous administration of bone marrow stromal cells on sevoflurane-induced neuronal apoptosis and neuroinflammation in neonatal rats.

Korean J Anesthesiol 2015 Aug 28;68(4):397-401. Epub 2015 Jul 28.

Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.

Background: Sevoflurane exposure during the early postnatal period causes neuroinflammation and neuronal apoptosis in rodents. Bone marrow stromal cells (BMSCs) have been shown to protect and repair the damaged central nervous system, for example in ischemic stroke models. In this study, we investigated whether intravenous administration of BMSCs ameliorated neurodegeneration, induced by sevoflurane exposure, in neonatal rats.

Methods: Sprague-Dawley rat pups (postnatal day 7) were exposed to 2% sevoflurane for 6 h (vehicle group, n = 7). BMSCs were administered 30 min after induction of sevoflurane anesthesia (BMSCs group, n = 7). The pups were exposed to carrier gas only, as a negative control (mock anesthesia group, n = 4). We assessed the therapeutic effects of BMSC treatment by measuring expression of the pro-inflammatory cytokine interleukin-6 (IL-6), and levels of cleaved caspase-3, in brain tissues immediately following sevoflurane anesthesia.

Results: Analysis of the cleaved caspase-3 bands revealed that levels of activated caspase-3 were elevated in the vehicle group compared with the mock anesthesia group, indicating that a single exposure to sevoflurane at subclinical concentrations can precipitate neuronal apoptosis. BMSC treatment did not suppress apoptosis induced by sevoflurane exposure (compared with the vehicle group). The vehicle group had higher proinflammatory cytokine IL-6 protein levels compared with the mock anesthesia group, indicating that sevoflurane exposure induces IL-6 expression. BMSC treatment suppressed sevoflurane-induced increases in IL-6 expression, indicating that these cells can inhibit the neuroinflammation induced by sevoflurane exposure (vehicle group vs. BMSC group).

Conclusions: Intravenous administration of BMSCs reduces neuroinflammation, but does not attenuate apoptosis induced by sevoflurane exposure.
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http://dx.doi.org/10.4097/kjae.2015.68.4.397DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524940PMC
August 2015

ERK2 Alone Drives Inflammatory Pain But Cooperates with ERK1 in Sensory Neuron Survival.

J Neurosci 2015 Jun;35(25):9491-507

Washington University Pain Center, Department of Anesthesiology, St. Louis, Missouri 63110, and

Unlabelled: Extracellular signal-regulated kinases 1 and 2 (ERK1/2) are highly homologous yet distinct components of signal transduction pathways known to regulate cell survival and function. Recent evidence indicates an isoform-specific role for ERK2 in pain processing and peripheral sensitization. However, the function of ERK2 in primary sensory neurons has not been directly tested. To dissect the isoform-specific function of ERK2 in sensory neurons, we used mice with Cre-loxP-mediated deletion of ERK2 in Nav1.8(+) sensory neurons that are predominantly nociceptors. We find that ERK2, unlike ERK1, is required for peripheral sensitization and cold sensation. We also demonstrate that ERK2, but not ERK1, is required to preserve epidermal innervation in a subset of peptidergic neurons. Additionally, deletion of both ERK isoforms in Nav1.8(+) sensory neurons leads to neuron loss not observed with deletion of either isoform alone, demonstrating functional redundancy in the maintenance of sensory neuron survival. Thus, ERK1 and ERK2 exhibit both functionally distinct and redundant roles in sensory neurons.

Significance Statement: ERK1/2 signaling affects sensory neuron function and survival. However, it was not clear whether ERK isoform-specific roles exist in these processes postnatally. Previous work from our laboratory suggested either functional redundancy of ERK isoforms or a predominant role for ERK2 in pain; however, the tools to discriminate between these possibilities were not available at the time. In the present study, we use new genetic knock-out lines to demonstrate that ERK2 in sensory neurons is necessary for development of inflammatory pain and for postnatal maintenance of peptidergic epidermal innervation. Interestingly, postnatal loss of both ERK isoforms leads to a profound loss of sensory neurons. Therefore, ERK1 and ERK2 display both functionally distinct and redundant roles in sensory neurons.
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http://dx.doi.org/10.1523/JNEUROSCI.4404-14.2015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4478259PMC
June 2015

[Anesthetic management of a pregnant woman with brain tumor].

Masui 2014 Oct;63(10):1142-5

A 35-year-old parturient, 35 weeks pregnant, pre- sented with intracranial tumor with increased intracra- nial pressure. She underwent emergency cesarean section under general anesthesia, followed by craniotomy. The intraoperative and postoperative courses were uneventful. The occurrence of brain tumors during pregnancy is very rare; meanwhile pregnancy may aggravate the natural history of an intracranial tumor, and may even unmask previously unknown diagnosis. The decision to proceed with cesarean section and neurosurgery depends on the site, size, type of tumor, neurological signs and symptoms, age of the fetus, and the patient's wishes. Therefore, close communication between the neurologist, neurosurgeon, anesthesiologist, obstetrician and the patient is very important.
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October 2014

[Potential influence of pre and intraoperative factors on postoperative recurrence and survival in patients undergoing radical resection of esophageal cancer].

Masui 2014 Dec;63(12):1344-9

Background: Several papers report that preoperative and intraoperative factors influence postoperative recurrence of malignancy. The purpose of this study is to define which factors affect the recurrence and survival of patients after the surgical resection of the esophageal cancer.

Methods: Ninety five patients underwent complete elective resection of the esophageal cancer. All patients were without preoperative chemotherapy and radiotherapy. We extracted 12 parameters, and cox regression analyses were used to assess the relation of 12 factors and the outcomes of patients. The 12 factors included preoperative factors (age, sex, weight stage of cancer, ASA PS, serum creatinine and total bilirubin), intraoperative variables (duration of anesthesia, blood transfusion, fluid balance, hypotensive episodes) and surgical Apgar score. Hypotensive episodes were defined as the systolic pressure lower than 70 mmHg occurring from the introduction of anesthesia to the end of anesthesia.

Results: Hypotensive episodes and blood transfusion significantly affected 1 year cancer specific survival. Stage of cancer and blood transfusion affected 5 year cancer specific survival.

Conclusions: We found that intraoperative hypotension affected 1-year cancer specific survival; however, the stage of cancer affected long-term survival instead of intraoperative factors. A low 5-year survival rate in esophageal cancer may have affected this result.
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December 2014

[Resveratrol did not prevent sevoflurane-induced neuroapoptosis in the neonatal mice brain].

Masui 2013 Oct;62(10):1184-7

Department of Anesthesiology and Pain Medicine, Tokyo Medical and Dental University, Tokyo 113-8510.

Background: In an animal model, neonatal exposure to sevoflurane induces neuroapoptosis, leading to memory deficits in adulthood. A recent study showed that resveratrol (20 mg x kg(-1)) prevent alcohol-induced cognitive deficits and neural apotosis in rat pups postnatally exposed to ethanol. We investigated if resveratorol prevent sevoflurane induced neuroapotosis.

Methods: Six-day-old mice were divided into two groups: resveratorol and control groups. Pups were given resveratrol orally 24h and 1h before sevoflurane anesthesia. Anesthesia was maintained for 6h. After anesthesia, apotosis was evaluated by immunohistochemical staining for activated caspase-3. Western blot analysis for cleaved poly-(adenosine diphosphate-ribose) polymerase was performed to examine apotosis.

Results: Neonatal exposure to sevoflurane induced severe neuroapotosis. There were no differences between control groups and resveratrol groups with regards to immunohistochemical staining and western blot analysis.

Conclusions: Resveratrol did not prevent sevoflurane-induced neuroapoptosis in the neonatal mice brain.
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October 2013

The determinants of propofol induction time in anesthesia.

Korean J Anesthesiol 2013 Aug 27;65(2):121-6. Epub 2013 Aug 27.

Department of Emergency Medicine, Nagoya University Hospital, Aichi, Japan.

Background: The required dose of anesthetics is generally smaller in patients with low cardiac output (CO). A high CO decreases the blood concentration of anesthetics during induction and maintenance of anesthesia. However, a high CO may also shorten the delivery time of anesthetics to the effect site, e.g. the brain. We assessed the time required for induction of anesthesia with propofol administered by target-controlled infusion (TCI), and investigated factors that modify the pharmacodynamics of propofol.

Methods: After measuring CO and blood volume (BV) by dye densitometry, propofol was infused using TCI to simulate a plasma concentration of 3 µg/ml. After infusion, the time taken to achieve bispectral index (BIS) values of 80 and 60 was determined. Age, sex, lean body mass (LBM), and cardiovascular parameters were analyzed as independent variables. The dependent variables were the time taken to achieve each BIS value and the plasma concentration of propofol (Cp) 10 min after the commencement of infusion.

Results: Multiple regression analysis revealed that a high CO significantly reduced the time taken to reach the first end point (P = 0.020, R(2) = 0.076). Age and LBM significantly prolonged the time taken to reach the second end point (P = 0.001). Cp was negatively correlated with BV (P = 0.020, R(2) = 0.073).

Conclusions: Cardiac output was a statistically significant factor for predicting the time required for induction of anesthesia in the initial phase, whereas, age and LBM were significant variables in the late phase. The pharmacodynamics of propofol was intricately altered by CO, age, and LBM.
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http://dx.doi.org/10.4097/kjae.2013.65.2.121DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766776PMC
August 2013

Mechanical allodynia but not thermal hyperalgesia is impaired in mice deficient for ERK2 in the central nervous system.

Pain 2012 Nov 16;153(11):2241-2252. Epub 2012 Aug 16.

Department of Anesthesiology, National Defense Medical College, Tokorozawa 359-8513, Japan Department of Anesthesiology, Tokyo Medical and Dental University Graduate School, Tokyo 113-8510, Japan Institute of Developmental Biology and Cancer Research, University of Nice Sophia-Antipolis, Centre National de la Recherche Scientifique, Unité mixte de Recherche 6543, Centre Antoine Lacassagne, Nice 06189, France Aging Regulation Research Team, Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo 173-0015, Japan.

Extracellular signal-regulated kinase (ERK) plays critical roles in pain plasticity. However, the specific contribution of ERK2 isoforms to pain plasticity is not necessarily elucidated. Here we investigate the function of ERK2 in mouse pain models. We used the Cre-loxP system to cause a conditional, region-specific, genetic deletion of Erk2. To induce recombination in the central nervous system, Erk2-floxed mice were crossed with nestin promoter-driven cre transgenic mice. In the spinal cord of resultant Erk2 conditional knockout (CKO) mice, ERK2 expression was abrogated in neurons and astrocytes, but indistinguishable in microglia compared to controls. Although Erk2 CKO mice showed a normal baseline paw withdrawal threshold to mechanical stimuli, these mice had a reduced nociceptive response following a formalin injection to the hind paw. In a partial sciatic nerve ligation model, Erk2 CKO mice showed partially restored mechanical allodynia compared to control mice. Interestingly, thermal hyperalgesia was indistinguishable between Erk2 CKO and control mice in this model. In contrast to Erk2 CKO mice, mice with a targeted deletion of ERK1 did not exhibit prominent anomalies in these pain models. In Erk2 CKO mice, compensatory hyperphosphorylation of ERK1 was detected in the spinal cord. However, ERK1 did not appear to influence nociceptive processing because the additional inhibition of ERK1 phosphorylation using MEK (MAPK/ERK kinase) inhibitor SL327 did not produce additional changes in formalin-induced spontaneous behaviors in Erk2 CKO mice. Together, these results indicate that ERK2 plays a predominant and/or specific role in pain plasticity, while the contribution of ERK1 is limited.
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http://dx.doi.org/10.1016/j.pain.2012.07.020DOI Listing
November 2012

Neonatal exposure to sevoflurane induces abnormal social behaviors and deficits in fear conditioning in mice.

Anesthesiology 2009 Mar;110(3):628-37

Department of Developmental Anatomy and Regenerative Biology, National Defense Medical College, Tokorozawa, Saitama, Japan.

Background: Neonatal exposure to anesthetics that block N-methyl-D-aspartate receptors and/or hyperactivate gamma-aminobutyric acid type A receptor has been shown to cause neuronal degeneration in the developing brain, leading to functional deficits later in adulthood. The authors investigated whether exposure of neonatal mice to inhaled sevoflurane causes deficits in social behavior as well as learning disabilities.

Methods: Six-day-old C57BL/6 mice were exposed to 3% sevoflurane for 6 h. Activated cleaved caspase-3 immunohistochemical staining was used for detection of apoptosis. Cognitive functions were tested by pavlovian conditioned fear test. Social behavior was tested by social recognition and interaction tests.

Results: Neonatal exposure to sevoflurane significantly increased the number of apoptotic cells in the brain immediately after anesthesia. It caused persistent learning deficits later in adulthood as evidenced by decreased freezing response in both contextual and cued fear conditioning. The social recognition test demonstrated that mice with neonatal exposure to sevoflurane did not develop social memory. Furthermore, these mice showed decreased interactions with a social target compared with controls in the social interaction test, indicating a social interaction deficit. The authors did not attribute these abnormalities in social behavior to impairments of general interest in novelty or olfactory sensation, because they did not detect significant differences in the test for novel inanimate object interaction or for olfaction.

Conclusions: This study shows that exposure of neonatal mice to inhaled sevoflurane could cause not only learning deficits but also abnormal social behaviors resembling autism spectrum disorder.
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http://dx.doi.org/10.1097/ALN.0b013e3181974fa2DOI Listing
March 2009

Isoflurane anesthesia inhibits clozapine- and risperidone-induced dopamine release and anesthesia-induced changes in dopamine metabolism was modified by fluoxetine in the rat striatum: an in vivo microdialysis study.

Neurochem Int 2008 Feb 22;52(3):384-91. Epub 2007 Jul 22.

Intensive Care Unit of University Hospital, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu city, Shizuoka 431-3192, Japan.

Previously, we have reported that halothane anesthesia increases the extracellular concentrations of dopamine (DA) metabolites in the rat striatum using in vivo microdialysis techniques, and we have suggested that volatile anesthetics affect DA release and metabolism in various ways. The present investigation assesses the effect of isoflurane, widely used in clinical anesthesia, on DA release and metabolism. A microdialysis probe was implanted in the striatum of male Sprague-Dawley rats (n=5-7 per group). After recovery, the probe was perfused with modified Ringer's solution and 40 microl of dialysate were injected into a high performance liquid chromatograph every 20 min. The rats were given saline or the same volume of 10 mg kg(-1) clozapine, risperidone, fluoxetine or citalopram. After the pharmacological treatment, the rats were anesthetized with 1.0% or 2.5% isoflurane for 1h. The data were analyzed using two-way analysis of variance (ANOVA). For each drug with significant (p<0.05) drug-time interactions, the statistical analysis included one-way ANOVA and Newman-Keuls post hoc comparisons. A high concentration of isoflurane (2.5%) anesthesia increased the extracellular concentration of DA metabolites during emergence from anesthesia. The levels of DA metabolites increased in an isoflurane concentration-dependent manner. Isoflurane attenuated DA release induced by clozapine and risperidone. Fluoxetine, but not citalopram, antagonized the isoflurane-induced increase in metabolites. The results of current investigation suggest that isoflurane enhances presynaptic DA metabolism, and that the oxidation of DA might be partially modulated by the activities of the dopaminergic-serotonergic pathway at a presynaptic site in the rat striatum.
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http://dx.doi.org/10.1016/j.neuint.2007.07.012DOI Listing
February 2008
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