Kyushu University Academic Staff Educational and Research Activities Database
List of Presentations
Kentaro Tokuda Last modified date:2020.05.27

Assistant Professor / Intensive Care Unit, kyushu University Hospital / Intensive Care Unit / Kyushu University Hospital


Presentations
1. Yukie Mizuta, Kentaro Tokuda, Jie Guo, Tomohiko Akahoshi, Masaharu Murata, Thiosulfate Reduces Doxorubicin-induced Cardiac Failure in a Murine Model, 48th Critical Care Congress, 2019.02.
2. Organ-protective effects of endogeneous gasotransmitters.
3. Kentaro Tokuda, Emergency intubation with/without neuromuscular blocking agents outside of the operating room., Korean Association for Respiratory Care, 2018.07, [URL], Tracheal intubation outside of the operating room (OR), i.e. intensive care unit, emergency department, general wards, etc., is more problematic than that performed in the OR. A number of researchers have reported that the incidence of difficult intubation and the rate of complications associated with tracheal intubation is higher in cases of non-OR intubation than in elective surgical patients. There are several reasons as to why airway management in critically ill patients can be challenging. First, the patients are in a life-threatening condition that requires emergency intubation. Because their physiological reserve is highly impaired, they can rapidly progress to severe hypoxemia during intubation procedure or to profound hypotension or even cardiac arrest due to the administration of sedatives prior to intubation. Second, the preparation time to intubation is limited, preventing critical care physicians from evaluating the airway of the patients adequately, and the patients might be at risk of aspiration due to insufficient fasting time. Third, the availability of airway devices as well as staff skilled in airway management is limited outside of the OR.
One of the most contested issues associated with airway management in critical care is whether or not neuromuscular blocking agents (NMBA) should be used for emergent tracheal intubation in critically ill patients. It has been claimed that maintaining spontaneous respiration during emergency intubation is the best way to prevent the airway management from deteriorating in such patients. However, recent evidence has shown that the use of NMBA during emergency intubation facilitates the intubation procedure, improves the success rate of the first intubation attempt, and decreases the rate of procedure-related complications. Regardless of the effects of NMBA, the presence of skilled personnel is crucial for a successful procedure, and an airway evaluation predicting the difficulty of intubation prior to the procedure is useful when it can be performed. As with the procedure in the OR, emergency tracheal intubation outside the OR should not be performed until the airway is precisely evaluated so that we can decide whether or not to administer NMBA.
In this lecture, I will focus on the potential risks as well as the advantages associated with the use of NMBA during emergency intubation of critically ill patients.
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4. Kentaro Tokuda, Jun Maki, Taku Nakagawa, Sumio Hoka , Management of Life-threatening Hypermagnesemia Induced by Repetitive Magnesium Cathartics. , Annual Meeting of the American Society of Anesthesiologists, 2017.10.
5. K. Tokuda, J. Maki, T. Fujiyoshi, N. Kaku, S. Mizuguchi, T. Akahoshi, S. Hoka, Y. Maehara, The efficacy of veno-venous extracorporeal membrane oxygenation for patients with acute respiratory failure. , 30th Annual Congress of European Society of Intensive Care Medicine, 2017.09.
6. Neuromuscular blocking agents should not (or could not) be used for tracheal intubation outside of the operating rooms..
7. 徳田 賢太郎, 牧 盾, 賀耒 典之, 水口 壮一, 深田 光敬, 赤星 朋比古, 外 須美夫, 前原 喜彦, The Presepsin Level on ICU Admission Is a Marker of the Severity of ICU Patients. , 46th Critical Care Congress (Society of Critical Care Medicine), 2017.01.
8. Kentaro Tokuda, Kenzo Araki, Hidekazu Setoguchi, Jun Maki, Sumio Hoka, Entrapped thoracic epidural catheter due to knotting: the utility of 3D-CT scans, Annual Meeting of American Society of the Anesthesiologists, 2015.10.
9. Kentaro Tokuda, Ken Yamaura, Midoriko Higashi, Sumio Hoka, Effects of cardiopulmonary bypass on the accuracy of non-invasive hemoglobin measurement by pulse co-oximetry, 28th Annual Congress of the European Society of Intensive Care Medicine , 2015.10.
10. Kentaro Tokuda, Improvement of postoperative analgesia by transversus abdominis plane block in patients with living donor hepatectomy, The 33rd Congress of the Scandinavian Society of Anaesthesiology and Intensive Care, 2015.06.
11. Kentaro Tokuda, Ken Yamaura, Midoriko Higashi, Sumio Hoka, The effect of cardiopulmonary bypass on the accuracy of non-invasive hemoglobin measurement by pulse co-oximetry, American society of Anesthesiologists 2014 Annual Meeting, 2014.10.
12. Kentaro Tokuda, Fumito Ichinose, Hepatoprotective effects of hydrogen sulphide against acute liver failure, European Society of Intensive Care Medicine 2014 Annual Meeting, 2014.09.
13. Kentaro Tokuda, Fumito Ichinose, Inhaled Hydrogen Sulfide Protects Mice against Acute Liver Failure, 14th Asian Australasian Congress of Anaesthesiologists, 2014.02, [URL], AIM: Acute liver failure is caused by massive hepatocyte apoptosis that is resistant to conventional medical therapies. Consequently, liver transplantation is required in many cases. An experimental liver failure model induced by galactosamine (Gal) and lipopolysaccharide (LPS) mimics clinical fulminant hepatitis. In this model, LPS stimulates macrophages to release TNFα, which induces apoptosis in Gal-sensitized hepatocytes, resulting in liver failure. Hydrogen sulfide (H2S), which is an endogeneously-produced gaseous signaling molecule, has anti-apoptotic as well as anti-inflammatory properties. Previously, we reported that H2S attenuates liver dysfunction arising from LPS-induced systemic inflammation. It has been also reported that H2S reduces hepatic ischemia/reperfusion injury by inhibition of apoptosis in the liver. However, whether H2S exerts hepatoprotective effects against fulminant hepatitis, in which both inflammatory responses and apoptosis play pivotal roles, remains unknown.
METHODS: Mice were challenged with saline or combination of Gal and LPS and thereafter randomized to breathe either air alone or air supplemented with H2S for 6h.
RESULTS: Mice that breathed air after Gal/LPS challenge showed poor survival rate (13%) and marked increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in plasma. In contrast, H2S inhalation for 6h after challenge markedly improved survival (60%, p < 0.05) and suppressed Gal/LPS-induced elevation of ALT and AST levels in plasma. Inhaled H2S suppressed TNFα in plasma at 1h after Gal/LPS challenge. Mice that breathed air after Gal/LPS challenge exhibited activation of caspase 3, 8, and 9 in the liver, whereas H2S breathing inhibited activation of caspase 3, 8, and 9. Gal/LPS challenge did not increase gene expression of anti-inflammatory IL-10, whereas H2S inhalation after Gal/LPS challenge significantly increased IL-10 gene expression.
CONCLUSION: These results suggest that H2S protects mice from acute liver failure at least in part by inhibition of caspase activation and by augmentation of anti-inflammatory IL-10 expression in the liver. .
14. Anti-inflammatory effects of hydrogen sulfide in systemic inflammation.
15. Kentaro Tokuda, Fumito Ichinose, Hydrogen Sulfide Protects Hepatocytes against Acute Liver Failure , Annual Meeting of American Society of Anesthesiologists 2012, 2012.10, Introduction: Acute liver failure is a fatal syndrome attributed to massive hepatocyte apoptosis that is resistant to conventional medical therapies. Consequently, liver transplantation is required in many cases. An experimental liver failure model induced by galactosamine (Gal) and lipopolysaccharide (LPS) mimics clinical fulminant hepatitis. In this model, LPS stimulates macrophages to release TNFα, which induces apoptosis in Gal-sensitized hepatocytes, resulting in liver failure. Hydrogen sulfide (H2S), which is an endogeneously-produced gaseous signaling molecule, has anti-apoptotic as well as anti-inflammatory properties. Previously, we reported that H2S attenuates liver dysfunction arising from LPS-induced systemic inflammation. It has also been reported that H2S reduces hepatic ischemia/reperfusion injury by inhibition of apoptosis in the liver. However, whether H2S exerts hepatoprotective effects against acute liver failure, in which both inflammatory responses and apoptosis have pivotal roles, remains unknown. Here, we examined the impact of H2S on acute liver failure in mice induced by Gal and LPS or TNFα.
Methods: Mice were challenged with saline or combination of Gal (700 mg/kg) and LPS (10 µg/kg) intraperitoneally and thereafter randomized to breathe either air alone or air supplemented with H2S (80 ppm) for 6h.
Results: Mice that breathed air after Gal/LPS challenge showed poor survival rate and marked increase of alanine/aspartate aminotransferase (ALT/AST) in plasma. In contrast, H2S inhalation for 6h after challenge markedly improved survival (Fig. 1) and suppressed Gal/LPS-induced elevation of ALT and AST levels in plasma. Inhaled H2S suppressed TNFα in plasma at 1h after Gal/LPS challenge. Mice that breathed air after Gal/LPS challenge exhibited activation of caspase 3, 8, and 9 in the liver, whereas H2S breathing inhibited activation of caspase 3, 8, and 9, suggesting inhaled H2S after Gal/LPS challenge suppressed both extrinsic and intrinsic pathways of caspase-dependent apoptosis in the liver (Fig. 2). Gal/LPS challenge increased phosphorylated STAT3 transcription factor. H2S inhalation after Gal/LPS challenge further augmented phosphorylation of STAT3 compared to air alone. The protective effects of H2S inhalation after Gal/LPS challenge were associated with upregulation of gene expression of anti-inflammatory IL-10, which stimulates STAT3 phosphorylation, in the liver. These results suggest that inhaled H2S contributes to survival of mice in acute liver failure at least in part through activation of IL-10/STAT3 pathway. To determine whether or not H2S protects hepatocytes directly, in vitro experiments using primary murine hepatocytes were conducted. GYY4137, an H2S donor, improved cell survival after stimulation with Gal/TNFα, suggesting H2S protects hepatocytes directly against lethal hepatic failure.
Conclusions: These results suggest that H2S protects mice from acute liver failure via direct hepatoprotective effects. These protective effects appear to be mediated at least in part by inhibition of caspase activation and by augmentation of IL-10/STAT3 signaling pathway in the liver. .
16. Kentaro Tokuda, Fumito Ichinose, Inhaled Hydrogen Sulfide Protects Mice against Gal/LPS-induced Acute Liver Failure
, Second International Conference on H2S Biology and Medicine, 2012.09, Introduction
Acute liver failure is a fatal syndrome attributed to massive hepatocyte apoptosis that is resistant to conventional medical therapies. Consequently, liver transplantation is required in many cases. An experimental liver failure model induced by galactosamine (Gal) and lipopolysaccharide (LPS) mimics clinical fulminant hepatitis. In this model, LPS stimulates macrophages to release TNFα, which induces apoptosis in Gal-sensitized hepatocytes, resulting in liver failure. Hydrogen sulfide (H2S), which is an endogeneously-produced gaseous signaling molecule, has anti-apoptotic as well as anti-inflammatory properties. Previously, we reported that H2S attenuates liver dysfunction arising from LPS-induced systemic inflammation. It has also been reported that H2S reduces hepatic ischemia/reperfusion injury by inhibition of apoptosis in the liver. However, whether H2S exerts hepatoprotective effects against acute liver failure, in which both inflammatory responses and apoptosis play pivotal roles, remains unknown. Here, we examined the impact of inhaled H2S on acute liver failure in mice induced by Gal and LPS.
Methods
Mice were challenged with saline or combination of Gal (700 mg/kg) and LPS (10 μg/kg) intraperitoneally and thereafter randomized to breathe either air alone or air supplemented with H2S (80 ppm) for 6h.Results
Mice that breathed air after Gal/LPS challenge showed poor survival rate (13%) and marked increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in plasma. In contrast, H2S inhalation for 6h after challenge markedly improved survival (60%, p < 0.05) and suppressed Gal/LPS-induced elevation of ALT and AST levels in plasma. Inhaled H2S suppressed TNFα in plasma at 1h after Gal/LPS challenge. Mice that breathed air after Gal/LPS challenge exhibited activation of caspase 3, 8, and 9 in the liver, whereas H2S breathing inhibited activation of caspase 3, 8, and 9, suggesting inhaled H2S after Gal/LPS challenge suppressed both extrinsic and intrinsic pathways of caspase-dependent apoptosis in the liver. Gal/LPS challenge increased phosphorylated STAT3 transcription factor. H2S inhalation after Gal/LPS challenge further augmented phosphorylation of STAT3 compared to air alone. The protective effects of H2S inhalation after Gal/LPS challenge were associated with upregulation of gene expression of anti-inflammatory IL-10, which stimulates STAT3 phosphorylation, in the liver. These results suggest that inhaled H2S contributes to survival of mice in acute liver failure at least in part through activation of IL-10/STAT3 pathway.Conclusions
These results suggest that H2S protects mice from acute liver failure at least in part by inhibition of caspase activation and by augmentation of IL-10/STAT3 signaling pathway in the liver. .
17. Perioperative management of very aged patients.
18. , [URL].
19. Non-linear regression curve model for desaturation in pulse oximetry during breath-holding in healthy volunteers..
20. A perioperative recording system on the server-based computing system., [URL].
21. A Comparison of Finger, Ear and Forehead SpO2 on Detecting Oxygen Desaturation in Healthy Volunteers., [URL].