Tetsuhiro Sakai

University of Texas Southwestern Medical Center, Dallas, TX, United States

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Publications (22)40.96 Total impact

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    ABSTRACT: We experienced an accidental use of suxamethonium for general anesthesia in a 26-year-old woman with hereditary hypocholinesterasemia that had not been recognized preoperatively. The patient was scheduled for total colectomy as her chronic ulcerative colitis could not be controlled with medications. Routine preoperative screening such as blood cell counts, biochemical data, chest x-ray and electrocardiogram were performed but serum cholinesterase (ChE) activity was not measured. As the preoperative patient condition was good with no abnormal history, anesthesia was induced and maintained with propofol, ketamine and fentanyl as usual. For muscle relaxation, suxamethonium was used for tracheal intubation, and vecuronium was used for the maintenance. After surgery, postanesthetic course was uneventful. One year later, as the patient was pregnant and scheduled for cesarean section, the preoperative screening was done. The biological data showed a hypocholinesterasemia without liver dysfunction. Thus, previous medical records of internal medicine were cheked. Surprisingly the record showed hypocholinesterasemia when she was 15 and 21 years of ages. However, as the physicians did not recognize hypocholinesterasemia, they did not inform the patient of it. Why did the patient have no prolonged apnea and emergence after the previous anesthesia? As the surgical time was exceeded 4 hrs, plasma suxamethonium could fortunately be less than its effective concentration at emergence. However, this case strongly suggests us that preoperative screening should be done without any omission. In addition, if serum ChE activity is not examined, use of suxamethonium should be avoided.
    No preview · Article · Sep 2006 · Masui. The Japanese journal of anesthesiology
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    ABSTRACT: We report here a case of obstruction of an reinforced endotracheal tube during laryngomicrosurgery under total intravenous anesthesia. In this case, we used a 6.0 mm ID reinforced endotracheal tube that had been used previously for other patients and sterilized two times by ethylene oxide gas. During the operation, the peak airway pressure increased gradually and eventually reached to 35 cmH2O. After the exchange of the endotracheal tube, ventilation was improved immediately. The endotracheal tube was occluded by dissection of internal wall. Several cases of reinforced tube obstruction have already been reported and in most of these cases the obstruction was related to their repeated use and nitrous oxide anesthesia. However, the present case showed that dissection of reinforced endotracheal tube could also occur during general anesthesia without using nitrous oxide. We should bear in mind that repeated use of reinforced endotracheal tube could induce a critical airway obstruction.
    No preview · Article · Dec 2003 · Masui. The Japanese journal of anesthesiology
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    Wei-Dong Mi · Hironori Ishihara · Tetsuhiro Sakai · Akitomo Matsuki
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    ABSTRACT: Apparently large plasma volumes derived by indocyanine green (PV-ICG) have been determined in the initial period after induction of anesthesia. We tested the hypothesis that possible overestimation of PV-ICG occurs shortly after anesthetic induction. Anesthesia was induced in 13 patients with fentanyl bolus 2 mug/kg and propofol infusion 0.5 mg(.)kg(-1.)min(-1) IV until patients lost consciousness and was then maintained with a propofol infusion. PV-ICG and the initial distribution volume of glucose (IDVG) were assessed at 15 min before and at 15 min after anesthetic induction. Plasma ICG and glucose concentrations were measured from serial blood samples taken before and through 7 min after injection of ICG 25 mg and glucose 5 g. PV-ICG and IDVG were calculated using a one-compartment model. PV-ICG was significantly increased by an average of 15.3% after induction, from 2.29 +/- 0.38 (SD) L to 2.64 +/- 0.31 L (P < 0.001). The mean hematocrit (Hct), concentrations of hemoglobin (Hb), and total plasma proteins at postinduction decreased compared with those at preinduction by 2.9%, 2.2%, and 2.3%, respectively (P < 0.05). Percentile increase in plasma volume calculated from Hb and Hct before and after induction was 4%. Consequently, an 11% overestimation in PV-ICG was observed. IDVG remained unchanged. Therefore, the ratio of PV-ICG/IDVG increased from 0.40 +/- 0.05 before induction to 0.48 +/- 0.06 after induction (P < 0.01). These results validate the hypothesis that possible overestimation of PV-ICG occurs during a definable period of time after propofol anesthetic induction. The present results also support the PV-ICG/IDVG ratio as a measure of possible overestimation of PV-ICG or fluid redistribution from the central to the peripheral tissues.
    Full-text · Article · Nov 2003 · Anesthesia & Analgesia
  • Weidong Mi · Tetsuhiro Sakai · Tsuyoshi Kudo · Mihoko Kudo · Akitomo Matsuki
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    ABSTRACT: To investigate the effect of different plasma levels of fentanyl on the concentration of propofol and the Bispectral Index (BIS) required for patients to regain consciousness and orientation following surgery. Prospective, open-label study. Operating room of a university hospital. 28 patients, aging 20 to 50 years, scheduled for elective, 1- to 4-hour surgeries under general anesthesia. BIS was continuously monitored from bifrontal montage (At1-Fpz and At2-Fpz) using an Aspect A-1,050 EEG system (Aspect, Natick, MA). Anesthesia was induced with bolus injections of fentanyl 2 microg/kg and propofol 2 mg/kg, and maintained with intermittent injections of fentanyl and constant infusion of propofol. Propofol infusion was stopped at the end of surgery. Consciousness and orientation were assessed as clinical endpoints once every 2 minutes following the end of the surgery. Blood samples were extracted for plasma propofol and fentanyl concentrations (PCp and FCp, respectively), and BIS values were recorded when patients regained consciousness and orientation. Patients were allocated to one of three groups depending on FCp on awakening: Group 1, FCp > 1 microg/L (n = 8); Group 2, FCp < 1 microg/L and >0.45 microg/L (n = 9); and Group 3, FCp < 0.45 microg/L (n = 11). PCp, BIS, recovery time, and other data were compared between the three groups. Demographic values, duration of surgery, and consumption of propofol and fentanyl were not different between the three groups. Group 3 patients regained consciousness with significantly higher propofol concentration (mean PCp = 3.2 mg/L) compared with those in Groups 1 and 2 (p < 0.05). However, the BIS values at both recovery endpoints were not different among the three groups. The plasma levels of fentanyl affect the concentrations of propofol required for patients to regain consciousness. The BIS values for wakefulness are unaltered at the different combinations of propofol and fentanyl concentrations. Thus, the BIS appears to be a useful and consistent indicator for level of consciousness during emergence from propofol/fentanyl intravenous anesthesia.
    No preview · Article · Mar 2003 · Journal of Clinical Anesthesia
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    ABSTRACT: During a period of five years from January 1996 through December 2000 total intravenous anesthesia with mainly propofol, fentanyl and ketamine was administered to 26,079 patients including cardiac and neurosurgical patients at the University of Hirosaki Hospital and five other affiliated hospitals. The patients studied ranged from 1 year 8 months to 93 years in age, 9.2 kg to 135.0 kg in body weight and from 18 min to 22 hours 50 min in anesthetic time. With adequate monitoring, fentanyl 1-2 micrograms.kg-1 was given at first, then total-dose of ketamine 1 mg.kg-1 and propofol 1-2 mg.kg-1 were administered for the induction of anesthesia in adult patients. A total dose of fentanyl 3-15 micrograms.kg-1 was given combined with propofol 5-10 mg.kg-1 and ketamine 0.3-1.0 mg.kg.h-1. In craniotomy patients, ketamine was excluded. For pediatric patients, sevoflurane anesthesia was employed to establish i.v. route, and intravenous agents were given almost same as in the same manner as in adult patients. None of them developed either cardiac arrest or severe cardiovascular insufficiencies due to anesthesia alone. Their postoperative hepatic and renal functions evaluated by various biochemical indices and urine output were adequately maintained during anesthesia and for a week postoperatively. They were followed up to 3 months postoperatively only to fail to detect any adverse events related directly to this method of anesthesia. These data suggest that total intravenous anesthesia with propofol, fentanyl and ketamine has a very wide margin of safety.
    No preview · Article · Jan 2003 · Masui. The Japanese journal of anesthesiology
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    ABSTRACT: Transcription of the genes for proinflammatory cytokines is regulated by nuclear factor kappa B (NF-κB) activation. Cardiopulmonary bypass (CPB) is characterized by a systemic endotoxemia demonstrated immediately following CPB institution followed by the systemic release of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α) and the interleukins (IL) 1, 6 and 8. However, the mechanism of the release of these proinflammatory cytokines remains to be determined.NF-κB is an inducible transcription factor implicated in activating various genes including those genes which encode for cytokines such as TNF, IL-1 and IL-6. The NF-κB protein is found in several cell types including inflammatory cells, for example peripheral blood monocytes, one of the cell types responsible for LPS-induced proinflammatory cytokine production. Therefore, we examined whether NF-κB is activated during CPB in order to define a mechanism of CPB-induced proinflammatory cytokine production and release.
    No preview · Article · Jul 2002 · International Congress Series
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    ABSTRACT: Ketamine reduces endotoxin-induced production of proinflammatory cytokines, including tumour necrosis factor-alpha (TNF), in several types of inflammatory cells, including monocytes and macrophages. Transcription of the genes that encode production of these proinflammatory cytokines is regulated by nuclear factor-kappa B (NF-kappaB). Cytoplasmic B protein is activated by endotoxin (LPS) as well as by TNF, allowing B protein to migrate into the cell nucleus to activate gene transcription for these inflammatory mediators. Because NF-kappaB is likely involved in brain injury and inflammatory neurodegenerative disease, such as multiple sclerosis, we examined whether ketamine inhibits LPS-induced activation of NF-kappaB in human glioma cells in vitro and intact mouse brain cells in vivo. Endotoxin-induced NF-kappaB expression in both the human glioma cells in vitro and the intact mouse brain cells in vivo was determined by electrophoretic mobility shift assays (EMSA) of nuclear extracts and measurement of NF-kappaB expression by densitometry. Endotoxin was injected intracerebroventricularly in vivo and intact brain was harvested. Klenow fragment labeling was used to identify NF-kappaB protein for both the in vivo and vitro experiments. Endotoxin treatment increased NF-kappaB expression (P < 0.05) both in vivo and vitro compared with control (untreated) cells. Ketamine suppressed endotoxin-induced neuronal NF-kappaB activation in a dose-dependent manner (P < 0.05, except for the 10(-5) M concentration in vitro) both in vivo and vitro. Ketamine inhibits endotoxin-induced NF-kappaB expression in brain cells in vivo and vitro and it is suggested that this may have implications in the neuroprotective effects of ketamine reported by other investigators.
    Preview · Article · Oct 2000 · Canadian Journal of Anaesthesia

  • No preview · Article · Sep 2000 · Anesthesiology
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    ABSTRACT: With the rise in the field of neuroimmunomodulation research, there is increased recognition of the influence of the nervous system and neuropeptides in peripheral disease. The neuropeptide α-melanocyte-stimulating hormone (α-MSH) is a neuroimmunomodulatory agent that modulates production of proinflammatory cytokines and inhibits peripheral inflammation via actions on CNS receptors. We examined whether central α-MSH operates by inhibiting activation of the nuclear factor kappa B (NF-κB) that is essential to the expression of proinflammatory cytokines and development of inflammation in the periphery. Electrophoretic mobility shift assays of nuclear extracts from the murine foot pad injected with TNF-α demonstrated that centrally administered α-MSH does inhibit NF-κB activation. Western blot analysis revealed that this inhibition was linked to central α-MSH-induced preservation of expression of IκBα protein in the peripheral tissue. The NF-κB and IκBα effects were inhibited in mice with spinal cord transection. Intraperitoneal (ip) injection of the nonspecific β-adrenergic receptor blocker propranolol, and of a specific β2-adrenergic receptor antagonist, likewise prevented these effects of central α-MSH; blockade of cholinergic, α-adrenergic, or β1-adrenergic receptors did not. Centrally administered α-MSH inhibited peripheral NF-κB activation and IκBα degradation even in mice with nonfunctional melanocortin 1 receptors (MC1R). These findings indicate that α-MSH can act centrally to inhibit NF-κB activation in peripheral acute inflammation via a descending neural pathway. The pathway involves β2-adrenergic receptors, but does not require activation of MC1R within the brain.
    No preview · Article · Oct 1999 · Journal of Neuroimmunology
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    ABSTRACT: The neuropeptide α-melanocyte-stimulating hormone (α-MSH) and its C-terminal tripeptide α-MSH11-13 modulate production of proinflammatory cytokines and inhibit inflammation. We examined whether systemic α-MSH and α-MSH11-13 inhibit activation of the nuclear transcription factor, nuclear factor kappa B (NF-κB), a factor that is essential to expression of proinflammatory cytokines, in experimental murine brain inflammation induced by lipopolysaccharide. Electrophoretic mobility shift assays of nuclear extracts demonstrated that parenteral α-MSH inhibited NF-κB activation. Western blot analysis revealed that this inhibition was linked to α-MSH-induced preservation of expression of IκBα protein in the brain. The effects of α-MSH on NF-κB and IκBα were paralleled by pretreatment with α-MSH11-13. Similar effects of the two peptides were observed in mice with nonfunctional melanocortin 1 receptors (MC1R), ruling out the possibility that this receptor subtype is essential to the influence on NF-κB. These findings indicate that α-MSH peptides given systemically can inhibit NF-κB activation induced in acute brain inflammation even in the absence of MC1R.
    No preview · Article · Jul 1999 · Brain Research
  • Satoshi Takahashi · Tetsuhiro Sakai · Akitomo Matsuki
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    ABSTRACT: Small volumes (4-6 mL/kg) of 7.5% hypertonic saline solution (HTS) are reported to be effective for resuscitation from circulatory shock. When infused rapidly into either hypovolemic or normovolemic subjects, HTS can cause an immediate and severe hypotension before cardiovascular improvement. In the present study, we examined the hypothesis that the early hypotension produced by HTS was mediated by an acute and transient depression of cardiac contractility. Left ventricular pressure and wall motions were measured simultaneously in 10 anesthetized dogs for the assessment of cardiac contractility. Infusion of HTS at 3 mL/kg in 1 min significantly decreased mean arterial blood pressure by 49%, from 95 +/- 4 to 51 +/- 5 mm Hg (P < 0.05, mean +/- SEM) at 45 s after the onset of infusion. This initial decrease in arterial blood pressure was abrupt and transient (106 +/- 9 s). Concomitantly, cardiac output and coronary blood flow increased significantly from 2.8 +/- 1.0 to 3.9 +/- 1.1 L/min and from 23.7 +/- 5.3 to 49.8 +/- 4.7 mL/min, respectively. Although heart rate remained constant, systolic shortenings of left ventricular diameter and wall thickness increased from 5.6% +/- 0.5% to 7.8% +/- 0.5% and from 13.9% +/- 0.6% to 15.1% +/- 1.2%, respectively, indicating an improvement in cardiac contractility. This was confirmed by subsequent analysis of the left ventricular end-systolic pressure-diameter relationship. Systemic and pulmonary vascular resistance decreased by 60% and 27%, respectively. Despite an initial period of hypotension after rapid infusion of HTS, mean arterial blood pressure, cardiac output, and contractility were all significantly increased at 5 min after HTS infusion. The results show that acute hypotension caused by rapid infusion of HTS was not mediated by cardiac depression but by a decrease in total peripheral resistance.
    No preview · Article · Feb 1998 · Anesthesia & Analgesia
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    Wei-Dong Mi · Tetsuhiro Sakai · Satoshi Takahashi · Akitomo Matsuki
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    ABSTRACT: Purpose To observe the changes in EEG bispectral index (BIS), 95% spectral edge frequency (95% SEF) and median frequency (MF) with haemodynamic changes to intubation during induction with propofol or propofol and 2 μg· kg−1 fentanyliv. Methods Twenty four ASA 1–11 patients were randomized to receive either propofol infusion preceded by normal saline (group P, n= 12) or propofol preceded by 2 μg· kg−1 fentanyl (group PF, n= 12). Intubation was performed five minutes after maintenance of BIS within 45 ± 5. EEG and haemodynamic variables were recorded at before induction, and before and after intubation. Results Haemodynamic responses to intubation were greater in group P than in group PF (P < 0.05). Postintubation SBP, DBP and HR increased, compared with preinduction values, more in group P than in group PF Postintubation BIS values increased from 45.5 ± 3.5 and 44.2 ± 4.1 to 51.1 ± 4.1 and 50.9 ± 5.3 in groups P and PF, respectively, compared with preintubation values. The BIS values were not different between treatment groups before and after intubation, and 95% SEF and MF values did not increase after intubation. Conclusion Fentanyl, 2 μg· kg−1iv, blunted the haemodynamic responses to intubation, but failed to attenuate the arousal of cerebral cortical activity. The different haemodynamic responses postintubation but similar BIS and 95% SEF changes in the two groups suggest that BIS or 95% SEF cannot predict the haemodynamic responses to intubation during anaesthesia induction with propofol and fentanyl.
    Preview · Article · Dec 1997 · Canadian Journal of Anaesthesia
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    Preview · Article · Apr 1997 · Anesthesia & Analgesia
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    ABSTRACT: In a prospective study, we determined the anesthetic induction dose of thiopental and the clinical variables influencing the appropriate induction dose of thiopental in 20 patients with the hypertrophic variety of Charcot-Marie-Tooth syndrome (CMT). As controls we chose 50 patients without CMT. Motor disturbance was evaluated in terms of muscle weakness of the distal lower and upper extremities. We examined sensory disturbance by evaluating loss of sensation in the index finger and great toe. The preinduction cardiac output was measured by echocardiography. Anesthesia was induced with repeated injections of 50 mg thiopental. The minimum induction dose of thiopental (MID) was confirmed when the eyelash reflex ceased. We maintained anesthesia with enflurane and nitrous oxide. The 95% confidence interval of the MID in patients used as the controls was 2.5-4.9 mg/kg. The MID in 11 patients with CMT was less than 2.5 mg/kg. MIDs in the patients with CMT were significantly smaller than those of the control patients (P < 0.0001). Also we found a strong relationship between the MID and the severity of both motor and sensory disturbances (P = 0.003 and 0.002, respectively). There was no relationship between the MID and other clinical variables, such as age, gender, inherited type, body weight, and preinduction cardiac output. Because delay in the recovery from anesthesia can be caused by an inappropriate dose of thiopental in CMT patients in whom motor and sensory function is seriously impaired, the dose of thiopental probably should be reduced and based on the individual patient's response.
    Full-text · Article · Feb 1996 · Anesthesia & Analgesia
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    ABSTRACT: Ketamine-induced sympathetic stimulation can be inhibited by administration of sedatives such as benzodiazepines, droperidol, or opioids. We have developed total intravenous anesthesia with ketamine in combination with droperidol and fentanyl (DFK) and have used this anesthetic method in more than 4000 surgical cases. In this study, we compared DFK in cardiac surgery with isoflurane-fentanyl anesthesia (AOI-F). Fourteen patients undergoing aortocoronary artery bypass graft surgery were randomly assigned to the DFK or AOI-F groups. The endocrine responses of the patients were evaluated from the plasma, levels of cortisol, antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and aldosterone. In both groups, anesthesia per se did not induced any significant changes in the hormones. Although cortisol and ADH increased during surgery, ANP and aldosterone did not change appreciably. All hormones were significantly elevated after the end of cardiopulmonary bypass. There were no significant differences in any of the hormones, blood pressure, and heart rate measured at different points in both groups. These results showed that DFK anesthesia as a total intravenous anesthesia deserves to be studied in more depth.
    No preview · Article · Sep 1995 · Journal of Anesthesia
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    ABSTRACT: Endocrine factors and cytokines are crucial to host responses to stress and infection. Because surgery is a major stressful condition, it is necessary to understand the influence of specific anesthetic procedures on immune-endocrine responses. The purpose of this study was to compare total intravenous anesthesia with propofol with conventional inhalational anesthesia on circulating cortisol, adrenocorticotropic hormone (ACTH), prolactin, alpha-melanocyte-stimulating hormone (αMSH), and the cytokine, interleukin-6 (IL-6) in healthy patients undergoing tubal ligation. The results show that circulating cortisol was significantly suppressed ous propofol completely abolished the response of circulating cortisol to surgery. Because ACTH responses to surgery were similar in the two groups, the inhibition likely occurred directly on the adrenal glands. This study is the first to report the effects of anesthesia on circulating αMSH, which was decreased significantly after induction with both anesthetic techniques and was still depressed at 90 min in the propofol patients. Other aspects of immune-endocrine responses to surgery were similar irrespective of anesthetic type, which further suggests a specific suppression of adrenal function by propofol.
    No preview · Article · Jul 1995 · Journal of Anesthesia
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    ABSTRACT: Cardiopulmonary bypass (CPB) makes prediction of any drug concentration diffcult because both hypothermia and hemodilution can alter the pharmacokinetics of the drug. Eleven patients undergoing cardiac surgery under CPB were anesthetized with continuous infusion of ketamine combined with intermittent administration of droperidol and fentanyl. The infusion rate of ketamine was 2 mg·kg−1·hr−1 following a bolus administration of 1.5 mg·kg−1 for the induction of anesthesia. Blood concentrations of ketamine and its main metabolite, norketamine, were measured at 0, 30, and 60 min after the start of and the end of CPB, and 0, 1, 2, and 24 h after the cessation of ketamine infusion. Hypothermia increased blood ketamine levels during CPB, but the norketamine levels did not change. Although acute hemodilution would decrease blood ketamine levels, their levels were already significantly increased at 30 min after CPB. Hypothermic factors have a more kinetically important role during CPB than hemodilution. Increases in blood norketamine levels following rewarming indicate that hypothermia could impair ketamine metabolism in the liver. Further increase in the plasma concentration of ketamine until 30 min after the end of CPB might be due to blood transfusion containing ketamine from the CPB reservoir.
    No preview · Article · May 1995 · Journal of Anesthesia

  • No preview · Article · Mar 1995 · Journal of Anesthesia

  • No preview · Article · Jan 1995 · Nihon Kyukyu Igakukai Zasshi

  • No preview · Article · Jul 1994 · Anesthesia & Analgesia

Publication Stats

336 Citations
40.96 Total Impact Points


  • 1999-2000
    • University of Texas Southwestern Medical Center
      • • Department of Anesthesiology and Pain Management
      • • Department of Physiology
      Dallas, TX, United States
  • 1995-2000
    • Hirosaki University
      • Department of Anesthesiology
      Khirosaki, Aomori, Japan
    • University of Texas at Dallas
      Richardson, Texas, United States