A suspected case of serotonin syndrome induced by palonosetron and ramosetron administration.

Serotonin syndrome occurs when serotonin (5-hydroxytryptamine, 5-HT) levels increase and is accompanied by symptoms of mental status changes, neuromuscular abnormalities, and autonomic hyperactivity. Serotonin receptor 3 antagonists, such as palonosetron or ramosetron, are commonly used for their antiemetic effects during general anesthesia. However, overdosage of these drugs carries a risk of serotonergic toxicity as they increase serum serotonin levels due to inhibition of serotonin reuptake. Serotonin syndrome caused by 5-HT3 antagonists is thought to be caused by the synergistic effects of high doses of serotonergic drugs or the combination of two or more serotonergic drugs with different mechanisms of action. The incidence of serotonin syndrome is unknown because it is a rare condition that cannot be selected for in randomized clinical trials. Therefore, physicians must focus on the clinical manifestations of the syndrome and manage patients before the condition becomes life-threatening.

Dexmedetomidine Improves Locomotor Function and Alleviates Thermal Hyperalgesia Following Sciatic Nerve Crush Injury in Rats.

PURPOSE: The effects of dexmedetomidine on locomotor function and thermal hyperalgesia in sciatic nerve crush injury (SNCI) were investigated using rats. METHODS: After exposing the right sciatic nerve, the sciatic nerve was crushed for 1 minute by a surgical clip. One day after nerve injury, dexmedetomidine (5, 25, and 50 µg/kg) was directly applied to the injured sciatic nerve once a day for 14 days. Walking track analysis was used to assess locomotor function and plantar test was conducted to assess thermal pain sensitivity. Immunohistochemistry was performed to determine the expression of c-Fos in the ventrolateral periaqueductal gray (vlPAG) and paraventricular nucleus (PVN). Western blot was used to evaluate the expression level of nerve growth factor (NGF) and myelin basic protein (MBP) in the sciatic nerve. RESULTS: SNCI resulted in deterioration of locomotor function and increased thermal pain sensitivity. The level of c-Fos expression in the PVN and vlPAG was increased and the level of NGF and MBP expression in the sciatic nerve was enhanced by SNCI. Dexmedetomidine treatment improved locomotor function and upregulated expression of NGF and MBP in the sciatic nerve of SNCI. Dexmedetomidine treatment alleviated thermal hyperalgesia and downregulated expression of c-Fos in the vlPAG and PVN after SNCI. CONCLUSION: Dexmedetomidine may be used as a potential new treatment drug for recovery of locomotion and control of pain in peripheral nerve injury.

Dexmedetomidine ameliorates memory impairment in sleep-deprived mice.

The selective α2-adrenergic receptor agonist dexmedetomidine acts as an analgesic, sedative, and anesthetic adjuvant. The most common consequence of sleep deprivation is memory impairment. We investigated whether dexmedetomidine can counteract memory impairment caused by sleep deprivation and suppress the production of inflammatory factors. For inducing sleep deprivation, adult male mice were placed inside a water cage containing 15 platforms immersed in water up to 1 cm for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (5, 10, and 20 µg/kg) and α2-adrenoceptor antagonist atipamezole (250 µg/kg) were intraperitoneally injected into the mice, once per day for six days. The step-down avoidance task and the Morris water maze test were performed. Western blot analysis was performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, brain-derived neurotrophic factor (BDNF), tyrosine kinase B (TrkB), nuclear transcription factor-κB (NF-κB), inhibitor of κBα (IκBα), and ionized calcium binding adapter molecule I (Iba-1) in the hippocampus. Immunohistochemistry was performed for the determination of Ki-67 and glial fibrillary acidic protein (GFAP) expression in the hippocampal dentate gyrus. Dexmedetomidine ameliorated sleep deprivation-induced deterioration of short-term memory and spatial learning ability. Dexmedetomidine inhibited production of inflammatory mediators caused by sleep deprivation. Dexmedetomidine also prevented the decrease in BDNF, TrkB expression, and cell proliferation induced by sleep deprivation. Dexmedetomidine could be used to counteract the neuropathological effects of sleep deprivation.

Stroke Volume Variation and Stroke Volume Index Can Predict Fluid Responsiveness after Mini-Volume Challenge Test in Patients Undergoing Laparoscopic Cholecystectomy.

Background and Objectives: For using appropriate goal-directed fluid therapy during the surgical conditions of pneumoperitoneum in the reverse Trendelenburg position, we investigated the predictability of various hemodynamic parameters for fluid responsiveness by using a mini-volume challenge test. Materials and Methods: 42 adult patients scheduled for laparoscopic cholecystectomy were enrolled. After general anesthesia was induced, CO2 pneumoperitoneum was applied and the patient was placed in the reverse Trendelenburg position. The mini-volume challenge test was carried out with crystalloid 4 mL/kg over 10 min. Hemodynamic parameters, including stroke volume variation (SVV), cardiac index (CI), stroke volume index (SVI), mean arterial pressure (MAP), and heart rate (HR), were measured before and after the mini-volume challenge test. The positive fluid responsiveness was defined as an increase in stroke volume index ≥10% after the mini-volume challenge. For statistical analysis, a Shapiro-Wilk test was used to test the normality of the data. Continuous variables were compared using an unpaired t-test or the Mann-Whitney rank-sum test. Categorical data were compared using the chi-square test. A receiver operating characteristic curve analysis was used to assess the predictability of fluid responsiveness after the mini-volume challenge. Results: 31 patients were fluid responders. Compared with the MAP and HR, the SVV, CI, and SVI showed good predictability for fluid responsiveness after the mini-volume challenge test (area under the curve was 0.900, 0.833, and 0.909, respectively; all p-values were <0.0001). Conclusions: SVV and SVI effectively predicted fluid responsiveness after the mini-volume challenge test in patients placed under pneumoperitoneum and in the reverse Trendelenburg position.

Effect of Polydeoxyribonucleotide on Lipopolysaccharide and Sevoflurane-Induced Postoperative Cognitive dysfunction in Human Neuronal SH-SY5Y Cells.

PURPOSE: Postoperative cognitive dysfunction (POCD) is a complication of surgery characterized by acute cognitive dysfunction, memory impairment, and loss of attention. The effect of polydeoxyribonucleotide (PDRN) on the POCD environment induced by lipopolysaccharide (LPS) and sevoflurane exposure were investigated in human neuronal SH-SY5Y cells. METHODS: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and WST-8 assays were performed to determine cell viability. Cyclic adenosine-3,5'-monophosphate (cAMP), tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 concentrations were measured using enzyme-linked immunoassay (ELISA). Immunocytochemistry was performed for vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF), and western blotting for TNF-α, IL-1ß, IL-6, and cAMP response element-binding protein (CREB). RESULTS: Induction of the POCD environment reduced cell viability in the MTT and WST-8 assays. PDRN treatment reduced TNF-α, IL-1ß, and IL-6 expression in POCD conditions, and significantly increased cAMP concentrations and the p-CREB/CREB ratio. PDRN treatment activated adenosine A2A receptors and then increased the expression of VEGF and BDNF, which had been reduced by LPS and sevoflurane exposure. CONCLUSION: PDRN treatment showed a therapeutic effect on the LPS and sevoflurane-induced POCD environment. PDRN was shown to have an excellent therapeutic effect on POCD, not only by promoting rapid anti-inflammatory effects in damaged cells, but also by enhancing the expression of BDNF and VEGF.

Total Intravenous Anesthesia Maintained the Degree of Pre-Existing Mitral Regurgitation Better than Isoflurane Anesthesia in Cardiac Surgery: A Randomized Controlled Trial.

Accurate assessment of mitral regurgitation (MR) is critical during mitral valve repair surgery. However, anesthesia may influence the degree of mitral regurgitation by changing pre- and after-load or cardiac contractility. Therefore, we compared changes in mitral regurgitation by total intravenous anesthesia (TIVA) and inhalation anesthesia in patients with pre-existing mitral regurgitation. This was a double-blind randomized controlled study conducted at a tertiary care center in 2018. Fifty-four mitral regurgitation patents undergoing elective cardiac surgery were randomly assigned to receive TIVA or isoflurane. Primary endpoint was change of regurgitation volume by anesthesia. The reduction of regurgitation volume by anesthesia was greater in the isoflurane group than in the TIVA group (mean (95% confidence interval CI): -0.20 (-6.15, 5.75) vs. -9.66 (-15.77, -3.56), mL·beat-1, p = 0.0266) and this phenomenon was more prominent with severe mitral regurgitation (grade 3 or 4) (mean (95% CI): -0.33 (-9.10, 8.44) vs. -16.20 (-24.22, -8.18), mL·beat-1, p = 0.0079). Among patients with MR grade 3 or 4, 94% remained the same with TIVA during anesthesia compared to 56% with isoflurane. In conclusion, TIVA maintained the pre-anesthetic state of mitral regurgitation relatively well, while the severity of mitral regurgitation tended to decrease with isoflurane anesthesia.

Comparison of oncological benefits of deep neuromuscular block in obese patients with gastric cancer (DEBLOQS_GC study): A study protocol for a double-blind, randomized controlled trial.

PURPOSE: Many studies have demonstrated the advantage of maintaining intraoperative deep neuromuscular block (NMB) with sugammadex. This trial is designed to evaluate the impact of muscle relaxation during laparoscopic subtotal gastrectomy on the oncological benefits, particularly in obese patients with gastric cancer. MATERIALS AND METHODS: This is a double-blind, randomized controlled multicenter prospective trial. Patients with clinical stage I-II gastric cancer with a body mass index of 25 and over, who undergo laparoscopic subtotal gastrectomy will be eligible for trial inclusion. The patients will be randomized into a deep NMB group or a moderate NMB group with a 1:1 ratio. A total of 196 patients (98 per group) are required. The primary endpoint is the number of harvested lymph nodes, which is a critical index of the quality of surgery in gastric cancer treatment. The secondary endpoints are surgeon's surgical condition score, patient's sedation score, and surgical outcomes including peak inspiratory pressure, operation time, postoperative pain, and morbidity. DISCUSSION: This is the first study that compares deep NMB with moderate NMB during laparoscopic gastrectomy in obese patients with gastric cancer. We hope to show the oncologic benefits of deep NMB compared with moderate NMB during subtotal gastrectomy. TRIAL REGISTRATION NUMBER: ClinicalTrials.gov (NCT03196791), date of registration: October 10, 2017.

Dexmedetomidine Ameliorates Sleep Deprivation-Induced Depressive Behaviors in Mice.

PURPOSE: Sleep deprivation induces depressive symptoms. Dexmedetomidine is a α2-adrenoreceptor agonist and this drug possesses sedative, anxiolytic, analgesic, and anesthetic-sparing effect. In this study, the action of dexmedetomidine on sleep deprivation-induced depressive behaviors was investigated using mice. METHODS: For the inducing of sleep deprivation, the mice were placed inside a water cage containing 15 platforms and filled with water up to 1 cm below the platform surface for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (0.5, 1, and 2 µg/kg) was intraperitoneally treated into the mice, one time per a day during 6 days. Then, forced swimming test and tail suspension test were conducted. Immunohistochemistry for tyrosine hydroxylase (TH), 5-hydroxytryptamine (5-HT; serotonin), tryptophan hydroxylase (TPH) and western blot for D1 dopamine receptor were also performed. RESULTS: Sleep deprivation increased the immobility latency in the forced swimming test and tail suspension test. The expressions of TPH, 5-HT, and D1 dopamine receptor were decreased, whereas, TH expression was increased by sleep deprivation. Dexmedetomidine decreased the immobility latency and increased the expressions of TPH, 5-HT, and D1 dopamine receptor, whereas, HT expression was decreased by dexmedetomidine treatment. CONCLUSION: In our results, dexmedetomidine alleviated sleep deprivation-induced depressive behaviors by increasing 5-HT synthesis and by decreasing dopamine production with up-regulation of D1 dopamine receptor.

Correlation between modified LEMON score and intubation difficulty in adult trauma patients undergoing emergency surgery.

Background: Prediction of difficult airway is critical in the airway management of trauma patients. A LEMON method which consists of following assessments; Look-Evaluate-Mallampati-Obstruction-Neck mobility is a fast and easy technique to evaluate patients' airways in the emergency situation. And a modified LEMON method, which excludes the Mallampati classification from the original LEMON score, also can be used clinically. We investigated the relationship between modified LEMON score and intubation difficulty score in adult trauma patients undergoing emergency surgery. Methods: We retrospectively reviewed electronic medical records of 114 adult trauma patients who underwent emergency surgery under general anesthesia. All patients' airways were evaluated according to the modified LEMON method before anesthesia induction and after tracheal intubation; the intubating doctor self-reported the intubation difficulty scale (IDS) score. A difficult intubation group was defined as patients who had IDS scores > 5. Results: The modified LEMON score was significantly correlated with the IDS score (P < 0.001). The difficult intubation group showed higher modified LEMON score than the non-difficult intubation group (3 [2-5] vs. 2 [1-3], respectively, P = 0.017). Limited neck mobility was the only independent predictor of intubation difficulty (odds ratio, 6.15; P = 0.002). Conclusion: The modified LEMON score is correlated with difficult intubation in adult trauma patients undergoing emergency surgery.

Face-to-face intubation using a lightwand in a patient with severe thoracolumbar kyphosis: a case report.

BACKGROUND: Severe deformity of the thoracolumbar spine may cause difficulty in airway management during induction of anesthesia. Therefore, special attention must be devoted to patient safety. CASE PRESENTATION: A 65-year-old male with severe thoracolumbar kyphosis was scheduled to undergo posterior spinal fusion under general anesthesia. Due to his inability to lie supine, conventional tracheal intubation under direct laryngoscopy was difficult. Alternatively, face-to-face tracheal intubation using a lightwand in the semi-recumbent position was performed. Intubation was successful on the first attempt without any complications. CONCLUSIONS: The face-to-face intubation technique using a lightwand is one of several alternative techniques for tracheal intubation in patients who cannot lie supine.

Pectoral nerve block (Pecs block) with sedation for breast conserving surgery without general anesthesia.

Most regional anesthesia in breast surgeries is performed as postoperative pain management under general anesthesia, and not as the primary anesthesia. Regional anesthesia has very few cardiovascular or pulmonary side-effects, as compared with general anesthesia. Pectoral nerve block is a relatively new technique, with fewer complications than other regional anesthesia. We performed Pecs I and Pec II block simultaneously as primary anesthesia under moderate sedation with dexmedetomidine for breast conserving surgery in a 49-year-old female patient with invasive ductal carcinoma. Block was uneventful and showed no complications. Thus, Pecs block with sedation could be an alternative to general anesthesia for breast surgeries.

Non-intubated thoracoscopic surgery for decortication of empyema under thoracic epidural anesthesia: a case report.

General anesthesia is the main strategy for almost all thoracic surgeries. However, a growing body of literature has reported successful cases of non-intubated thoracic surgery with regional anesthesia. This alternative strategy not only prevents complications related to general anesthesia, such as lung injury, incomplete re-expansion and intubation related problems, but also accords with trends of shorter hospital stay and lower overall costs. We experienced a successful case of non-intubated thoracoscopic decortication for a 68-year-old man who was diagnosed as empyema while the patient kept spontaneously breathing with moderate sedation under thoracic epidural anesthesia. The patient showed a fast recovery without concerns of general anesthesia related complications and effective postoperative analgesia through thoracic epidural patient-controlled analgesia device. This is the first report of non-intubated thoracoscopic surgery under thoracic epidural anesthesia in Korea, and we expect that various well designed prospective studies will warrant the improvement of outcomes in non-intubated thoracoscopic surgery.

Dexmedetomidine alleviates cerebral ischemia-induced short-term memory impairment by inhibiting the expression of apoptosis-related molecules in the hippocampus of gerbils.

Cerebral ischemia results from cerebrovascular occlusion, which leads to neuronal cell death and eventually causes neurological impairments. Dexmedetomidine is a potent and highly selective α2-adrenoreceptor agonist with actions such as sedation, anxiolysis, analgesia and anesthetic-sparing effects. We investigated the effect of dexmedetomidine on apoptosis in the hippocampus after transient global ischemia in gerbils. Transient global ischemia was induced by ligation of both common carotid arteries. Dexmedetomidine was administrated intraperitoneally at three respective doses (0.1, 1 and 10 µg/kg) once per day for 14 consecutive days beginning a day after surgery. Short-term memory was assessed by use of a step-down avoidance task. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assay, immunohistochemistry for caspase-3, and western blot analysis of Bcl-2-associated X protein, B-cell lymphoma 2, Bid, cytochrome c, apoptotic protease activating factor-1 and caspase-9 in the hippocampus. Induction of global ischemia deteriorated short-term memory by enhancing the expression of apoptosis-related molecules in the hippocampus. Treatment with dexmedetomidine suppressed the expression of apoptosis-related molecules under ischemic conditions, resulting in short-term memory improvement. Under normal conditions, dexmedetomidine exerted no significant effect on apoptosis in the hippocampus. The present results suggest that the α2-adrenoceptor agonist dexmedetomidine may be a useful therapeutic agent for the treatment of ischemic brain diseases.

Dexmedetomidine promotes the recovery of the field excitatory postsynaptic potentials (fEPSPs) in rat hippocampal slices exposed to oxygen-glucose deprivation.

Dexmedetomidine (DEX), a selective α2 adrenergic agonist, is an anesthetic and sedative agent, and is reported to exert neuroprotective effects after hypoxic ischemia. However, there are few studies on the electrophysiological effect of DEX in hippocampal slices under ischemic conditions. The effects of DEX on field potential in hippocampal slices exposed to oxygen-glucose deprivation (OGD) were evaluated. Hippocampal slices were prepared from rats, and the evoked field excitatory postsynaptic potentials (fEPSPs) were recorded using the MED 64 system. Hypoxic-ischemia was induced by perfusion with glucose-free artificial cerebrospinal fluid (aCSF) bubbled with 95% N2 and 5% CO2, and hippocampal slices were perfused with DEX-added aCSF before, during, and after OGD induction. In the normal hippocampal slices, perfusion with 1 and 10µM DEX did not significantly decrease the normalized fEPSP amplitude, but 100µM DEX significantly reduced the fEPSP amplitude compared with its baseline control. The induction of OGD remarkably decreased the fEPSP amplitude, whereas the pre-, co-, and post-treatment of 10µM DEX gradually promoted recovery after washing out, and consequently the amplitude of fEPSP in DEX pre-, co-, and post-treated OGD slices were significantly higher than that in the untreated OGD slices at 10min and 60min after washing out. In particular, co-treatment with DEX conspicuously promoted the recovery of the fEPSP amplitude at the beginning of washing out. These results suggest the possibility of DEX as a therapeutic agent to prevent hypoxic-ischemic brain damage and promote functional recovery after ischemia.

Rocuronium Bromide Inhibits Inflammation and Pain by Suppressing Nitric Oxide Production and Enhancing Prostaglandin E2 Synthesis in Endothelial Cells.

PURPOSE: Rocuronium bromide is a nondepolarizing neuromuscular blocking drug and has been used as an adjunct for relaxation or paralysis of the skeletal muscles, facilitation of endotracheal intubation, and improving surgical conditions during general anesthesia. However, intravenous injection of rocuronium bromide induces injection pain or withdrawal movement. The exact mechanism of rocuronium bromide-induced injection pain or withdrawal movement is not yet understood. We investigated whether rocuronium bromide treatment is involved in the induction of inflammation and pain in vascular endothelial cells. METHODS: For this study, calf pulmonary artery endothelial (CPAE) cells were used, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Western blot, nitric oxide detection, and prostaglandin E2 immunoassay were conducted. RESULTS: Rocuronium bromide treatment inhibited endothelial nitric oxide synthase and suppressed nitric oxide production in CPAE cells. Rocuronium bromide activated cyclooxygenase-2, inducible nitric oxide synthase and increased prostaglandin E2 synthesis in CPAE cells. CONCLUSIONS: Rocuronium bromide induced inflammation and pain in CPAE cells. Suppressing nitric oxide production and enhancing prostaglandin E2 synthesis might be associated with rocuronium bromide-induced injection pain or withdrawal movement.

The comparison of monitored anesthesia care with dexmedetomidine and spinal anesthesia during varicose vein surgery.

PURPOSE: The purpose of this study was to investigate the effectiveness and safety of monitored anesthesia care (MAC) using dexmedetomidine for its sedative and analgesic effect during varicose vein surgery. METHODS: Forty-two patients, who underwent varicose vein surgery, were divided into the MAC group (n = 20) or the spinal anesthesia group (n = 22) for randomized clinical trial. In the MAC group, dexmedetomidine was administered by a loading dose of 1 µg/kg for 10 minutes, followed by a maintenance infusion of 0.2-1.0 µg/kg/hr. Ketamine was used for intermittent injection. In the spinal anesthesia group, midazolam was used for sedation. Intraoperative vital signs, the number of adverse events, and the satisfaction of patients and surgeons concerning the anesthetic condition were compared between the two groups. RESULTS: Systolic blood pressure was intraoperatively significantly different over time between the two groups. The groups had statistical differences in the change in heart rate with regard to time. In the postanesthetic care unit, patients and surgeons in the MAC group had a lower satisfaction score, compared to patients and surgeons in the spinal anesthesia group. However, in the recovery period, patients had a positive perception concerning MAC anesthesia. In addition, without significant adverse events, the MAC group had a shorter time to possible ambulation, which indicated an early recovery. CONCLUSION: We believe that MAC using dexmedetomidine in combination with ketamine may be an alternative anesthetic technique for varicose vein surgery with regard to a patient's preference and medical condition.

Laparoscopic cholecystectomy in patients with anesthetic problems.

Laparoscopic cholecystectomy is a standard operation for benign gallbladder disease. As experience with laparoscopic cholecystectomy has increased, the procedure has become possible in patients with anesthetic problems. Patients with ankylosing spondylitis or severe kyphosis represent a challenging group to anesthesiologists and laparoscopic surgeons since these diseases are associated with difficult intubation, restrictive ventilatory defects, and cardiac problems. The relatively new approach of awake fiberoptic intubation is considered to be the safest option for patients with anticipated airway difficulties. Laparoscopic cholecystectomy is usually performed under general anesthesia but considerable difficulties in anesthetic management are encountered during laparoscopic surgery; for example, hemodynamic instability may develop in patients with cardiopulmonary dysfunction due to pneumoperitoneum and position changes during the operation. Nonetheless, regional anesthesia can be considered as a valid option for patients with gallbladder disease who are poor candidates for general anesthesia due to cardiopulmonary problems. We report three cases of laparoscopic cholecystectomy successfully performed in patients with anesthetic problems that included cardiopulmonary disease, severe kyphosis, and ankylosing spondylitis.

Rocuronium anaphylaxis in a 3-year-old girl with no previous exposure to neuromuscular blocking agents.

During the perioperative period, anaphylactic reactions rarely occur. Neuromuscular blocking agents (NMBAs) are responsible for 60-70% of perioperative anaphylactic reactions. This case, we report a case of rocuronium-induced anaphylaxis in a 3-year-old girl with no previous exposure to NMBAs. This case cautions and informs practitioners that an IgE-mediated anaphylactic reaction with rocuronium is possible even in young children with no previous exposure to NMBAs.

Isoflurane Induces Transient Anterograde Amnesia through Suppression of Brain-Derived Neurotrophic Factor in Hippocampus.

OBJECTIVE: Transient anterograde amnesia is occasionally observed in a number of conditions, including migraine, focal ischemia, venous flow abnormalities, and after general anesthesia. The inhalation anesthetic, isoflurane, is known to induce transient anterograde amnesia. We examined the involvement of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) in the underlying mechanisms of the isoflurane-induced transient anterograde amnesia. METHODS: Adult male Sprague-Dawley rats were divided into three groups : the control group, the 10 minutes after recovery from isoflurane anesthesia group, and the 2 hours after recovery from isoflurane anesthesia group (n=8 in each group). The rats in the isoflurane-exposed groups were anesthetized with 1.2% isoflurane in 75% nitrous oxide and 25% oxygen for 2 hours in a Plexiglas anesthetizing chamber. Short-term memory was determined using the step-down avoidance task. BDNF and TrkB expressions in the hippocampus were evaluated by immunofluorescence staining and western blot analysis. RESULTS: Latency in the step-down avoidance task was decreased 10 minutes after recovery from isoflurane anesthesia, whereas it recovered to the control level 2 hours after isoflurane anesthesia. The expressions of BDNF and TrkB in the hippocampus were decreased immediately after isoflurane anesthesia but were increased 2 hours after isoflurane anesthesia. CONCLUSION: In this study, isoflurane anesthesia induced transient anterograde amnesia, and the expressions of BDNF and TrkB in the hippocampus might be involved in the underlying mechanisms of this transient anterograde amnesia.