A 56-year-old male with a gastrointestinal stromal tumor (GIST) underwent surgical resection of the tumor. Nine months after surgery, imatinib therapy was initiated because of the discovery of metastatic tumors in the left adrenal gland and in a lymph node of the peritoneum. Seventeen months later, the patient achieved complete remission (CR) and imatinib therapy was continued. However, 48 months after initiation of imatinib therapy, computed tomography scans revealed a left adrenal gland metastasis and the patient underwent left adrenalectomy. Immunohistochemical staining indicated that the spindle-shaped cells of the resected tumor were positive for C-kit, thus confirming metastasis of the GIST. This is the first report from Korea of an adrenal gland metastasis from a GIST. Worldwide, only two such cases have been reported. Here, we describe the first case of a distant recurrence of a GIST in the left adrenal gland after CR had been achieved with the aid of surgical resection and imatinib therapy.
Adrenal Glands* ; Adrenalectomy ; Gastrointestinal Stromal Tumors* ; Humans ; Imatinib Mesylate ; Korea ; Lymph Nodes ; Male ; Middle Aged ; Neoplasm Metastasis* ; Peritoneum ; Recurrence

BACKGROUND AND OBJECTIVES: The aim of this study was to investigate the relationship between inhalation anesthetics and hearing in mice. MATERIALS AND METHODS: As inhalation anesthetics, isoflurane was used. Auditory brainstem response and distortion product otoacoustic emission were used as measurement of hearing. Mice were divided into 2 groups. 'Isoflurane group' consisted of mice that were anesthetized with an inspired concentration of 2.0 vol% isoflurane with 2 L/min of oxygen (n=10). 'Control group' consisted of mice that were anesthetized with ketamine and xylazine (n=10). RESULTS: Auditory brainstem response thresholds in mice anesthetized with ketamine and xylazine was not different from those in mice anesthetized with isoflurane. Threshold of DPOAE was higher in mice with isolurane than with ketamine and xylazine. Changes of efferent control may be induced by isoflurane and consequently change the threshold of DPOAE in mice. CONCLUSIONS: These results infer that, there was a change of central nervous system induced by inhalation anesthetics, this change also can be applied to the strategies for prevention of hearing loss.
Anesthetics ; Anesthetics, Inhalation ; Animals ; Central Nervous System ; Evoked Potentials, Auditory, Brain Stem ; Hearing ; Hearing Loss ; Isoflurane ; Ketamine ; Mice ; Oxygen ; Xylazine

BACKGROUND: The addition of epinephrine to local anesthetics has been known to prolong the duration of neural blokade and to increase the intensity of analgesia, but underlying mechanisms are unclear. This study was designed to investigate electrophysiologically the analgesic effects of epinephrine and its interaction with tetracaine. METHODS: Whole cell patch clamp recordings were made from acutely dissociated neurons from adult rat dorsal root ganglion (DRG). Using voltage clamp method, we compared the IC50 values of tetracaine for Na+ and Ca2+ channel suppression in the absence and presence of a fixed dose of epinephrine. Action potentials evoked by current pulses were also investigated to evaluate the effect of tetracaine and epinephrine on the excitability of DRG neurons. RESULTS: Clinical doses of epinephrine did not alter the dose-response curves of tetracaine for peak Na+ and Ca2+ channel current, but the amplitude of action potential spikes was reduced and firing rates evoked by sustained current pulse increased. The addition of epinephrine did not affect the changes of action potential parameters caused by tetracaine alone. CONCLUSIONS: The ability of epinephrine to increase the intensity of analgesia induced by tetracaine seems more likely due to an analgesic action at the level of spinal cord rather than a direct analgesic action at a level of primary sensory neurons. Local vasoconstriction and stimulation of descending inhibitory system via alpha-adrenergic pathway may play a role.
Action Potentials ; Adult ; Analgesia ; Anesthetics, Local ; Animals ; Diagnosis-Related Groups ; Epinephrine* ; Fires ; Ganglia, Spinal* ; Humans ; Inhibitory Concentration 50 ; Neurons ; Rats ; Sensory Receptor Cells ; Spinal Cord ; Spinal Nerve Roots* ; Tetracaine* ; Vasoconstriction

BACKGROUND: Epidural analgesia, via either a thoracic or lumbar route, is commonly used to provide postoperative analgesia following thoracotomy for pulmonary resection, but little data indicate which location is better in terms of postoperative analgesia, side effects, or associated complications. METHODS: 54 patients, who undergo a lateral thoracotomy, were randomized to receive a mixture of fentanyl and 0.15% bupivacaine at 0.5microgram/kg/hr of fentanyl via either a thoracic (Group T) or a lumbar (Group L) catheter. Postoperative pain was assessed 6hrs after the operation and everyday for 5 days on a visual analog scale (VAS). Postoperative side effects and patients satisfaction of epidural analgesia were assessed by 4 grades system. RESULTS: The VAS scores during coughing were higher than those of resting state without intergroup differences. The incidences and severity of side effects (nausea, vomiting, pruritus, sedation) were not different between group T and group L, but the incidence of urinary retention attributable to use of the lumbar epidural route was significantly higher than with the thoracic route (p<0.05). CONCLUSIONS: The authors conclude that there is no clinical advantage of thoracic over lumbar epidural fentanyl in the thoracotomy patients with respect to analgesia and incidences of most side effects except urinary retention.
Analgesia ; Analgesia, Epidural* ; Bupivacaine ; Catheters ; Cough ; Fentanyl* ; Humans ; Incidence ; Pain, Postoperative ; Pruritus ; Thoracotomy* ; Urinary Retention ; Visual Analog Scale ; Vomiting

BACKGROUND: Propofol and barbiturates are both known to protect cells of several organs against ischemia/reperfusion injury, but there are few reports on any possible protective effects on human hepatocytes. We investigated the activities of both agents on human hepatic SNU761 cells under hydrogen peroxide (H2O2)-induced oxidative stress. METHODS: To determine whether propofol and pentobarbital protect hepatocytes from H2O2-induced toxicity, we used SNU761 cells, a human hepatocellular carcinoma (HCC) cell line. Cells were pretreated with different dosages (1, 10, 50 micrometer) of propofol or pentobarbital (1, 10, 50, 100, 400 micrometer) 30 min before H2O2 application. Lactate dehydrogenase (LDH) was measured to assess and quantify cell death. To determine the nature of cell death, treated hepatocytes were doubly stained with fluorescein isothiocyanate (FITC)-labeled Annexin V and propidium iodide (PI), and analyzed by flow cytometry. RESULTS: Pretreatment with propofol, but not pentobarbital, suppressed H2O2-induced LDH release. In Annexin V-FITC/PI binding analysis, propofol decreased the number of necrotic and late apoptotic cells, but no significant decreases in such cell numbers were seen when pentobarbital was used. CONCLUSIONS: Unlike pentobarbital, propofol, at clinical concentrations, protected SNU-761 HCC cells against oxidative stress.
Annexin A5 ; Apoptosis ; Barbiturates ; Carcinoma, Hepatocellular ; Cell Count ; Cell Death ; Cell Line ; Flow Cytometry ; Fluorescein ; Hepatocytes ; Humans ; Hydrogen ; Hydrogen Peroxide ; Isothiocyanates ; L-Lactate Dehydrogenase ; Necrosis ; Oxidative Stress ; Pentobarbital ; Propidium ; Propofol

BACKGROUND: The present investigation was undertaken to evaluate the protective effect of propofol and etomidate against hydrogen peroxide (H2O2) induced oxidative damage in human hepatic SNU761 cells by measuring lactate dehydrogenase (LDH). METHODS: The cell line of human hepatocellular carcinoma was grown for 24 hours in dissociated cell culture. They were divided into eight groups: negative control (NC) group with no drug administration, positive control (PC) group with H2O2 250 micrometer and other groups pretreated with propofol (P; 1, 10, 50 micrometer) or etomidate (ET; 1, 10, 50 micrometer) followed H2O2 administration. After 7 hours, cell death was assessed by morphology under the light microscope and quantified by measuring the LDH in the culture media. RESULTS: In the light microscopic findings, the intact cells were increased in all three propofol groups compared to group PC. H2O2-induced LDH production was also significantly suppressed in all three propofol groups compared to group PC (P < 0.001). There were no significant differences in the microscopic findings and LDH production between the etomidate groups and group PC. CONCLUSIONS: These results suggest that the propofol has protective effect on the hepatocyte against H2O2-induced oxidative stress.
Carcinoma, Hepatocellular ; Cell Culture Techniques ; Cell Death ; Cell Line ; Culture Media ; Etomidate ; Hepatocytes ; Humans ; Hydrogen ; Hydrogen Peroxide ; L-Lactate Dehydrogenase ; Light ; Oxidative Stress ; Propofol

BACKGROUND: It is well known that the loud noise exposure can lead to noise-induced hearing loss (NIHL). Drilling during mastoid surgery may result in NIHL. The noise level produced by drilling of the mastoid bone can exceed 125 dB HL (hearing level); therefore, mastoid surgery itself is associated with a lower incidence of NIHL than expected. The aim of this study was to analyze the effects of isoflurane on NIHL and hair cell morphological changes. METHODS: BALB/c mice were divided into 2 groups; a control group (n = 20) and an isoflurane group (n = 20). The mice of both groups were exposed to 120 dB SPL (sound pressure level) broadband white noise for 3 hours per day, for 3 consecutive days. The mice in the isoflurane group were anesthetized with isoflurane while exposed to the noise. The auditory brainstem response (ABR) thresholds were determined 1 day before and after the noise-exposure and then again after 7 days. Both cochlea were removed and stained using fluorescent isothiocyanate (FITC) phalloidin. RESULTS: 1 day prior to noise-exposure, the ABR thresholds were those of a normal hearing level in both the control and isoflurane groups. In the control group, the mean hearing threshold was 78.0+/-2.6 dB HL after 1 day of noise-exposure and 81.5+/-3.4 dB HL after 1 week; in the isoflurane group, the mean hearing threshold was 49+/-11.7 dB HL after 1 day and 30.5+/-9.3 dB HL after 1 week. The hearing thresholds after noise exposure in the control were significantly higher than those in the isoflurane group (P<0.05). CONCLUSIONS: The occurrence of NIHL decreased and the hair cell damage suppressed in the mice exposed to intense noise while anesthetized by isoflurane.
Animals ; Cochlea ; Evoked Potentials, Auditory, Brain Stem ; Hair ; Hearing ; Hearing Loss, Noise-Induced* ; Incidence ; Isoflurane* ; Mastoid ; Mice* ; Noise ; Phalloidine

A 20-year-old man presented to our outpatient clinic with hemoptysis, cough, and pleuritic chest pain. His chest radiograph and pulmonary function tests (PFT) were normal. A bronchoscopy showed a small yellowish patch with a regular surface. A direct bronchoscopic biopsy was performed. The pathologic findings showed a benign granular cell tumor. The respiratory symptoms resolved after biopsying the tumor. On follow?up, there were no signs of recurrence of the granular cell tumor after a period of 24 months.
Adult ; Chest Pain/*diagnosis/pathology ; Granular Cell Tumor/*diagnosis/pathology ; *Hemoptysis ; Humans ; Male ; Tracheal Neoplasms/*diagnosis/pathology

BACKGROUND: The present investigation was undertaken to evaluate the neuroprotective effect of etomidate against N-methyl-D- aspartate (NMDA) induced neurotoxicity in rat cortical neurons by measuring lactate dehydrogenase (LDH). METHODS: The cerebral cortical neurons of fetal rat were grown for 12 days in dissociated cell culture. They were divided into four groups: first group acted as control with no drug administration and other groups treated with either NMDA 100microM or Etomidate (ET) 10microM + NMDA 100microM or ET 100microM + NMDA 100microM After 24 hrs, cell death was assessed by morphology under the light microscope and quantified by measuring the LDH in the culture media. RESULTS: In the light microscopic findings, the intact cortical neurons were increased in the ET groups. NMDA-induced LDH production also significantly suppressed in ET group (P<0.05). There were no significant difference between the ET 10microM and 100microM groups. CONCLUSIONS: These results suggest that the etomidate has protective effect on the cultured rat cortical neurons against NMDA-induced neurotoxicity.
Animals ; Aspartic Acid ; Cell Culture Techniques ; Cell Death ; Culture Media ; Etomidate* ; L-Lactate Dehydrogenase ; N-Methylaspartate* ; Neurons* ; Neuroprotective Agents ; Rats*