Unexpected extrusion of the implantable pulse generator of the spinal cord stimulator - A case report -

Background@#Despite significant technological advances in the implantable pulse generator (IPG), complications can still occur. We report a case that unexpected extrusion of the IPG of spinal cord stimulation (SCS) was promptly identified and successfully removed without any complications. Case: After a car accident 4 years ago, a 55-year-old man who was diagnosed with complex local pain syndrome in his right leg. The SCS was inserted with 2 leads, with the IPG being implanted in the right lower abdomen region. Four years later, he developed extrusion of the IPG from his abdominal region. This unexpected extrusion may have been related to pressure necrosis caused by continued compression of pocket site where a belt was frequently tied. The IPG and the leads were successfully removed without infection occurring. @*Conclusions@#To prevent unexpected extrusion of IPG, it is necessary to consider in advance whether the pocket site is pressed against the belt.

Celiac Plexus Neurolysis for the Treatment of Patients with Terminal Cancer at a Tertiary University Hospital in Korea / 한국호스피스완화의료학회지

Purpose@#The aim of this study was to investigate celiac plexus neurolysis (CPN) for the treatment of cancerous upper abdominal pain in a tertiary university hospital in Korea. @*Methods@#At the tertiary university hospital in Korea, electronic medical records of cancer patients who underwent CPN and died in the hospital from November 2009 to June 2018 were retrospectively analyzed. @*Results@#The total number of subjects was 51. The 17 patients were from the Department of Gastroenterology (33.0%), followed by 11 patients from the Department of Hemato-oncology (21.6%), 11 patients from the Department of Anesthesia and Pain Medicine (21.6%), 9 patients from the Department of General Surgery (17.6%). The diagnosis was pancreatic cancer in 15 patients (29.4%), stomach cancer in 8 patients (15.7%), hepatobiliary cancer in 20 patients (39.2%), colon cancer in 1 patient (2.0%), esophageal cancer in 2 patient (3.9%) and intra-abdominal metastasis in 5 patients (9.8%). The mean survival time after the surgery was 66.4±55.0 days. The pain intensity before and 1 week after the procedure significantly decreased, but the amounts of opioids consumed before and 1 week after the procedure were not statistically significant. Side effects occurred after the procedure including temporary localized pain in 24 patients (47.0%), hypotension in 12 (23.5%), and diarrhea in 6 (11.8%). @*Conclusion@#CPN is an effective and safe procedure for reducing upper abdominal pain caused by cancer, and it is necessary to perform CPN within the appropriate time by establishing a system of interdepartmental cooperation.

Optimal effect-site concentration of remifentanil to prevent hemodynamic changes during nasotracheal intubation using a video laryngoscope

Background@#Nasotracheal intubation is the most commonly used method to secure the field of view when performing surgery on the oral cavity or neck. Like orotracheal intubation, nasotracheal intubation uses a laryngoscope. Hemodynamic change occurs due to the stimulation of the sympathetic nervous system. Recently, video laryngoscope with a camera attached to the end of the direct laryngoscope blade has been used to minimize this change. In this study, we investigated the optimal effect-site concentration (Ce) of remifentanil for minimizing hemodynamic responses during nasotracheal intubation with a video laryngoscope. @*Methods@#Twenty-one patients, aged between 19 and 60 years old, scheduled for elective surgery were included in this study. Anesthesia was induced by slowly injecting propofol. At the same time, remifentanil infusion was initiated at 3.0 ng/ml via target-controlled infusion (TCI). When remifentanil attained the preset Ce, nasotracheal intubation was performed using a video laryngoscope. The patient's blood pressure and heart rate were checked pre-induction, right before and after intubation, and 1 min after intubation. Hemodynamic stability was defined as an increase in systolic blood pressure and heart rate by 20% before and after nasotracheal intubation. The response of each patient determined the Ce of remifentanil for the next patient at an interval of 0.3 ng/ml. @*Results@#The Ce of remifentanil administered ranged from 2.4 to 3.6 ng/ml for the patients evaluated. The estimated optimal effective effect-site concentrations of remifentanil were 3.22 and 4.25 ng/ml, that were associated with a 50% and 95% probability of maintaining hemodynamic stability, respectively. @*Conclusion@#Nasotracheal intubation using a video laryngoscope can be successfully performed in a hemodynamically stable state by using the optimal remifentanil effect-site concentration (Ce50 , 3.22 ng/ml; Ce95 , 4.25 ng/ml).

Effects of remifentanil preconditioning on factors related to uterine contraction in WISH cells

BACKGROUND: Preterm labor and miscarriage may occur in stressful situations, such as a surgical operation or infection during pregnancy. Pharyngeal and buccal abscess and facial bone fractures are inevitable dental surgeries in pregnant patients. Remifentanil is an opioid analgesic that is commonly used for general anesthesia and sedation. Nonetheless, no study has investigated the effects of remifentanil on amniotic epithelial cells. This study evaluated the effects of remifentanil on the factors related to uterine contraction and its mechanism of action on amniotic epithelial cells.METHODS: Amniotic epithelial cells were preconditioned at various concentrations of remifentanil for 1 h, followed by 24-h lipopolysaccharide (LPS) exposure. MTT assays were performed to assess the cell viability in each group. The effects of remifentanil on factors related to uterine contractions in amniotic epithelial cells were assessed using a nitric oxide (NO) assay, western blot examinations of the expression of nuclear factor-kappa B (NF-κB), cyclooxygenase 2 (COX2), and prostaglandin E2 (PGE₂), and RT-PCR examinations of the expression of the proinflammatory cytokines interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α).RESULTS: Remifentanil did not affect viability and nitric oxide production of amniotic epithelial cells. Western blot analysis revealed that remifentanil preconditioning resulted in decreased expressions of NF-κB and PGE2 in the cells in LPS-induced inflammation, and a tendency of decreased COX2 expression. The results were statistically significant only at high concentration. RT-PCR revealed reduced expressions of IL-1β and TNF-α.CONCLUSION: Preconditioning with remifentanil does not affect the viability of amniotic epithelial cells but reduces the expression of factors related to uterine contractions in situations where cell inflammation is induced by LPS, which is an important inducer of preterm labor. These findings provide evidence that remifentanil may inhibit preterm labor in clinical settings.

Remifentanil promotes osteoblastogenesis by upregulating Runx2/osterix expression in preosteoblastic C2C12 cells

BACKGROUND: The imbalance between osteoblasts and osteoclasts can lead to pathological conditions such as osteoporosis. It has been reported that opioid adversely affect the skeletal system, but it is inconsistent. Remifentanil is currently used as an adjuvant analgesic drug in general anesthesia and sedation. The aim of the present study was to investigate the effect of remifentanil on the osteoblast differentiation and mechanism involved in this effect. METHODS: The C2C12 cells (mouse pluripotent mesenchymal cell line) were used as preosteoblast. Osteoblastic differentiation potency was determined by alkaline phosphatase (ALP) staining. C2C12 cell migration by remifentanil was evaluated using Boyden chamber migration assay. The expression of Runx2 and osterix was evaluated by RT-PCT and western blot analysis to investigate the mechanism involved in remifentanil-mediated osteoblast differentiation. RESULTS: ALP staining showed that remifentanil increased significantly osteoblast differentiation. In Boyden chamber migration assay, C2C12 cell migration was increased by remifentanil. RT-PCR and western blot analysis showed that the expression of Runx2 and osterix was upregulated by remifentanil. CONCLUSIONS: We demonstrated that remifentanil increased osteoblast differentiation in vitro by upregulation of Runx2 and osterix expression. Therefore, remifentanil has the potential for assisting with bone formation and bone healing.

Colonic hypoperfusion following ligation of the inferior mesenteric artery in rectosigmoid colon cancer patients

PURPOSE: Colon perfusion status is one of the most important factors for the determination of postoperative anastomotic complications. Colonic hypoperfusion can be induced by inferior mesenteric artery (IMA) ligation in some patients. This study aimed to evaluate atherosclerotic risk assessment and vascular parameters of CT angiography as predictors of colonic hypoperfusion. METHODS: This prospective study was conducted at a tertiary referral hospital and included 46 rectosigmoid colon cancer patients undergoing laparoscopic anterior resection between August 2013 to July 2014. Atherosclerotic risk scores were assessed using the Framingham cardiovascular risk score system. The IMA length, branching pattern, atherosclerotic calcification, and intermesenteric artery and mesenteric vascular diameters were evaluated using CT angiography. Mesenteric marginal artery pressures were measured before and after IMA clamping. The mean arterial pressure (MAP) index was calculated by dividing the mesenteric marginal MAP into the systemic MAP to determine the mesenteric hypoperfusion status after IMA clamping. A critically low MAP index was defined as <0.4. RESULTS: Critically low MAP index (<0.4) was observed in 6 cases (13.0%) after IMA clamping. Atherosclerotic calcification of the IMA and superior mesenteric artery occurred in 11 (23.9%) and 5 patients (10.9%), respectively. Low MAP index was associated with high atherosclerotic risk score and short IMA length, rather than atherosclerotic calcification and other vascular parameters of the major mesenteric arteries. Multivariate analysis indicated that high atherosclerotic risk and short IMA length were independent predictors of critically low MAP index. CONCLUSION: Atherosclerotic risk assessment and IMA length were useful predictors of the mesenteric hypoperfusion status following IMA ligation during laparoscopic rectosigmoid colon surgery.

Fatal neurological complication after liver transplantation in acute hepatic failure patient with hepatic encephalopathy / 고신대학교의과대학학술지

Liver transplantation is a current definitive treatment for those with end-stage liver disease. Hepatic encephalopathy is a common complication of hepatic failure, which can be improved and aggravated by various causes. It is important to differentiate hepatic encephalopathy from other diseases causing brain dysfunction such as cerebral hemorrhage, which is also related to high mortality after liver transplant surgery. A 37-year-old patient was presented with acute liver failure and high ammonia levels and seizure-like symptoms. Computed tomography (CT) of his brain showed mild brain atrophy, regarded as a symptom of hepatic encephalopathy, and treated to decrease blood ammonia level. Deceased donor liver transplantation was performed and liver function and ammonia level normalized after surgery, but the patient showed symptoms of involuntary muscle contraction and showed loss of pupil reflex and fixation without recovery of consciousness. Brain CT showed brain edema and bilateral cerebral infarction, and the patient died after a few days. The purpose of this case report is to emphasize the importance of preoperative neurological evaluation, careful transplantation decision, and proper perioperative management of liver transplantation in patients with acute hepatic encephalopathy.

Remifentanil Negatively Regulates RANKL-Induced Osteoclast Differentiation and Bone Resorption by Inhibiting c-Fos/NFATc1 Expression

Remifentanil is commonly used in operating rooms and intensive care units for the purpose of anesthesia and sedation or analgesia. Although remifentanil may significantly affect the bone regeneration process in patients, there have been few studies to date on the effects of remifentanil on bone physiology. The purpose of this study was to investigate the effects of remifentanil on osteoclast differentiation and bone resorption. Bone marrow-derived macrophages (BMMs) were cultured for 4 days in remifentanil concentrations ranging from 0 to 100 ng/ml, macrophage colony-stimulating factor (M-CSF) alone, or in osteoclastogenic medium to induce the production of mature osteoclasts. To determine the degree of osteoclast maturity, tartrate-resistant acid phosphatase (TRAP) staining was performed. RT-PCR and western blotting analyses were used to determine the effect of remifentanil on the signaling pathways involved in osteoclast differentiation and maturation. Bone resorption and migration of BMMs were analyzed to determine the osteoclastic activity. Remifentanil reduced the number and size of osteoclasts and the formation of TRAP-positive multinuclear osteoclasts in a dose-dependent manner. Expression of c-Fos and NFATC1 was most strongly decreased in the presence of RANKL and remifentanil, and the activity of ERK was also inhibited by remifentanil. In the bone resorption assay, remifentanil reduced bone resorption and did not significantly affect cell migration. This study shows that remifentanil inhibits the differentiation and maturation of osteoclasts and reduces bone resorption.

Fatal vocal cord granuloma after orthognathic surgery

Endotracheal intubation is commonly associated with laryngeal injury that often resolves spontaneously without any complication. However, stenosis or granulomatous lesions are generally found on the tracheal wall or vocal process at the tube cuff level, caused by excessive cuff pressure. We present a case of fatal vocal cord granuloma leading to dyspnea following orthognathic surgery and sustained intubation for 14 hours.

Optimal effective-site concentration of remifentanil for sedation during plate removal of maxilla

BACKGROUND: Removal of the plate following Le Fort I osteotomy and BSSO (bilateral sagittal split osteotomy) is a common procedure. However, patients who undergo plate removal experience intense pain and discomfort. This study investigated the half-maximal effective concentration (Ce50 ) of remifentanil in the prevention of plate removal pain under sedation using dexmedetomidine. METHODS: The study evaluated 18 patients, between 18 and 35 years of age, scheduled for elective surgery. Remifentanil infusion was initiated after sedation using dexmedetomidine, and started at a dose of 1.5 ng/mL on the first patient via target-controlled infusion (TCI). Patients received a loading dose of 1.0 µg/kg dexmedetomidine over 10 min, followed by a maintenance dose of 0.7 µg/kg/h. When the surgeon removed the plate, the patient Modified Observer's Assessment of Alertness/Sedation (MOAA/S) score was observed. RESULTS: The Ce of remifentanil ranged from 0.9 to 2.1 ng/mL for the patients evaluated. The estimated effect-site concentrations of remifentanil associated with a 50% and 95% probability of reaching MOAA/S score of 3 were 1.28 and 2.51 ng/mL, respectively. CONCLUSIONS: Plate removal of maxilla can be successfully performed without any pain or adverse effects by using the optimal remifentanil effect-site concentration (Ce50 , 1.28 ng/mL; Ce95 , 2.51 ng/mL) combined with sedation using dexmedetomidine.

Medical adhesive related skin injury after dental surgery

An 87-year-old woman was referred for the extraction of residual teeth and removal of tori prior to prosthetic treatment. After surgery under general anesthesia, the surgical tape was removed to detach the bispectral index sensor and the hair cover. After the surgical tape was removed, skin injury occurred on the left side of her face. After epidermis repositioning and ointment application, a dressing was placed over the injury. Her wound was found to have healed completely on follow-up examination. Medical adhesive related skin injury (MARSI) is a complication that can occur after surgery and subjects at the extremes of age with fragile skin are at a higher risk for such injuries. Careful assessment of the risk factors associated with MARSI is an absolute necessity.

Effect of remifentanil on pre-osteoclast cell differentiation in vitro

BACKGROUND: The structure and function of bone tissue is maintained through a constant remodeling process, which is maintained by the balance between osteoblasts and osteoclasts. The failure of bone remodeling can lead to pathological conditions of bone structure and function. Remifentanil is currently used as a narcotic analgesic agent in general anesthesia and sedation. However, the effect of remifentanil on osteoclasts has not been studied. Therefore, we investigated the effect of remifentanil on pre-osteoclast (pre-OCs) differentiation and the mechanism of osteoclast differentiation in the absence of specific stimulus. METHODS: Pre-OCs were obtained by culturing bone marrow-derived macrophages (BMMs) in osteoclastogenic medium for 2 days and then treated with various concentration of remifentanil. The mRNA expression of NFATc1 and c-fos was examined by using real-time PCR. We also examined the effect of remifentanil on the osteoclast-specific genes TRAP, cathepsin K, calcitonin receptor, and DC-STAMP. Finally, we examined the influence of remifentanil on the migration of pre-OCs by using the Boyden chamber assay. RESULTS: Remifentanil increased pre-OC differentiation and osteoclast size, but did not affect the mRNA expression of NFATc1 and c-fos or significantly affect the expression of TRAP, cathepsin K, calcitonin receptor, and DC-STAMP. However, remifentanil increased the migration of pre-OCs. CONCLUSIONS: This study suggested that remifentanil promotes the differentiation of pre-OCs and induces maturation, such as increasing osteoclast size. In addition, the increase in osteoclast size was mediated by the enhancement of pre-OC migration and cell fusion.

The Association of Preoperative Body Mass Index with Acute Kidney Injury in Liver Transplantation Recipients: A Retrospective Study / 대한구급학회지

BACKGROUND: Liver transplantation (LT) is a complicated procedure with a high incidence of postoperative acute kidney injury (AKI). Previous studies indicate that even transient or mild post-LT AKI can result in critical conditions, including prolonged stays in hospitals and intensive care units and increased morbidity and mortality. The aim of this study was to investigate the association between body mass index (BMI) and occurrence of AKI in LT recipients. METHODS: Medical data from 203 patients who received LT surgery from January 2010 to August 2016 in a single university hospital setting were retrospectively collected and analyzed. Patients were classified as either underweight (BMI <20 kg/m²) or normal weight (20 ≤ BMI < 30 kg/m²). Demographic data, anesthetic methods, complications, and perioperative laboratory test values of each patient were assessed. Propensity analyses and logistic regression were performed to evaluate the association between BMI and post-LT AKI. RESULTS: There was no significant difference in occurrence of post-LT AKI between underweight and normal weight patients. The underweight patient group had significantly longer hospital stay compared with the normal weight patient group (P = 0.023). CONCLUSIONS: BMI classification was neither a positive nor negative predictor of postoperative AKI occurrence. However, patients with lower BMI had significantly longer hospital stay compared with their counterparts. Although our study was limited by its retrospective design, our observations suggest that lower BMI might play a role in post-LT AKI.

Effects of Remifentanil Preconditioning Attenuating Oxidative Stress in Human Dermal Fibroblast

Human dermal fibroblast is essential in wound healing of the skin through the synthesis of extracellular matrix proteins. With respect to oxidative stress, the effects of remifentanil on human dermal fibroblast have received little attention. Therefore, we investigated the effects of remifentanil on the apoptosis and autophagic reaction of human dermal fibroblasts under oxidative stress. The subjects were divided into the following groups: Control group: cells were incubated at 37℃ in a humidified atmosphere with 5% CO₂. Hydrogen peroxide (H₂O₂) group: cells were exposed to H₂O₂ for 2 h. RPC/H₂O₂ group: cells were pretreated with remifentanil for 2 h and exposed H₂O₂ for 2 h. 3-MA/RPC/H₂O₂ group: cells were pretreated with 3-methyladenine (3-MA) and remifentanil for 1 h and 2 h, respectively. We measured cell viability using MTT assay. Western blot analysis was used to determine the expression levels of proteins associated with apoptosis and autophagy. Quantification of apoptotic cells was performed using flow cytometer analysis, and autophagic vacuoles were observed under a fluorescence microscope. Remifentanil treatment increased the proliferation of human dermal fibroblast and decreased apoptotic cell death, enhancing autophagic activity under oxidative stress. However, 3-MA, the autophagy pathway inhibitor, inhibited the protective effect of remifentanil in oxidative stress. This study demonstrates that remifentanil activated autophagy and decreased apoptotic death of human dermal fibroblasts under oxidative stress. Our results suggest that remifentanil may help in the treatment of oxidative stress.

Propofol protects human keratinocytes from oxidative stress via autophagy expression

BACKGROUND: The skin consists of tightly connected keratinocytes, and prevents extensive water loss while simultaneously protecting against the entry of microbial pathogens. Excessive cellular levels of reactive oxygen species can induce cell apoptosis and also damage skin integrity. Propofol (2,6-diisopropylphenol) has antioxidant properties. In this study, we investigated how propofol influences intracellular autophagy and apoptotic cell death induced by oxidative stress in human keratinocytes. METHOD: The following groups were used for experimentation: control, cells were incubated under normoxia (5% CO₂, 21% O₂, and 74% N₂) without propofol; hydrogen peroxide (H₂O₂), cells were exposed to H₂O₂ (300 µM) for 2 h; propofol preconditioning (PPC)/H₂O₂, cells pretreated with propofol (100 µM) for 2 h were exposed to H₂O₂; and 3-methyladenine (3-MA)/PPC/H₂O₂, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to H₂O₂. Cell viability, apoptosis, and migration capability were evaluated. Relation to autophagy was detected by western blot analysis. RESULTS: Cell viability decreased significantly in the H₂O₂ group compared to that in the control group and was improved by propofol preconditioning. Propofol preconditioning effectively decreased H₂O₂-induced cell apoptosis and increased cell migration. However, pretreatment with 3-MA inhibited the protective effect of propofol on cell apoptosis. Autophagy was activated in the PPC/H₂O₂ group compared to that in the H₂O₂ group as demonstrated by western blot analysis and autophagosome staining. CONCLUSION: The results suggest that propofol preconditioning induces an endogenous cellular protective effect in human keratinocytes against oxidative stress through the activation of signaling pathways related to autophagy.

Propofol protects against oxidative-stress-induced COS-7 cell apoptosis by inducing autophagy

BACKGROUND: In oxidative stress, reactive oxygen species (ROS) production contributes to cellular dysfunction and initiates the apoptotic cascade. Autophagy is considered the mechanism that decreases ROS concentration and oxidative damage. Propofol shows antioxidant properties, but the mechanisms underlying the effect of propofol preconditioning (PPC) on oxidative injury remain unclear. Therefore, we investigated whether PPC protects against cell damage from hydrogen peroxide (H₂O₂)-induced oxidative stress and influences cellular autophagy. METHOD: COS-7 cells were randomly divided into the following groups: control, cells were incubated in normoxia (5% CO₂, 21% O₂, and 74% N₂) for 24 h without propofol; H₂O₂, cells were exposed to H₂O₂ (400 µM) for 2 h; PPC + H₂O₂, cells pretreated with propofol were exposed to H₂O₂; and 3-methyladenine (3-MA) + PPC + H₂O₂, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to H₂O₂. Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) reduction. Apoptosis was determined using Hoechst 33342 staining and fluorescence microscopy. The relationship between PPC and autophagy was detected using western blot analysis. RESULTS: Cell viability decreased more significantly in the H₂O₂ group than in the control group, but it was improved by PPC (100 µM). Pretreatment with propofol effectively decreased H₂O₂-induced COS-7 cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol during apoptosis. Western blot analysis showed that the level of autophagy-related proteins was higher in the PPC + H₂O₂ group than that in the H2O2 group. CONCLUSION: PPC has a protective effect on H₂O₂-induced COS-7 cell apoptosis, which is mediated by autophagy activation.

The Association of Preoperative Body Mass Index with Acute Kidney Injury in Liver Transplantation Recipients: A Retrospective Study / 대한중환자의학회지

BACKGROUND: Liver transplantation (LT) is a complicated procedure with a high incidence of postoperative acute kidney injury (AKI). Previous studies indicate that even transient or mild post-LT AKI can result in critical conditions, including prolonged stays in hospitals and intensive care units and increased morbidity and mortality. The aim of this study was to investigate the association between body mass index (BMI) and occurrence of AKI in LT recipients. METHODS: Medical data from 203 patients who received LT surgery from January 2010 to August 2016 in a single university hospital setting were retrospectively collected and analyzed. Patients were classified as either underweight (BMI <20 kg/m²) or normal weight (20 ≤ BMI < 30 kg/m²). Demographic data, anesthetic methods, complications, and perioperative laboratory test values of each patient were assessed. Propensity analyses and logistic regression were performed to evaluate the association between BMI and post-LT AKI. RESULTS: There was no significant difference in occurrence of post-LT AKI between underweight and normal weight patients. The underweight patient group had significantly longer hospital stay compared with the normal weight patient group (P = 0.023). CONCLUSIONS: BMI classification was neither a positive nor negative predictor of postoperative AKI occurrence. However, patients with lower BMI had significantly longer hospital stay compared with their counterparts. Although our study was limited by its retrospective design, our observations suggest that lower BMI might play a role in post-LT AKI.

Optimal dose of dexmedetomidine for sedation during epidural anesthesia

BACKGROUND: Sedation during epidural anesthesia can reduce patients' anxiety and discomfort. Dexmedetomidine has sedative, hypnotic, and analgesic effects, with minimal respiratory depression. However, the use of dexmedetomidine is associated with prolonged recovery. This study investigated the optimal dose of intravenous dexmedetomidine for proper sedation with minimal recovery time in epidural anesthesia. METHODS: Sixty-three patients (American Society of Anesthesiologists physical status I/II) were randomized into two groups. Following epidural anesthesia, a loading dose (1 µg/kg) of dexmedetomidine was administered for 10 min followed by maintenance infusion as follows: Group A (n = 32; dexmedetomidine 0.6 µg/kg/h) and Group B (n = 31; dexmedetomidine 1.0 µg/kg/h). Heart rate, blood pressure, and bispectral index score (BIS) were recorded during surgery. The length of stay and modified Aldrete score (MAS) were measured in the postanesthesia care unit (PACU). RESULTS: Length of stay in the PACU was longer in Group B than in Group A (P < 0.05). The MAS was higher in Group A after 30 min in the PACU (P < 0.05). The BIS did not significantly differ between the two groups from baseline to 150 min after infusion of dexmedetomidine. BIS values were significantly higher in Group A at 160 min (P < 0.05). The mean arterial pressure in Group B was significantly lower in the PACU. CONCLUSIONS: Length of stay in the PACU was longer in Group B than in Group A (P < 0.05). The MAS was higher in Group A after 30 min in the PACU (P < 0.05). The BIS did not significantly differ between the two groups from baseline to 150 min after infusion of dexmedetomidine. BIS values were significantly higher in Group A at 160 min (P < 0.05). The mean arterial pressure in Group B was significantly lower in the PACU.

Remifentanil induces autophagy and prevents hydrogen peroxide-induced apoptosis in Cos-7 cells

BACKGROUND: This study investigated the effect of remifentanil pretreatment on Cos-7 cells exposed to oxidative stress, and the influence of remifentanil on intracellular autophagy and apoptotic cell death. METHODS: Cells were divided into 4 groups: (1) Control: non-pretreated cells were incubated in normoxia (5% CO₂, 21% O₂, and 74% N₂). (2) H₂O₂: non-pretreated cells were exposed to H₂O₂ for 24 h. (3) RPC+H₂O₂: cells pretreated with remifentanil were exposed to H₂O₂ for 24 h. (4) 3-MA+RPC+H₂O₂: cells pretreated with 3-Methyladenine (3-MA) and remifentanil were exposed to H₂O₂ for 24 h. We determined the cell viability of each group using an MTT assay. Hoechst staining and FACS analysis of Cos-7 cells were performed to observe the effect of remifentanil on apoptosis. Autophagy activation was determined by fluorescence microscopy, MDC staining, and AO staining. The expression of autophagy-related proteins was observed using western blotting. RESULTS: Remifentanil pretreatment increased the viability of Cos-7 cells exposed to oxidative stress. Hoechst staining and FACS analysis revealed that oxidative stress-dependent apoptosis was suppressed by the pretreatment. Additionally, fluorescence microscopy showed that remifentanil pretreatment led to autophagy-induction in Cos-7 cells, and the expression of autophagy-related proteins was increased in the RPC+H₂O₂ group. CONCLUSIONS: The study showed that remifentanil pretreatment stimulated autophagy and increased viability in an oxidative stress model of Cos-7 cells. Therefore, we suggest that apoptosis was activated upon oxidative stress, and remifentanil preconditioning increased the survival rate of the cells by activating autophagy.

Effects of propofol-induced autophagy against oxidative stress in human osteoblasts

BACKGROUND: Oxidative stress occurs during the aging process and other conditions such as bone fracture, bone diseases, and osteoporosis, but the role of oxidative stress in bone remodeling is unknown. Propofol exerts antioxidant effects, but the mechanisms of propofol preconditioning on oxidative stress have not been fully explained. Therefore, the aim of this study was to evaluate the protective effects of propofol against H2O2-induced oxidative stress on a human fetal osteoblast (hFOB) cell line via activation of autophagy. METHODS: Cells were randomly divided into the following groups: control cells were incubated in normoxia (5% CO2, 21% O2, and 74% N2) without propofol. Hydrogen peroxide (H2O2) group cells were exposed to H2O2 (200 µM) for 2 h, propofol preconditioning (PPC)/H2O2 group cells were pretreated with propofol then exposed to H2O2, 3-methyladenine (3-MA)/PPC/H2O2 cells were pretreated with 3-MA (1 mM) and propofol, then were exposed to H2O2. Cell viability and apoptosis were evaluated. Osteoblast maturation was determined by assaying bone nodular mineralization. Expression levels of bone related proteins were determined by western blot. RESULTS: Cell viability and bone nodular mineralization were decreased significantly by H2O2, and this effect was rescued by propofol preconditioning. Propofol preconditioning effectively decreased H2O2-induced hFOB cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol. In western blot analysis, propofol preconditioning increased protein levels of collagen type I, BMP-2, osterix, and TGF-β1. CONCLUSIONS: This study suggests that propofol preconditioning has a protective effect on H2O2-induced hFOB cell death, which is mediated by autophagy activation.