Ji-Uk Yoon

Maintenance anaesthetics during remifentanil-based anaesthesia might affect postoperative pain control after breast cancer surgery

BACKGROUND Although remifentanil provides profound analgesia during operation, postoperative occurrence of hyperalgesia and tolerance after remifentanil administration could be a challenge to the postoperative pain control. In this investigation, we sought to determine the effect of maintenance with propofol or sevoflurane on postoperative analgesia after remifentanil-based anaesthesia. METHODS Two hundred and fourteen women undergoing breast cancer surgery under remifentanil-based general anaesthesia were randomly included in this prospective and double-blind trial. The patients were anaesthetized with sevoflurane (S) or propofol (P) under high (H) or low (L) effect-site concentration (Ce) of remifentanil-based anaesthesia using a target-controlled infusion system; the patients were allocated into the SH, SL, PH, and PL groups. Pain intensity (visual analogue score, VAS) and cumulative morphine requirements were recorded 30 min, 1, 6, 12, and 24 h after operation. RESULTS The patient characteristics were similar. Cumulative morphine consumption at 24 h after surgery was higher in the SH group [38.6 (sd 14.9)] compared with the SL [31.5 (3.7)], PH [31.7 (8.3)], and PL groups [30.1 (6.1)] (P<0.001). The VAS scores during 24 h after surgery were also higher in the SH group than the SL, PH, and PL groups (P<0.001). CONCLUSIONS Remifentanil hyperalgesia was induced by high dose of remifentanil-based anaesthesia during sevoflurane anaesthesia, whereas that was not apparent during propofol anaesthesia. Also, remifentanil hyperalgesia did not occur during low dose of remifentanil-based anaesthesia. Maintenance of propofol during high-dose remifentanil-based anaesthesia provided better postoperative analgesia.

The median effective effect-site concentration of remifentanil for minimizing the cardiovascular changes to endotracheal intubation during desflurane anesthesia in pediatric patients

Background Desflurane has the most rapid onset and offset of action among the volatile anesthetic agents used for general anesthesia, but it can cause airway reactivity, tachycardia, and hypertension during induction, especially in pediatric patients. This study was designed to determine a median effective effect-site concentration (EC50) of remifentanil to prevent the cardiovascular changes due to tracheal intubation during the 1 minimum alveolar concentration (MAC) desflurane inhalation, which was required to prevent movement in response to a noxious stimulus in 50% of subjects, in pediatric patients. Methods Twenty-four pediatric patients between the ages 5-15 years were enrolled in this study. We injected thiopental intravenously, at the same time remifentanil was infused by Target Controlled Infusion (TCI) device. When the target effect-site concentration (Ce) of remifentanil reached a preset level, desflurane was administrated through the facial mask. Then, we assessed the signs of desflurane related airway reactivity and cardiovascular changes for 2 min. The up-and-down criteria was a 20% change in systolic blood pressure (SBP) and a heart rate (HR) between just prior to intubation and 1 min after intubation. The EC50 of remifentanil was calculated from 8 independent pairs using Dixons up-and-down method. Results We studied 24 pediatric patients in range of 1-5 ng/ml of the Ce of remifentanil. No patient showed airway reactivity during the study. The EC50 of remifentanil to suppress the hemodynamic changes after tracheal intubation during desflurane anesthesia was calculated as 3.4 ± 0.9 ng/ml. Conclusions In pediatric anesthesia, the EC50 of remifentanil to minimize the cardiovascular changes due to tracheal intubation during 1 MAC desflurane anesthesia was 3.4 ± 0.9 ng/ml.

Accidental epidural injection of rocuronium

Epidural administration of local anesthetics or opioid during general anesthesia is a widespread method for postoperative analgesia. Despite the availability of this technique, inadvertent administration of nonepidural medications into the epidural space can be associated with serious neurological complications. We report a case of accidental epidural rocuronium injection.

Remifentanil Protects Human Keratinocytes against Hypoxia–Reoxygenation Injury through Activation of Autophagy

The proliferation, differentiation, and migration of keratinocytes are essential in the early stages of wound healing. Hypoxia-Reoxygenation (H/R) injury to keratinocytes can occur in various stressful environments such as surgery, trauma, and various forms of ulcers. The effects of remifentanil on human keratinocytes under hypoxia-reoxygenation have not been fully studied. Therefore, we investigated the effects of remifentanil on the proliferation, apoptosis, and autophagic activation of human keratinocytes during hypoxic-reoxygenation. Human keratinocytes were cultured under 1% oxygen tension for 24 h. The cells were then treated with various concentrations of remifentanil (0.01, 0.1, 0.5, and 1 ng/mL) for 2 h. Thereafter, the cells were reoxygenated for 12 h at 37°C. We measured cell viability via MTT assay. Using quantitative real-time PCR and western blot analysis, we measured 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 brought about an increase in the proliferation of human keratinocytes damaged by hypoxia-reoxygenation and decreased the apoptotic cell death, enhancing autophagic activity. However, the autophagy pathway inhibitor 3-MA inhibited the protective effect of remifentanil in hypoxia-reoxygenation injury. In conclusion, the current study demonstrated that remifentanil treatment stimulated autophagy and reduced apoptotic cell death in a hypoxia-reoxygenation model of human keratinocytes. Our results provide additional insights into the relationship between apoptosis and autophagy.

Effects of Remifentanil Preconditioning on Osteoblasts under Hypoxia-Reoxygenation Condition

Background: Ischemia-reperfusion of bone occurs in a variety of clinical conditions, such as orthopedic arthroplasty, plastic gnathoplasty, spinal surgery, and amputation. Usually, cellular models of hypoxia-reoxygenation reflect in vivo models of ischemia-reperfusion. With respect to hypoxia-reoxygenation conditions, the effects of remifentanil on osteogenesis have received little attention. Therefore, we investigated the effects of remifentanil on the proliferation and differentiation of osteoblasts during hypoxic-reoxygenation. Methods: After remifentanil (0.1, 1 ng/mL) preconditioning for 2 hours, human osteoblasts were cultured under 1% oxygen tension for 24 hours. Thereafter, the cells were reoxygenated for 12 hours at 37 °C. The naloxone groups were treated with naloxone for 30 minutes before remifentanil treatment. We measured cell viability via MTT assay. Osteoblast maturation was determined by assay of bone nodular mineralization. Quantitative PCR and western blot methods were used to determine BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-β1, HIF-1α, and RUNX2 expression levels. Results: Osteoblast viability and bone nodular mineralization by osteoblasts is recovered by remifentanil preconditioning from hypoxia-reoxygenation insult. During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-β1, HIF-1α, and RUNX2 in osteoblasts. Conclusions: Under hypoxia-reoxygenation conditions, remifentanil preconditioning enhanced the cell viability and maturation of osteoblasts, and stimulated the expression of proteins associated with osteoblast proliferation and differentiation of the osteoblast. Our results suggest that remifentanil may help in the treatment of bone stress injuries.

Hypothermic cardiopulmonary bypass for minimally invasive mitral valve plasty in adult moyamoya disease

A 43-year-old man underwent minimally invasive mitral valve plasty of a flail mitral valve. Four years previously, he had been diagnosed with moyamoya disease (MMD) by cerebral magnetic resonance imaging/angiography findings. In MMD, risk factors for cerebral stroke include changes in arterial carbon dioxide partial pressure, blood pressure, and body temperature. And during cardiopulmonary bypass (CPB), these hemodynamic changes can be challenging. However, hypothermia during CPB can decrease cerebral oxygen consumption and have a cerebral protective effect. We performed a minimally invasive mitral valve plasty, using hypothermic CPB, in a patient with MMD, without any neurological deficits.

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.

Protective effects of remifentanil against H2O2-induced oxidative stress in human osteoblasts

Background Bone injury is common in many clinical situations, such as surgery or trauma. During surgery, excessive reactive oxygen species (ROS) production decreases the quality and quantity of osteoblasts. Remifentanil decreases ROS production, reducing oxidative stress and the inflammatory response. We investigated remifentanils protective effects against H2O2-induced oxidative stress in osteoblasts. Methods To investigate the effect of remifentanil on human fetal osteoblast (hFOB) cells, the cells were incubated with 1 ng/ml of remifentanil for 2 h before exposure to H2O2. For induction of oxidative stress, hFOB cells were then treated with 200 µM H2O2 for 2 h. To evaluate the effect on autophagy, a separate group of cells were incubated with 1 mM 3-methyladenine (3-MA) before treatment with remifentanil and H2O2. Cell viability and apoptotic cell death were determined via MTT assay and Hoechst staining, respectively. Mineralized matrix formation was visualized using alizarin red S staining. Western blot analysis was used to determine the expression levels of bone-related genes. Results Cell viability and mineralized matrix formation increased on remifentanil pretreatment before exposure to H2O2-induced oxidative stress. As determined via western blot analysis, remifentanil pretreatment increased the expression of bone-related genes (Col I, BMP-2, osterix, and TGF-β). However , pretreatment with 3-MA before exposure to remifentanil and H2O2 inhibited remifentanils protective effects on hFOB cells during oxidative stress. Conclusions We showed that remifentanil prevents oxidative damage in hFOB cells via a mechanism that may be highly related to autophagy. Further clinical studies are required to investigate its potential as a therapeutic agent.

Primary right atrial angiosarcoma misdiagnosed as aortic intramural hematoma.

The overall incidence of cardiac tumor is very low, and malignant cardiac tumors account for only 25% of all cardiac tumors. Angiosarcomas are the most common type of malignant cardiac tumors, characterized by rapidly proliferating, extensively infiltrating anaplastic cells derived from blood vessels and lining irregular blood-filled spaces. We present a 26-year-old man with angiosarcoma involving the right atrium, which was misdiagnosed as aortic intramural hematoma by computed tomography, finally confirmed by transesophageal echocardiography during the operation.

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.