RESUMEN
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.
RESUMEN
Vascular injury caused by a central venous catheter (CVC) has been reported to be a rare complication, especially delayed vascular injury due to CVC has a few cases and it can be fatal because of delayed recognition and more serious complications. A 59-year-old woman with no available medical history was admitted for treatment of ovarian cancer. For the surgery, a triple-lumen CVC was placed through the left subclavian vein. Parenteral nutrition through the CVC was used for postoperative nutritional management in the first postoperative day. On the sixth postoperative day (POD), the patient suddenly complained of dyspnea. The CT revealed bilateral pleural effusion and irregular soft tissue density and air bubble in anterior mediastinum suggesting migration of the distal portion of the CVC into the anterior mediastium. In the intensive care unit (ICU) bilateral thoracentesis and percutaneous drainage were performed. She was discharged from the ICU in 3 days later and transferred to the general ward. This case emphasizes the possibility of the delayed vascular injury related to CVC and some strategies for prevention of vascular injury.
RESUMEN
In oral and maxillofacial surgery, many complications associated with nasotracheal tube can be caused. In this case, we reported ballooning tube damage of nasotracheal tube during orthognathic double-jaw surgery and replacement of tube through cut down of tube and tube exchange using airway exchange catheter. The patient scheduled for high Le Fort I osteotomy and bilateral sagittal split osteotomy was intubated nasotracheally with nasal endotracheal tube. During maxilla osteotomy, air bubble was detected in the oral blood. In spite of our repeated ballooning, the results were the same so we changed damaged tube using airway exchange catheter aseptically. Tiny and superficial cutting site was detected in the middle of pilot tube. As we know in our case, tiny injury impeded a normal airway management and prevention is important.
