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Tonsillectomy is a frequently performed surgical procedure in children, requiring post-operative analgesia. This study evaluated the efficacy and safety of nalbuphine or sufentanil combined with dexmedetomidine for patient-controlled intravenous analgesia (PCIA) after pediatric tonsillectomy adenoidectomy. A total of 400 patients undergoing tonsillectomy with and without adenoidectomy were included in the study. Patients received a PCIA pump (0.5 mg/kg nalbuphine, 2 µg/kg dexmedetomidine and 0.9% sodium chloride to a total volume of 100 ml) for postoperative pain management were classified into Group ND (n = 200). Patients received a PCIA pump (2 µg/kg sufentanil, 2 µg/kg dexmedetomidine and 0.9% sodium chloride to a total volume of 100 ml) for postoperative pain management were classified into Group SD (n = 200). More stable hemodynamic changes were noted in Group ND than Group SD from 1 h to 48 h after operation. At 6, 12, 24, and 48 h after operation, the children in Group ND had higher Ramsay sedation scores than those in Group SD. The times to push the PCIA button in Group ND and Group SD were 2.44 ± 0.74 and 2.62 ± 1.00, showing significant differences (p = 0.041). The VASR scores of children in Group ND were significantly lower within 6, 12, and 24 h than those in Group SD (p < 0.05). The VASC scores of children in Group ND were significantly lower within four time points (2, 6, 12, and 24 h) than those in Group SD (p < 0.05). At 1st day after surgery, the children in Group ND had lower levels of serum ACTH, IL-6, and COR levels than those in Group SD (p < 0.001). The incidence rates of nausea and vomiting, and pruritus were significantly higher in Group SD than Group ND (5.00% vs. 11.00%, p = 0.028; 1.00% vs. 4.50%, p = 0.032). The total incidence rate of adverse reactions was significantly higher in Group SD than Group ND (15.00% vs. 31.00%, p = 0.0001). The study demonstrated that dexmedetomidine added to nalbuphine PCIA enhanced the analgesic effects, attenuated the postoperative pain, and reduced the stress response after pediatric tonsillectomy adenoidectomy.
RESUMEN
Objective: This study was designed to investigate the effects of three different doses of dexmedetomidine in caudal blocks on postoperative stress and pain after pediatric urethroplasty. Methods: A total of 160 children who underwent elective urethroplasty were enrolled in this study. They were randomly divided into four groups: groups D1, D2, and D3, in which the patients were injected respectively with a mixed solution of 1, 1.5, or 2 µg kg-1 of dexmedetomidine and 0.25% ropivacaine into the sacral canal; and group R, in which the patients were injected with 0.25% ropivacaine into the sacral canal. Cortisol and interleukin-6 (IL-6) levels within 24 h, the incidence of adverse events in the circulatory system during surgery, onset time of the caudal block, duration of postoperative analgesia, the incidence of agitation during recovery, and other anesthetic adverse reactions were observed and recorded. Results: Compared with group R, cortisol and IL-6 levels in groups D1, D2, and D3 decreased within 24 h after the operation (T2-T6). The incidence of intraoperative hypertension, tachycardia, and shivering during the recovery period decreased, the onset time of the caudal block decreased, and the duration of postoperative analgesia increased (p < 0.01). Compared with group D1, the duration of postoperative analgesia increased in groups D2 and D3 (p < 0.01). Compared with groups D1 and D2, the incidence of excessive sedation and bradycardia in group D3 increased (p < 0.05). Conclusion: The administration of 1.5 µg kg-1 of dexmedetomidine appears to be most feasible in accelerating the onset of the caudal block, reducing stress and inflammation, stabilizing the circulation, increasing the duration of postoperative analgesia, and reducing anesthesia- and operation-associated adverse events.
RESUMEN
OBJECTIVE: Myocardial ischemia reperfusion (MI/RI) stresses the pathological process of progressive aggravation of tissue damage in ischemic myocardium. Isoflurane (ISO) is cardioprotective in MI/RI. Thus, this work aimed to identify the mechanism of isoflurane (ISO) post-treatment in MI/RI by regulating microRNA-378 (miR-378) and mitogen-activated protein kinase 1 (MAPK1). METHODS: A MI/RI model was established by ligating the left anterior descending coronary artery in mice. The modeled mice were injected with ISO or miR-378 or MAPK1 to define their roles in hemodynamics, myocardial injury, cell apoptosis and inflammatory infiltration of mice. CD45, miR-378 and MAPK1 levels were detected. Dual luciferase reporter gene assay was utilized for detection of the targeting connection of miR-378 and MAPK1. RESULTS: Reduced miR-378 and elevated MAPK1 existed in MI/RI. ISO elevated miR-378 to target MAPK1. ISO improved hemodynamics and myocardial injury, reduced apoptosis rate and inflammatory infiltration in MI/RI mice. Up-regulated miR-378 further enhanced the protective effect of ISO on MI/RI mice. Depleting MAPK1 reversed the effects of suppressed miR-378 on MI/RI. CONCLUSION: This study highlights that elevating miR-378 strengthens the isoflurane-mediated effects on MI/RI in mice via suppressing MAPK1, which provides a potential treatment for MI/RI.
RESUMEN
Sevoflurane is the most commonly used general anesthetic in pediatric patients. But preclinical studies indicate that sevoflurane could have neurotoxicity in newborn and old animals, and this raises concern regarding its safety. In this study, we explored the potential mechanisms of sevoflurane-induced neurotoxicity in human SH-SY5Y neuronal cells. We showed that prolonged exposure to 2% sevoflurane caused a significant increase in the Bag family protein Bag2 in a time- and dose-dependent manner. We investigated the possible role of Bag2 upon exposure to sevoflurane by silencing Bag2 in neuronal cells. Knockdown of Bag2 caused increased overall reactive oxygen species (ROS) and generation of lipid peroxidation products 4-hydroxynonenal (4-HNE). Upon sevoflurane exposure, Bag2-silent cells have reduced glutathione (GSH) and glutathione peroxidase activity. Under the sevoflurane treatment, Bag2-deficient cells have reduced mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) production, while knockdown cells have less viability and higher lactic dehydrogenase (LDH) release as well as a higher percentage of apoptotic cells. The knockdown cells also had higher levels of mitochondrial cytochrome C release, a higher ratio of Bax/Bcl-2 and increased caspase cleavage by sevoflurane. Overall, our data support an important role of Bag2 in sevoflurane-induced neurotoxicity.
RESUMEN
Brainderived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) serves a significant role in neural protection by activating the phosphatidylinositol 3kinase (PI3K)/Akt signaling pathway, which also was associated with the neuroprotective the treatment with dexmedetomidine (DEX). The present study aimed to further explore whether treatment with DEX postIR increased the expression level of BDNF and VEGF in the rat brain. A total of 30 healthy, clean male Wistar rats were randomly divided into 3 experimental groups: Control group, ischemia/reperfusion (I/R) group and DEX treatment group. Subsequently, BDNF and VEGF mRNA and protein expression levels were analyzed. The results indicated that the mRNA expression levels of BDNF and VEGF were higher in the I/R and DEX groups compared with expression levels in the Control group at 6 h and 1 day posttreatment; the levels of BNDF mRNA expression were higher in the DEX group compared with the I/R group. The levels of BDNF and VEGF protein expression in the I/R and DEX groups were also significantly higher compared with those in the Control group. I/R surgery significantly increased the expression of BDNF and VEGF protein DEX group at 6 h, day 1 and day 3 compared with expression levels in the I/R group. Results from the present study indicated that postsurgical treatment with DEX may increase the expression of BDNF and VEGF following I/R, which may serve a role in nerve protection.