ABSTRACT
Abstract Objective: Emergence delirium is a common complication in children. Recorded mother's voice, as a non-pharmacological measure, is increasingly used to prevent the emergence of delirium in pediatric patients, but sufficient evidence is still needed to prove its efficacy. Methods: Embase, PubMed, Cochrane Library, Web of Science, CINAHL, and Sinomed databases were searched for randomized controlled trials exploring the efficacy of recorded mother's voice in preventing the emergence of delirium in pediatric patients undergoing general anesthesia. The original data were pooled for the meta-analysis with Review Manager 5.4.1. This study was conducted based on the Cochrane Review Methods. Results: Eight studies with 724 children were included in the analysis. Recorded mother's voice reduced the incidence of emergence delirium when compared with either no voice (RR: 0.45; [95 % CI, 0.34 - 0.61]; p < 0.01; I2 = 7 %) or stranger's voice (RR: 0.51; [95 % CI, 0.28 - 0.91]; p = 0.02; I2 = 38 %) without increasing other untoward reactions. In addition, it shortened the post-anesthesia care unit stay time when compared with no voice (MD = -5.64; [95 % CI, -8.43 to -2.58]; p < 0.01, I2 = 0 %), but not stranger's voice (MD = -1.23; [95 % CI, -3.08 to 0.63]; p = 0.19, I2 = 0 %). It also shortened the extubation time and reduced the incidence of postoperative rescue analgesia. Conclusion: The current analysis indicated that recorded mother's voices could reduce the incidence of emergency delirium, shorten post-anesthesia care unit stay time and extubation time, and decrease the incidence of postoperative rescue analgesia in children.
ABSTRACT
Dexmedetomidine (DEX) is known to provide neuroprotection against cerebral ischemia and reperfusion injury (CIRI), but the exact mechanisms remain unclear. This study was conducted to investigate whether DEX pretreatment conferred neuroprotection against CIRI by inhibiting neuroinflammation through the JAK2/STAT3 signaling pathway. Middle cerebral artery occlusion (MCAO) was performed to establish a cerebral ischemia/reperfusion (I/R) model. Specific-pathogen-free male Sprague-Dawley rats were randomly divided into Sham, I/R, DEX, DEX+IL-6, and AG490 (a selective inhibitor of JAK2) groups. The Longa score, TTC staining, and HE staining were used to evaluate brain damage. ELISA was used to exam levels of TNF-α. Western blotting was used to assess the levels of JAK2, phosphorylated-JAK2 (p-JAK2), STAT3, and phosphorylated-STAT3 (p-STAT3). Our results suggested that both pretreatment with DEX and AG490 decreased the Longa score and cerebral infarct areas following cerebral I/R. After treatment with IL-6, the effects of DEX on abrogating these pathological changes were reduced. HE staining revealed that I/R-induced neuronal pathological changes were attenuated by DEX application, consistent with the AG490 group. However, these effects of DEX were abolished by IL-6. Furthermore, TNF-α levels were significantly increased in the I/R group, accompanied by an increase in the levels of the p-JAK2 and p-STAT3. DEX and AG490 pretreatment down-regulated the expressions of TNF-α, p-JAK2, and p-STAT3. In contrast, the down-regulation of TNF-α, p-JAK2, and p-STAT3 induced by DEX was reversed by IL-6. Collectively, our results indicated that DEX pretreatment conferred neuroprotection against CIRI by inhibiting neuroinflammation via negatively regulating the JAK2/STAT3 signaling pathway.