The Analgesic Effect of Ultrasound-guided Erector Spinae Plane Block in Median Sternotomy Cardiac Surgery in Adults: A Systematic Review and Meta-analysis of Randomized Controlled Trials.

OBJECTIVES: To assess the analgesic effect of erector spinae plane block in adults undergoing median sternotomy cardiac surgery. DESIGN AND SETTING: The Cochrane, Embase, and PubMed databases from inception to January 2024 were searched. The study has been registered in the International Prospective Register of Systematic Reviews (CRD42023470375). PARTICIPANTS: Eight randomized controlled trials involving 543 patients, comparing with no block or sham block, were included, whether it was a single injection or continuous. MEASUREMENTS AND MAIN RESULTS: The primary outcomes were pain scores and opioid consumption. Erector spinae plane block reduced pain scores immediately after extubation (mean difference [MD], -1.19; 95% confidence interval [CI], -1.67 to -0.71; p for heterogeneity = 0.10), at 6 hours after extubation (MD, -1.96; 95% CI, -2.85 to -1.08; p for heterogeneity < 0.0001), and at 12 hours after extubation (MD, -0.98; 95% CI, -1.55 to -0.40; p for heterogeneity < 0.00001). The decrease in pain scores reached the minimal clinically important difference within 6 hours. Opioid consumption 24 hours after surgery decreased by 35.72 mg of oral morphine equivalents (95% CI, -50.88 to -20.57; p for heterogeneity < 0.0001). Sensitivity analysis confirmed the stability of results. The quality of primary outcomes was rated as very low to moderate. CONCLUSIONS: Erector spinae plane block decreased pain scores within 12 hours after extubation, reached the minimal clinically important difference within 6 hours, and decreased opioid consumption 24 hours after surgery, based on data of very low to moderate quality. However, high-quality randomized controlled trials are necessary to validate these findings.

Influence of (ATP)-Binding Cassette Transporter Subfamily B Member 1 (ABCB1) Gene Polymorphism on the Efficacy of Remifentanil.

BACKGROUND The aim of this study was to investigate the influence of adenosine triphosphate (ATP)-binding cassette transporter subfamily B member 1 (ABCB1) gene polymorphism on the efficacy of Remifentanil. MATERIAL AND METHODS A total of 276 patients undergoing elective surgeries were included to collect general clinical information and detect the polymorphism of ABCB1 rs1045642 using the TaqMan-MGB probe, and they were divided into 3 groups - a genotype AA group, a genotype AG group, and a genotype GG group - based on different genotypes of ABCB1 rs1045642. RESULTS The comparisons showed that there were no differences in sex, age, body mass index (BMI), smoking, drinking status, or ASA class among the 3 groups (P˃0.05). The genotype GG group had higher consumption of Remifentanil than the genotype AA group (P˂0.05), but the genotype AG group was not different from the genotype AA and GG groups (P˃0.05). Comparison of the surgery duration revealed no difference among the 3 groups (P˃0.05). The analepsia time, autonomous respiratory recovery time, and orientation recovery time in the genotype GG group were longer than in the genotype AA group (P˂0.05), but the genotype AG group was not different from the genotype AA and GG groups (P˃0.05). There were no differences in adverse reactions among the 3 groups (P˃0.05). CONCLUSIONS ABCB1 gene polymorphism can affect the clinical efficacy of Remifentanil.

Effects of ADAM2 silencing on isoflurane-induced cognitive dysfunction via the P13K/Akt signaling pathway in immature rats.

Volatile anesthetics, including isoflurane, have been reported to have negative effects on cognitive dysfunction characterized by cognitive deficits following anesthesia. The aim of the current study was to investigate the effects involved with disintegrin and metallopeptidase domain 2 (ADAM2) silencing on isoflurane-induced cognitive dysfunction via the P13 K/Akt signaling pathway in immature rats. One week old healthy Sprague-Dawley (SD) rats were recruited and administered isoflurane anesthesia. The rats were then subjected to shADAM2 or wortmannin (PI3K/Akt signaling pathway inhibitor) to identify the effects of ADAM2 and the PI3K/Akt signaling pathway on the cognitive function of rats. Morris water maze and passive-avoidance tests were performed to examine the cognitive function of the rats. TUNEL staining was conducted to detect neuronal apoptosis in the hippocampal CA1 region. The obtained experimental results demonstrated that isoflurane anesthesia led to increased escape latency, reaction time, number of errors and TUNEL-positive neurons, along with a decreased latency time. In response to treatment with shADAM2, escape latency, reaction time, number of errors and TUNEL-positive cells were all noted to have decreased, in addition to elevated latency time, while contrasting trends were observed in regard to treatment with wortmannin. Taken together, the key findings of the present study revealed that shADAM2 activated the PI3K/Akt signaling pathway, resulting in elevated expressions of PI3K and Akt. Our study ultimately identified that ADAM2 silencing alleviates isoflurane-induced cognitive dysfunction by activating the P13 K/Akt signaling pathway in immature rats.

IL-17A promotes the neuroinflammation and cognitive function in sevoflurane anesthetized aged rats via activation of NF-κB signaling pathway.

BACKGROUND: To investigate the role of IL-17A in the neuroinflammation and cognitive function of aged rats anaesthetized with sevoflurane through NF-κB pathway. METHOD: The aged and young adult rats were randomly divided into Control (inhale oxygen only), Sevoflurane (inhale oxygen and sevoflurane), Sevo (Sevoflurane) + anti-IL-17A (injected with IL-17A antibody, inhale oxygen and sevoflurane), and Sevo + NC groups (injected with IgG2a antibody, inhale oxygen and sevoflurane). Cognitive function was evaluated by Morris water maze and contextual fear conditioning tests. Tumor necrosis factor (TNF)-α, Interleukin (IL)-1ß, IL-6 and monocyte chemoattractant protein (MCP)-1 expressions in the hippocampus of rats were detected by ELISA (enzyme-linked immunosorbent assay) assay, and Nuclear factor (NF)-κB pathway-related proteins by Western blot. RESULTS: Sevoflurane anaesthetized aged rats showed longer escape latency and swimming distance, fewer platform crossing times, shortened stay time in the platform quadrant compared to Control rats; In addition, increased levels in hippocampal expression of malondialdehyde (MDA), IL-17A, NF-κB p65, inducible nitric oxide synthase (iNOS) and COX-2, as well as a reduced level of superoxide dismutase (SOD) were also observed in these animals. However, the sevoflurane anesthetized aged rats treated with anti-IL-17A presented a completely opposite tendency concerning the above factors (all P < 0.05). Nevertheless, there was no significant difference in the acquisition of learning or memory, neuroinflammation and oxidative stress of young adult rats in all groups (all P > 0.05). CONCLUSION: Anti-IL-17A may alleviate neuroinflammation and oxidative stress via inhibiting NF-κB pathway, thereby attenuating post-operative cognitive dysfunction (POCD) in aged rats anaesthetized with sevoflurane.