Pre-anesthetic use of butorphanol for the prevention of emergence agitation in thoracic surgery: A multicenter, randomized controlled trial.

Background: Emergence agitation (EA) is common in patients after general anesthesia (GA) and is associated with poor outcomes. Patients with thoracic surgery have a higher incidence of EA compared with other surgery. This study aimed to investigate the impact of pre-anesthetic butorphanol infusion on the incidence of EA in patients undergoing thoracic surgery with GA. Materials and methods: This prospective randomized controlled trial (RCT) was conducted in 20 tertiary hospitals in China. A total of 668 patients undergoing elective video-assisted thoracoscopic lobectomy/segmentectomy for lung cancer were assessed for eligibility, and 620 patients were enrolled. In total, 296 patients who received butorphanol and 306 control patients were included in the intention-to-treat analysis. Patients in the intervention group received butorphanol 0.02 mg/kg 15 min before induction of anesthesia. Patients in the control group received volume-matched normal saline in the same schedule. The primary outcome was the incidence of EA after 5 min of extubation, and EA was evaluated using the Riker Sedation-Agitation Scale (RSAS). The incidence of EA was determined by the chi-square test, with a significance of P < 0.05. Results: In total, 296 patients who received butorphanol and 306 control patients were included in the intention-to-treat analysis. The incidence of EA 5 min after extubation was lower with butorphanol treatment: 9.8% (29 of 296) vs. 24.5% (75 of 306) in the control group (P = 0.0001). Patients who received butorphanol had a lower incidence of drug-related complications (including injecting propofol pain and coughing with sufentanil): 112 of 296 vs. 199 of 306 in the control group (P = 0.001) and 3 of 296 vs. 35 of 306 in the control group (P = 0.0001). Conclusion: The pre-anesthetic administration of butorphanol reduced the incidence of EA after thoracic surgery under GA. Clinical trial registration: [http://www.chictr.org.cn/showproj.aspx?proj=42684], identifier [ChiCTR1900025705].

Comparison of the postoperative effect between epidural anesthesia and continuous wound infiltration on patients with open surgeries: A meta-analysis.

PURPOSE: The study aimed to compare the effect of epidural anesthesia (EA) and continuous wound infiltration (CWI) on surgical patients. METHODS: The literature retrieval was conducted in relevant databases from their inception to June 2018 with the predefined searching strategy and selection criteria. Then, the Cochrane Collaboration's tool was used to assess the quality of included studies. In addition, odds ratio (OR) and standardized mean difference (SMD) with its corresponding 95% confidence interval (CI) were used as a measure of effect size for evaluating outcomes indicators. RESULTS: Totally, sixteen RCTs were included. The incidence of hypotension in EA group was significantly higher than CWI group (OR = 3.7398; 95% CI: 1.0632 to 13.1555). In addition, EA provided better pain relief than CWI on rest at 72 h (SMD = -0.6037; 95% CI: -1.0767 to -0.1308) after surgery. Additionally, there were no significant differences in pain score on rest and mobilization at 2 h, 12 h, 24 h and 48 h. Moreover, the subgroup analysis showed that pain scores in EA group was significantly reduced at 2 h on rest and 12 h on mobilization than CWI group after liver resection surgery, as well as at 72 h on rest after colorectal surgery. CONCLUSION: CWI is superior to EA with a lower incidence of complications for use in surgery, and EA may provide better pain control than CWI on pain relief after surgery.

The inhibiting effect of intravenous anesthesia on adrenal gland functions under the sepsis condition.

This study aims to explore the effect of intravenous anesthesia on the adrenal gland functions of rats with sepsis as well as on their lungs and adrenal gland tissues in order to provide a theoretical reference for the cure of sepsis. Female Sprague Dawley (SD) rats were taken as the research objects in this study. Venous channels of rats were constructed by catheterization through the external jugular vein, and the cecal ligation and puncture technique was adopted to duplicate the sepsis rat models. The level of tumor necrosis factor-α (TNF-α) in serum was detected using enzyme-linked immunosorbent assay (ELISA), and necrocytosis was observed by the fluorescent staining method. The results showed that the survival rates of groups A, B, C, and D were 100%, 60%, 60%, and 50%, respectively, while their concentrations of TNF-α in serum were101.26 ± 43.38, 1398.68 ± 178.56, 451.16 ± 78.68, and 649.83 ± 98.56 pg/mL, respectively. Results of fluorescent staining showed that the number of living cells per unit view in group A was 1428 ± 166 and those of groups B, C and D were 175 ± 56, 618 ± 76, and 468 ± 55, respectively. Besides, it was found that changes of inflammatory pathology of lung tissues of each group were significant. In conclusion, etomidate does not affect the survival of sepsis rats and does not exacerbate lung tissue inflammation in sepsis rats. Instead, it can inhibit TNF-α in serum of sepsis rats, as well as the apoptosis of adrenal cells in sepsis rats.

Transcriptome sequencing combined with bioinformatics predicts potential genes and pathways associated with bupivacaine-induced apoptosis.

This study aimed to explore the potential genes and pathways associated with bupivacaine-induced apoptosis. Human neuroblastoma cell line SH-SY5Y was used in this study. The effect of bupivacaine on cell viability of SH-SY5Y was detected by Cell Counting Kit-8. Transcriptome sequencing was performed for SH-SY5Y cells that were treated and untreated with bupivacaine based on the HiSeq 4000 sequencing platform. The sequencing results were analyzed using bioinformatics methods, including differentially expressed genes (DEGs) identification, functional enrichment analysis, protein-protein interaction (PPI) network analysis and module analysis. The cell viability of SH-SY5Y cells decreased significantly after bupivacaine treatment (p < .01). Based on the HiSeq 4000 sequencing platform, we obtained a global overview of the transcriptome of SH-SY5Y treated with/without bupivacaine. Bioinformatics analysis identified 335 up-regulated and 294 down-regulated DEGs in bupivacaine group. They were significantly enriched in cell cycle-associated functions and pathways and cAMP signaling pathway. In the PPI network, proliferating cell nuclear antigen (PCNA), v-Akt murine thymoma viral oncogene homolog 3 (AKT3), cyclin-dependent kinase inhibitor 1A (CDKN1A) and cell division cycle 6 (CDC6) had high topology scores. Module analysis obtained two sub-network modules (cluster 1 and cluster 2). PCNA, CDC6, CDKN1A and AKT3 may play important roles in bupivacaine-induced apoptosis. Additionally, bupivacaine may also induce apoptosis via pathways of cell cycle and cAMP signaling pathway.

siRNA-mediated downregulation of GluN2B in the rostral anterior cingulate cortex attenuates mechanical allodynia and thermal hyperalgesia in a rat model of pain associated with bone cancer.

It has previously been suggested that the upregulation of GluN2B-containing N-methyl D-aspartate receptors (GluN2B) within the rostral anterior cingulate cortex (rACC) may contribute to the development of chronic pain. The present study used a rat model of bone cancer pain in order to investigate whether lentiviral-mediated delivery of small interfering RNAs targeting GluN2B (LV-GluN2B) could attenuate pain associated with bone cancer, by selectively decreasing GluN2B expression within the rACC. Sprague Dawley rats were inoculated with osteosarcoma cells into the intramedullary space of the right tibia in order to induce persistent bone cancer-associated pain. Intra-rACC administration of the lentiviral siRNA was performed in the tumor bearing rats; and reverse transcription-quantitative polymerase chain reaction and western blotting were performed in order to detect the expression levels of GluN2B. Pain behavior changes were evaluated via paw withdrawal threshold and latency determinations. Marked and region-selective decreases in the mRNA and protein expression levels of GluN2B were detected in the rACC following the intra-rACC administration of LV-GluN2B. Furthermore, the rats also exhibited pain behavior changes corresponding to the decreased levels of GluN2B. By post-operative day 14, inoculation of osteosarcoma cells had significantly enhanced mechanical allodynia and thermal hyperalgesia in the rats, which were subsequently attenuated by the intra-rACC administration of LV-GluN2B. Notably, the paw withdrawal threshold and latency of the tumor-bearing rats had recovered to normal levels, by day 14 post-administration. The results of the present study suggest that GluN2B within the rACC may be a potential target for RNA interference therapy for the treatment of pain associated with bone cancer. Furthermore, the lentiviral vector delivery strategy may be a promising novel approach for the treatment of bone cancer pain.

Identification of anesthetic-induced expression changes using DNA microarray.

The present study aimed to identify changes in atrial gene expression induced by sevoflurane and propofol using DNA microarray. The expression profiles of GSE4386 in atrial samples, obtained from patients who had received either the anesthetic gas sevoflurane or the intravenous anesthetic propofol prior to and following off-pump coronary artery bypass graft (CABG) surgery, were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) in the sevoflurane and the propofol groups were then identified and compared. Subsequently, a functional enrichment analysis was performed for the DEGs. The interactive functional modules for common, sevoflurane-specific and propofol-specific DEGs were then constructed for analysis of the biological processes. The percentages of common DEGs were 31.3 (275/879) and 94.8% (275/290) in the sevoflurane group and propofol groups, respectively. The functional categories for the common, sevoflurane-specific and propofol-specific DEGs were similar. Overall, two, one, and one functional modules were identified for the common DEGs, propofol specific DEGs and sevoflurane specific DEGs, respectively. DEGs in the modules were involved in cellular processes, including the 'regulation of transcription' and 'regulation of cellular process', which were similar to the functional annotations for the DEGs. Therefore, sevoflurane and propofol may synergistically reduce myocardial reperfusion injury in patients undergoing off-pump CABG surgery.