The effect of magnesium sulfate on emergence agitation in surgical adult patients undergoing general anesthesia: A systematic review and meta-analysis of randomized controlled trials.

STUDY OBJECTIVE: Investigating the effect of magnesium sulfate (MS) on emergence agitation (EA) in adult surgical patients following general anesthesia (GA). DESIGN: Systematic literature review and meta-analysis (PROSPERO number: CRD42023461988). SETTING: Review of published literature. PATIENTS: Adults undergoing GA. INTERVENTIONS: Intravenous administration of MS. MEASUREMENTS: We searched PubMed/MEDLINE, EMBASE, the Cochrane Library, Scopus, and Web of Science for publications until September 14, 2023. The primary outcome was the incidence of EA, while the secondary outcomes included the impact of MS on postoperative agitation score (PAS), emergence variables and adverse events. Relative risk (RR) with 95% confidence interval (CI) measured dichotomous outcome, while standardized mean difference (SMD) or mean difference (MD) with 95% CI measured continuous outcomes. MAIN RESULTS: Meta-analysis of five randomized controlled trials (RCTs) indicated that MS was associated with a lower incidence of EA at various time points (0 min: RR = 0.62, 95% CI [0.41, 0.95]; p = 0.183, I2 = 43.6%; 5 min: RR = 0.29, 95% CI [0.16, 0.52]; p = 0.211, I2 = 36%; 10 min: RR = 0.14, 95% CI [0.06, 0.32]; p = 0.449, I2 = 0%; 15 min: RR = 0.11, 95% CI [0.02, 0.55]; p = 0.265, I2 = 19.5%; 30 min: RR = 0.05, 95% CI [0.00, 0.91]; the postoperative period: RR = 0.21, 95% CI [0.09, 0.49]; p = 0.724, I2 = 0%;). Additionally, MS was associated with a reduced PAS at various time points except for 0 min. However, no significant differences were observed in extubation time, the length of stay in the post-anesthesia care unit, postoperative nausea and vomiting or total complications. CONCLUSIONS: Limited available evidence suggests that MS was associated with a lower incidence of EA. Nevertheless, further high-quality studies are warranted to strengthen and validate the effect of MS in preventing EA in adult surgical patients.

Silencing the expression of lncRNA SNHG15 may be a novel therapeutic approach in human breast cancer through regulating miR-345-5p.

Background: Long noncoding RNA (lncRNA) short nucleolar RNA host gene 15 (SNHG15) has been found to have an oncogenic function in numerous malignancies. Nevertheless, the biological function and regulatory mechanisms of SNHG15 in breast cancer have not been fully elucidated. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of SNHG15 and in MDA-MB-231 breast cancer cells. The expression of SNHG15 was silenced using small interfering RNA (siRNA) technology. The proliferation and migration of the cells were examined by colony formation assays, cell counting kit 8 (CCK-8) assays, and transwell assays. For the zebrafish xenograft injection experiments, cultured cells labelled with the fluorescent dye CM-DiI were injected into the perivitelline space of the larvae. Results: This present study revealed that the expression of lncRNA SNHG15 (lnc-SNHG15) was significantly upregulated in breast cancer cells, and its overexpression was associated with the tumor. The relative expression of lnc-SNHG15 could be downregulated using siRNAs, and silencing lnc-SNHG15 inhibited the proliferation and the migration of MDA-MB-231 cells. In vivo experiments using the zebrafish xenograft model showed similar results. Mechanistically, the knockdown effect of lnc-SNHG15 could be restored by inhibiting the expression of the miR-345-5p, confirming the negative regulation between lnc-SNHG15 and miR-345-5p. Interestingly, cisplatin treatment combined with SNHG15 knockdown effectively inhibited MDA-MB-231 cell proliferation and migration in the zebrafish xenograft compared to negative controls. Conclusions: In conclusion, lnc-SNHG15 knockdown increased miR-345-5p expression and negated cisplatin resistance in breast cancer cells, and thus, lnc-SNHG15 may be a potential novel target for breast cancer therapy.

Anesthetic management for resection of a giant emphysematous bulla: a case report.

Anesthetic management for patients with a giant emphysematous bulla (GEB) is challenging. This case report describes a patient who developed 95% pulmonary compression by a GEB. A 14-Ga indwelling catheter was placed in the GEB before surgery to allow for slow re-expansion of the collapsed lung tissue. This prevented rupture of the GEB during anesthesia. Additionally, positive-pressure ventilation was performed to reduce the risk of re-expansion pulmonary edema. This respiratory management strategy may be beneficial for patients with a GEB who develop pulmonary dysfunction during thoracic surgery.

The effectiveness of preemptive analgesia for relieving postoperative pain after video-assisted thoracoscopic surgery (VATS): a prospective, non-randomized controlled trial.

BACKGROUND: The effectiveness of preemptive analgesia (PA) for relieving postoperative pain and reducing the side effects of analgesics following video-assisted thoracoscopic surgery (VATS) has not yet been determined. This study intends to test the clinical application value of PA in the perioperative period of VATS. METHODS: From January 2018 to August 2018, we divided patients who underwent VATS in our hospital into a trial group (PA group) and a control group (traditional analgesia group, TA group). The PA group received a PA program, and the TA group was administered a conventional postoperative analgesia scheme. We compared the two groups according to the intensity of postoperative pain using the numeric rating scale (NRS), the incidence rate of analgesic drug-related adverse reactions, and the severity of stress-induced inflammation. RESULTS: One hundred five cases from the PA group, and 80 cases from the TA group were included in the analysis. There were no significant differences between the two groups in baseline characteristics (P>0.05). The PA group had a lower incidence rate of side effects from the analgesics compared to the TA group, and there was a statistical difference at 48 and 72 hours after surgery (P<0.05). The PA group had a slightly lower score than the TA group for postoperative resting pain. However, this difference was not statistically significant (P>0.05). The motion pain NRS score of the PA group was lower than the TA group, and although there were no significant differences at 4, 24, and 48 hours (P>0.05), there was a statistically significant difference at 72 hours (P<0.05). In the subset of patients with motion pain NRS ≥3 points, the PA group was marginally higher than the TA group at 4 hours (P>0.05) but was lower than the TA group at 24, 48, and 72 hours, with a statistically significant difference at 24 and 72 hours (P<0.05). There were no statistically significant differences in perioperative stress indexes between the two groups (P>0.05). CONCLUSIONS: PA can relieve postoperative pain following VATS and reduce the incidence rate of analgesic drug-related adverse effects.

Protective effect of dexmedetomidine against diabetic hyperglycemia-exacerbated cerebral ischemia/reperfusion injury: An in vivo and in vitro study.

AIMS: Dexmedetomidine (Dex) has been noted to have neuroprotective effect against cerebral ischemia-reperfusion (I/R) injury. However, the effect of Dex in diabetic hyperglycemia-exacerbated cerebral I/R injury and its underlying mechanism remain unclear. MAIN METHODS: The infarct volume and brain edema were evaluated by 2,3,5-triphenyltetrazolium chloride staining and standard wet-dry method. Modified neurological severity score was utilized to assess the neurological deficits. The oxidative stress and inflammation were evaluated by detecting reactive oxygen species (ROS), malondialdehyde (MDA), tumor necrosis factor (TNF)-α and interleukin (IL)-1ß. Terminal deoxynucleotidyl transferase dUTP nick end labeling assay and cell count kit-8 were applied to measure cell apoptosis and viability. KEY FINDINGS: Dex treatment reduced infarct volume, decreased brain water content and improved neurological deficit in middle cerebral artery occlusion/reperfusion (MCAO/R) mice. Dex treatment reduced the levels of ROS, MDA, TNF-α and IL-1ß in the entire middle cerebral artery territory of diabetic mice subjected to MCAO/R, as well as in primary culture of mouse hippocampal neurons stimulated with 50 mM glucose and oxygen glucose deprivation/reperfusion. Dex treatment inhibited neuronal apoptosis induced by diabetic hyperglycemia-exacerbated cerebral I/R injury. Dex upregulated nuclear factor of activated T-cells 5 (NFAT5) and Sirtuin 1 (SIRT1) expression, induced NF-E2-related factor 2 (Nrf2) translocation from cytoplasm to nucleus and inhibited the acetylation of Nrf2. However, these changes triggered by Dex treatment were abrogated by NFAT5 knockdown. SIGNIFICANCE: Dex protects against diabetic hyperglycemia-exacerbated cerebral I/R injury through attenuation of oxidative stress, inflammation and apoptosis. The underlying mechanism is at least the NFAT5/SIRT1/Nrf2 signaling pathway dependent.

Isoflurane protects against injury caused by deprivation of oxygen and glucose in microglia through regulation of the Toll-like receptor 4 pathway.

Oxygen and glucose deprivation (OGD) are the most important factors related to tissue damage resulting from stroke. Microglial cells have been found to be very vulnerable to ischemia and OGD. It has been reported that isoflurane exposure can protect the mammalian brain from insults such as ischemic stroke; however, the effects of isoflurane on OGD-induced injury in microglia are as yet unknown. In this study, we investigated the effects of isoflurane on OGD-induced injury in microglia. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) revealed that OGD did indeed induce cell death in microglia. However, isoflurane preconditioning attenuated OGD-induced cell death. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay demonstrated that isoflurane treatment alleviated OGD-induced apoptosis. Toll-like receptor 4 (TLR4) plays a considerable role in the induction of innate immune and inflammatory responses. Our results indicate that isoflurane preconditioning inhibits the upregulation of TLR4 as well as the activation of its downstream molecules, such as c-Jun N-terminal kinase (JNK) and nuclear factor kappa B (NF-κB), in BV-2 microglia exposed to OGD. Importantly, we also found that isoflurane pretreatment significantly reduces the production of proinflammatory factors such as tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), IL-ß, and nitric oxide (NO). The results indicate that TLR4 and its downstream NF-κB-dependent signaling pathway contribute to the neuroprotection of microglia exposed to OGD/reoxygenation by administration of isoflurane.

Prediction of effect-site concentration of sufentanil by dose-response target controlled infusion of sufentanil and propofol for analgesic and sedation maintenance in burn dressing changes.

This study was to investigate the feasibility and efficiency of by target-controlled infusion (TCI) for analgesia and sedation during burn dressing change, and to predict the effect-site concentration of sufentanil. Eighty burn patients were randomly and evenly divided into four groups according to target sufentanil effect-site concentration (0.2, 0.3, 0.4 and 0.5 ng/ml). The sufentanil-propofol TCI was carried out during dressing changes. The effect-site concentration of propofol was maintained at 1.2 µg/ml. The dose-response relationships of sufentanil for providing adequate analgesia were evaluated by visual analog scales and Ramsay sedation scores. The effect-site concentration of sufentanil was calculated by Probit regression analysis. Incidence of respiratory depression, doctors and patients' satisfaction and adverse events were assessed. The EC50 and EC95 of sufentanil to maintain anesthesia for uncovering the inner layer dressings during TCI were 0.278 ng/ml (95% CI 0.231-0.318 ng/ml) and 0.394 ng/ml (95% CI 0.366-0.530 ng/ml), respectively, while the EC50 and EC95 of sufentanil to maintain anesthesia for wound management were 0.349 ng/ml (95% CI 0.299-0.366 ng/ml) and 0.465 ng/ml (95% CI 0.430-0.563 ng/ml), respectively. Doctors and patients' satisfaction were significantly higher in the 0.4 and 0.5 ng/ml groups than the 0.2 ng/ml group. One and three patients had respiratory depression in the 0.4 and 0.5 ng/ml groups, respectively. No adverse events occurred after operations. In conclusion, low dose sufentanil-propofol TCI for anesthesia and sedation maintenance in burn dressing changes is feasible and effective, and wound management requires higher effect-site concentrations of sufentanil than disclosing inner layer dressings.

[Effect of transcutaneous acupoint electrical stimulation on lipid peroxidation and cognitive function in patients experiencing craniotomy].

OBJECTIVE: To observe the effect of transcutaneous acupoint electrical stimulation (TAES) on serum superoxide dismutase (SOD) activity, malondialdehyde (MDA) and S100beta contents in craniotomy patients for studying its cerebral protection mechanism. METHODS: Fifty patients scheduled for neurosurgery were randomly divided into TAES group (n = 25) and control group (n=25) with randomized block method. For patients of TAES group, TAES was applied to bilateral Hegu (LI 4) and Quchi (LI 11), Zusanli (ST 36) and Sanyinjiao (SP 6) from 30 minutes on before anesthesia to the end of operation. Patients of control group were anesthetized with sevoflurane inhalation and intermittent (i.v.) of sulfenany and vecurnium bromide. Blood samples were taken for assaying serum SOD activity, MDA and S100beta contents with purinase oxydasis, biochemiluminescence and enzyme linked immunosorbent assay separately. Scores of cognitive ability were given by using Mini Mental State Examination (MMSE). RESULTS: In comparison with pre-anesthesia, serum SOD activity decreased significantly 1 h after craniotomy in control group, at the end of operation in both control and TAES groups (P<0.05, P<0.01), and increased markedly 48 h after operation in control group (P<0.05). Serum MDA in control group increased significantly 48 h after operation, while that in TAES group reduced apparently 24 h after operation (P<0.01). Serum S100beta content in TAES group decreased remarkably 48 h after operation (P<0.01). Serum SOD activity of TAES group was significantly higher than that of control group 24 h after operation (P<0.05). Compared with control group, serum MDA contents of 24 h and 48 h after operation and serum S100beta levels at 1 h after craniotomy and 48 h after operation were markedly lower in TAES group (P<0.01, P<0.05). No significant differences were found between two groups in the cognitive function scores (P>0.05). CONCLUSION: TAES can increase serum SOD activity and reduce MDA and S100beta levels in patients undergoing craniotomy, which may contribute to its effect in reducing lipid peroxidation induced cerebral injury. But its impact on the patient's cognitive function needs study further.