Influence of Minimum Alveolar Concentration and Inhalation Duration of Sevoflurane on Facial Nerve Electromyography in Hemifacial Spasm: A Randomized Controlled Trial.

BACKGROUND: The lateral spread response (LSR) is an electromyography feature of hemifacial spasm; intraoperative reduction in the LSR is associated with positive surgical outcomes. This study examined the effects of different minimum alveolar concentrations (MACs) and durations of sevoflurane inhalation on the LSR. METHODS: Eighty patients undergoing microvascular decompression surgery for hemifacial spasm were randomly allocated to receive propofol-remifentanil total intravenous anesthesia alone or in combination with sevoflurane at 0.5, 0.75, or 1 MAC. The LSR and orbicularis oculi muscle wave were recorded before and at 15 and 30 minutes after the start of sevoflurane administration. RESULTS: Sevoflurane reduced the LSR amplitude in a dose-dependent and duration-dependent manner. The curve representing the LSR amplitude preservation ratio change according to sevoflurane concentration is best fitted by regression analysis using a cubic model, as the cubic equations had the largest coefficient of determination; at 15 minutes ( R2 =0.76, F =78.36, P <0.05) and at 30 minutes ( R2 =0.882, F =189.94, P <0.05). The inhibitory effect of sevoflurane on the LSR amplitude was greater in the first 15 minutes than in the second 15 minutes of sevoflurane administration. Sevoflurane at 1 MAC for 30 minutes mildly decreased the amplitude of the orbicularis oculi muscle wave. The latencies of the LSR and the orbicularis oculi muscle wave were not affected by sevoflurane at all MACs studied. CONCLUSIONS: The combination of intravenous propofol-remifentanil anesthesia with 0.5 MAC sevoflurane allows reliable intraoperative LSR monitoring in hemifacial spasm patients. Our findings support the central rather than peripheral hypothesis of the LSR.

Manual Removal versus Spontaneous Delivery of the Placenta at Cesarean Section: A Meta-Analysis of Randomized Controlled Trials.

PURPOSE: Several randomized clinical trials (RCTs) investigated the effects of the manual placental removal on hemorrhage or other hemorrhage-related complications compared with the spontaneous placental removal during cesarean section (CS), while the results remained controversial and were inconsistent. The purpose of this meta-analysis was to quantify the pooled effects of the methods of placental removal on hemorrhage during CS. PATIENTS AND METHODS: A systematic literature search was conducted using PubMed, EMBASE, Web of Science, and Google Scholar. Heterogeneity was tested by I 2 statistics and Q-statistic. The random-effects model or fixed-effects model were used to calculate the pooled effect for the included studies according to heterogeneity. And the term of standardized mean difference (SMD) with 95% confidence intervals (CI) was pooled and estimated the effects across all studies. RESULTS: A total of nine RCTs were included in this meta-analysis. Compared with spontaneous group, manual placental removal increased the amount of hemorrhage (SMD = 0.53, 95% CI [0.12, 0.94]; Z = 2.54, P = 0.011) and increased the risk of endometritis (OR = 1.84, 95% CI [1.31, 2.58]; Z = 3.52, P < 0.0001). In contrast, there was no significant difference concerning the operating time (SMD = -0.30, 95% CI [-0.85, 0.24]; Z = 1.09, P = 0.276), the length of hospital stays (SMD = 0.11, 95% CI [-0.08, 0.30]; Z = 1.11, P = 0.265), and blood transfusion requirement (OR = 1.36, 95% CI [0.91, 2.04]; Z = 1.52, P = 0.129), respectively. CONCLUSION: Comparing with spontaneous placental removal, manual placental removal appeared to be less positive effect during CS. Because of the limitations of this meta-analysis, more high-quality RCTs are needed to confirm our findings.

Coronary angiography or not after cardiac arrest without ST segment elevation: A systematic review and meta-analysis.

OBJECTIVE: This meta-analysis aimed to review the available evidence and evaluate the necessity of immediate coronary angiography (CAG) to obtain positive outcomes for out-of-hospital cardiac arrest (OHCA) patients without ST segment elevation. DATA SOURCES: Web of Science, PubMed, Embase, Chinese National Knowledge Infrastructure, Wanfang, and SinoMed databases. STUDY SELECTION: We included observational and case-control studies of outcomes among individuals without ST segment elevation experiencing OHCA who had immediate, delayed, or no CAG. DATA EXTRACTION: We extracted study details, as well as patient characteristics and outcomes. DATA SYNTHESIS: Six studies (n = 2665) investigating mortality until discharge demonstrated a significant increase in survival benefit with early CAG (odds ratio [OR] = 1.78; 95%CI = 1.51-2.11; I = 81%; P < .0001). Seven studies (n = 2909) showed a significant preservation of neurological functions with early CAG at discharge (OR = 1.66; 95%CI = 1.37-2.02; P < .00001). Four studies (n = 1357) investigating survival outcomes with middle-term follow-up revealed no significant benefit with early CAG (OR = 1.21; 95%CI = 0.93-1.57; I = 66%; P = .15). CONCLUSIONS: Our meta-analysis demonstrates that there may be significant benefits in performing immediate CAG on patients who experience OHCA without ST segment elevation.

Lidocaine mediates the progression of cerebral ischemia/reperfusion injury in rats via inhibiting the activation of NF-κB p65 and p38 MAPK.

BACKGROUND: Lidocaine is a commonly used local anesthetic, and low-dose lidocaine has neuroprotective effects on cerebral ischemia/reperfusion (CI/R) injury; the mechanism for this, however, is still unclear. The aim of this study was to investigate the role and the possible mechanisms of lidocaine on CI/R injury in rats. METHODS: We constructed a rat (male Sprague-Dawley rats, 6-8 weeks old) model of CI/R injury induced by middle cerebral artery occlusion (MCAO). Histopathology, neuronal apoptosis, oxidative stress, and inflammatory response were evaluated using hematoxylin and eosin (HE) staining, Nissl staining, enzyme-linked immunosorbent assay (ELISA) and western blotting, respectively. In addition, brain water content, infarct volume, neurological deficit score each evaluated. RESULTS: The findings showed that lidocaine improved spatial learning and memory impairment, protected I/R-induced brain injury and attenuated neuronal death and apoptosis. Furthermore, lidocaine also regulated the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), IL-6, IL-10, iNOS, and IL-4.Notably, lidocaine markedly inhibited the expression of p65 and p38. CONCLUSIONS: The results indicate that lidocaine protects against cerebral injury induced by I/R in rats via the nuclear factor kappa-B (NF-κB) p65 and p38 mitogen-activated protein kinase (MAPK) signaling pathway, it provided a candidate for the treatment of CI/R-induced injury.

Sedative depth on neurological outcomes in a juvenile rat model of cardiopulmonary resuscitation.

The guidelines for cardiopulmonary resuscitation (CPR) in pediatric advanced life support suggest that midazolam is the preferred agent for sedation in patients with mild hypothermia, whereas children with cardiac arrest (CA) are at a crucial stage regarding their immature nervous system. Studies have shown that midazolam may have a detrimental effect on the developmental of the pediatric nervous system. Our previous study found that midazolam induced neuronal damage after CPR in young rats. It is speculated that: midazolam causes the potential injury of neurons by inhibiting mitochondrial autophagy expression and is an important factor for the poor prognosis in children after successful CPR. This project intends to adopt the modified asphyxiant CPR model in juvenile rats. Survival rate, neurological function and histopathological changes were evaluated to determine the protective effects of appropriate sedation depth on cerebral ischemia-reperfusion injury in juvenile rats after CPR. Combined with cell biology and molecular biology related technologies, the mechanism by which the mitochondrial pinkl-parkin signaling pathway induces autophagy to inhibit neuronal apoptosis may be key factor in the protective effects of sedation depth on the brain. The aim of this study is to provide experimental evidence and elucidate the mechanisms of improvement of cerebral ischemia-reperfusion injury by sedation depth in children after successful CPR and to lay a theoretical and experimental basis for clinical treatment.

Analgesic therapy improves arterial endothelial function following non-cardiovascular surgery: A randomized, placebo-controlled trial.

Pain subsequent to non-cardiac surgery may affect the endothelial function, which in turn contributes to myocardial injury (MI). The present study examined whether effective pain control is able to improve the postoperative endothelial function. Patients (n=160) undergoing laparoscopic cholecystectomy were randomly assigned into two groups, treated with tramadol analgesic or saline (placebo) following surgery. On preoperative day 1 (baseline) and postoperatively at 2 h, 1 day and 5 days, pain was assessed on a visual analogue scale (VAS), and B-mode ultrasound was used to measure brachial endothelium-dependent flow-mediated dilation (FMD) and nitroglycerin-induced dilation. At 2 h postoperatively, the FMD in the two groups was significantly lower compared with that at the other three time points (P≤0.005), while VAS was significantly higher (P<0.05). Patients in the tramadol group presented significantly reduced VAS values in comparison with those in the placebo group at 2 h and 1 day postoperatively (P=0.013 and 0.031, respectively), as well as significantly higher FMD at 2 h (6.7±1.5 vs. 6.0±1.7%; P=0.001) and 1 day postoperatively (7.3±1.3 vs. 6.9±1.4%; P=0.03). A VAS score of <5 was independently associated with postoperative FMD of ≥7 (odds ratio, 2.5; 95% confidence interval, 1.0-6.0; P=0.047). Backward multivariate linear regression also demonstrated that FMD was independently correlated with age and VAS score (B=-1.403, P=0.011; B=-0.579, P=0.003). The response to nitroglycerin-induced dilation remained stable in all patients at baseline and at all postoperative time points. In conclusion, analgesic treatment may improve the arterial endothelial function following non-cardiac surgery, which may help prevent postoperative MI.

[The optimal concentration for the protective effect of emulsified isoflurane on the neonatal rat cardiac myocytes hypoxia/reoxygenation injury of primary culture].

OBJECTIVE: To optimize the concentration of emulsified isoflurane (EI) for the protective effect on primary cultured neonatal rat hypoxia/reoxygenation (H/R) cardiac myocytes. METHODS: To prepare the H/R injury model on the basis of in-vitro neonatal rat cardiac myocytes culture and divide them into 13 groups at random, namely, normal control group (N group), H/R group, H/R+fat emulsion group (F group), the one, two, three, four, five, six, seven, eight, nine and ten times of 0.28 mmol/L EI designated as EI1-EI10 group. The supernatants of cell culture from each group were detected for lactate dehydrogenase (LDH) activity and the level of cardiac troponin-I (cTnI). The cellular homogenates of each group were prepared for the detection of superoxide dismutase (SOD) and malondialdehyde (MDA). Inverted microscope was applied to observe the characteristics of cardiac myocytes growth and changes of its forms. RESULTS: Compared to N group, the LDH, MDA and cTnI of others all increased (P < 0.05) and SOD decreased (P < 0.05). Compared to H/R group, LDH, MDA and cTnI of each EI dose group decreased significantly (P < 0.05), but SOD increased (P < 0.05). Compared to EI6 group, the LDH, MDA and cTnI in the other groups of EI increased (P < 0.05) and the SOD decreased (P < 0.05). As the EI concentration (increasing by multiple) increased, the LDH, MDA and cTnI in the EI1 to EI6 group decreased gradually and SOD gradually increased (P < 0.05), the LDH, MDA and cTnI in the EI7 to EI10 group increased gradually and SOD gradually decreased (P < 0.05). CONCLUSION: EI has the protective effect on the neonatal rat cardiac myocytes with H/R injury, the optimal concentration for the protective effect on cardiac myocytes is 1.68 mmol/L, and its mechanism may be associated with its anti-oxidation effect.