Objective To evaluate the effect of rocuronium on entropy to endotracheal intubation during anesthesia induction with propofol. Methods Forty patients anesthetized induction with propofol using a target-controlled infusion were randomly divided into two groups: rocuronium group (R group, 20 cases) received 0.6 mg/kg rocuronium or saline group (S group, 20 cases) received saline. 2-3 min later, endotracheal intubation was performed. Response entropy(RE) and state entropy(SE) were recorded during baseline(Ta), at steady state(Tb), 2 min after rocuro nium or saline administration (Tc) and 0, 1, 2 and 3 min after endotracheal intubation (T0, T1, T2, T3). Results At T2, the RE-SE was higher in S group than that in R group. Endotracheal intubation induced increasing in RE and SE. Comparing T2 and T0 values in R group and S group, SE increased from 42 ± 7 to 50 ± 8 and 43 ± 13 to 55 ± 12, and RE increased from 45 ± 6 to 54 ± 9 and 48 ± 16 to 66 ± 15, respectively. At T0, RE and RE-SE were higher in S group. Conclusion Rocuronium affects RE-SE and RE and RE-SE responses to endotracheal intubation and may confound interpretation of entropy monitoring.

【Objective】 To explore the protective effects of exogenous hydrogen sulfide （H2S） on oxygen glucose deprivation and re-oxygenation （OGD/R）-induced SH-SY5Y cell injury. 【Methods】 OGD/R model was established in SH-SY5Y cells. Based on interferences， SH-SY5Y cells were divided into control group （no interference）， OGD/R model group， and treatment groups （OGD/R model treated with different concentrations of NaHS （H2S donor）. The cells were cultured in low glucose medium without fetal bovine serum under 37 ℃， 93% N2 and hypoxia （2% O2） for 12 h， then in complete medium under normoxia （5% O2 ） for 24 h. CCK-8 was used to detect cell viability， and flow cytometry was used for assaying the level of cellular apoptosis. Western blot was used to detect the expression levels of endoplasmic reticulum stress-related proteins including glucose regulatory protein 78 （GRP78）， CCAAT/enhancer-binding homologous protein （CHOP）， NF-κB P65 and COX-2. 【Results】 The cell viability was lower in OGD/R model group than in the control group （P<0.05）. NaHS treatment at a concentration of 0-0.5 mmol/L increased cell viability in OGD/R model group in a dose-dependent manner （P<0.05）. In contrast， NaHS （C>0.5 mmol/L） decreased cell viability of OGD/R （P<0.05）. The apoptosis level of early stage in OGD/R model group was significantly higher than that in control group （P<0.05）. NaHS treatment at concentrations of 0.2 and 0.4 mmol/L lowered the apoptosis level of early stage in OGD/R model group （P<0.05）. Western blot showed that the protein expression levels of GRP78， CHOP， NF-κB p65， and COX-2 were significantly higher in OGD/R model group than those in control group （P<0.05）. When compared with OGD/R model group， the expression levels of GRP78， CHOP， NF-κBp65 and COX-2 were decreased by NaHS at concentrations of 0.2， 0.4 and 4 mmol/L （P<0.05）， but there was no statistically significant difference among the treatment groups （P>0.05）. 【Conclusion】 NaHS can rescue cell viability of OGD/R-induced cell injury. It may be achieved by inhibiting the activation of NF-κBp65 and COX-2 proteins induced by endoplasmic reticulum stress to reduce the level of cell apoptosis.