ABSTRACT
Objective:To evaluate the effect of gender on neuromuscular blockade of rocuronium in epileptics.Methods:Forty American Society of Anesthesiologists physical status Ⅱ or Ⅲ patients, aged 18-59 yr, with body mass index of 18.5-24.0 kg/m 2, scheduled for elective surgery for treatment of epilepsy under general anesthesia, were divided into 2 groups ( n=20 each) according to gender: male group (group M) and female group (group F). Neuromuscular conduction function was monitored with a muscle relaxation monitor.Ulnar nerve was stimulated in TOF mode (frequency 2 Hz, wave width 0.2 ms, stimulation current 70 mA and interval 12 s). Rocuronium 0.8 mg/kg was injected intravenously during anesthesia induction, and endotracheal intubation was performed when T l reached maximum inhibition.The conditions of endotracheal intubation were evaluated by the modified method.When T 1 recovered to 25% during operation, rocuronium 0.15 mg/kg was intravenously injected.Sugammadex sodium 2 mg/kg was injected intravenously when T 1 recovered to 50% after surgery.The onset time (T onset), peak time (T peak), 10% recovery time (T 10%), 10%-25% recovery time (T 10%-25%), 25%-50% recovery time (T 25%-50%), 50%-75% recovery time (T 50%-75%) and 75%-90% recovery time (T 75%-90%) of rocuronium were recorded.Peripheral venous blood samples (3 ml) were collected when T 1 recovered to 25% and 75%, and the concentration of rocuronium was detected by liquid chromatography-tandem mass spectrum.The consumption of rocuronium per unit of weight per minute was calculated. Results:There was no significant difference between the two groups in terms of T onset, T peak, T 10%, T 10%-25%, T 25%-50%, T 50%-75%, T 75%-90%, endotracheal intubation conditions, blood concentration of rocuronium at varied time points, or consumption of rocuronium per unit of weight per minute ( P>0.05). Conclusion:Gender exerts no effect on the neuromuscular blockade of rocuronium in epileptics.
ABSTRACT
Objective To investigate the role of TLR4/NF-κB signal pathway in pathogenesis of brain inju-ry during deep hypothermia circulatory arrest(DHCA). Methods BV2 microglia cells were subjected to oxygen-glucose deprivation/reoxygenation(OGD/R),in vitro model for DHCA. The BV2 were randomly divided into the control group(C group)and the experimental group(O group). BV2 viability was determined by CCK-8 assay. TLR4 and its downstream signaling molecules ,MyD88 and phosphorylated NF-κB (p-p65) expressions were detected by Western blotting. TLR4 mRNA expression in BV2 microglial cells were determined by RT-PCR. Level of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in culture medium was detected by ELASA. Results Compared with the group C,BV2 microglia cell viability in experiment group was obviously weaker(P<0.05). Expressions of TLR4,MyD88 and phosphorylated NF-κB(p-p65)from the experiment group increased remarkedly than those from the group C (P < 0.05). TLR4 mRNA level was higher significantly in the group O than in the group C (P < 0.01). Production of IL-6 and TNF-α in the group O were up-regulated apparently compared to the group C(P<0.01). Conclusion TLR4/NF-κB signaling pathway contributed to activation of BV2 microglia cells treated by OGD/Reoxygenation ,which was probably the exactly way that involved in pathogenesis of brain injury during deep hypothermia circulatory arrest.
ABSTRACT
Objective To investigate the role of TLR4/NF-κB signal pathway in pathogenesis of brain inju-ry during deep hypothermia circulatory arrest(DHCA). Methods BV2 microglia cells were subjected to oxygen-glucose deprivation/reoxygenation(OGD/R),in vitro model for DHCA. The BV2 were randomly divided into the control group(C group)and the experimental group(O group). BV2 viability was determined by CCK-8 assay. TLR4 and its downstream signaling molecules ,MyD88 and phosphorylated NF-κB (p-p65) expressions were detected by Western blotting. TLR4 mRNA expression in BV2 microglial cells were determined by RT-PCR. Level of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in culture medium was detected by ELASA. Results Compared with the group C,BV2 microglia cell viability in experiment group was obviously weaker(P<0.05). Expressions of TLR4,MyD88 and phosphorylated NF-κB(p-p65)from the experiment group increased remarkedly than those from the group C (P < 0.05). TLR4 mRNA level was higher significantly in the group O than in the group C (P < 0.01). Production of IL-6 and TNF-α in the group O were up-regulated apparently compared to the group C(P<0.01). Conclusion TLR4/NF-κB signaling pathway contributed to activation of BV2 microglia cells treated by OGD/Reoxygenation ,which was probably the exactly way that involved in pathogenesis of brain injury during deep hypothermia circulatory arrest.
ABSTRACT
Objective To explore the expression of TLR4/NF-κB pathway in cerebral injury resulting from DHCA ( deep hypothermia circulatory arrest ) as well as the effect of SACP ( selective antegrade cerebral perfusion). Methods Twelve pigs were randomly assigned to DHCA group (n = 6) or SACP group (n = 6) at 18 ℃ for 80 min. IL-6 was assayed by ELISA. Apoptosis and NF-κB proteins were detected by fluorescence TUNEL and Western blot, respectively. The level of TLR4 was determined through qRT-PCR and Western blot. Results Serum IL-6 level of SACP group was significantly lower at the end of circulation arrest and experiment and apoptotic index and NF-κB protein were apparently lower in SACP group (P < 0.05). The level of TLR4 protein and mRNA from SACP group decreased significantly (P < 0.05). Conclusions TLR4/NF-κB pathway plays a critical role in pathogenesis of DHCA cerebral injury and attenuating TLR4/NF-κB cytokines probably contributes to neuroprotection of SACP. TLR4/NF-κB pathway may be a novel target for DHCA.