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1.
The Journal of Clinical Anesthesiology ; (12): 666-668, 2014.
Article in Chinese | WPRIM | ID: wpr-453296

ABSTRACT

Objective To investigate the effect of dexmedetomidine on excitatory aminoacid (EAA)and inhibition of amino acid(IAA)in cerebro-spinal fluid(CSF)of patients undergoing in-tracranial tumor surgery,and to explore the cerebral protective mechanism of dexmedetomidine in neurosurgery.Methods Sixty patients aged 18-64 years old,ASA Ⅰ or Ⅱ,weighing 50-90 kg un-dergoing elective intracranial tumor surgery were randomly divided into dexmedetomidine group (group D)and control group(group C).Dexmedetomidine 1 μg/kg was infused before anesthesia in-duction for more than 10 minutes and pumped continously with 0.2-0.7 μg·kg-1·h-1 in group D, while in group C midazolam 0.03-0.05 mg/kg was injected followed by intermittent administration of 0.03-0.05 mg/kg.BIS value was maintained between 40-50.MAP and HR was recorded at the time points before induction(T0 ),dura mater incision(T1 ),tumor resection(T2 ),at the end of the surgery (T3 ).And we collected CSF at T0 ,T3 ,6 hours after the surgery(T4 ),12 hours after the surgery (T5 ),24 hours after the surgery(T6 ),then the concentrations of EAA and IAA were determined with high-performance liquid chromatography (HPLC)at T0 ,T3 ,T4 ,T5 and T6 .Results The MAP and HR in group D at T1-T3 were much lower than that in T0 and in group C(P <0.05).Compared with T0 ,the Glu and Asp in CSF significantly increased in group C at T3-T6 and were much higher than those in group D (P < 0.05 ),GABA was significantly decreased and much lower than group D(P <0.05).Compared with T0 ,the Glu and Asp in group D at T3-T5 were increased and GABA was decreased, but without statistic significance. At T6 , the values recovered to the level at T0 . Conclusion Dexmedetomidine can be used to maintain hemodynamic stability in intracranial tumor surgery,and may play a role in cerebral protection through inhibiting expression of Glu and Asp (EAA).

2.
Chinese Journal of Anesthesiology ; (12): 1370-1373, 2011.
Article in Chinese | WPRIM | ID: wpr-417574

ABSTRACT

ObjectiveTo investigate the effects of partial hepatic ischemia/reperfusion (I/R) on choline acetyltransferase(ChAT) expression in hippocampal neuron in mice.MethodsOne hundred adult male mice,aged 2 months,weighing 20-25 g,were randomly divided into 5 groups (n =20 each): normal control group(group C),sham operation group(group S),groups I/R1,I/R2,I/R3.Partial hepatic ischemia was produced by clamping left hepatic artery and portal vein for 20,30,40 min respectively followed by reperfusion in groups I/R1,I/R2,I/R3.Passive avoidance task was performed with 10 mice in each group at 4-9 and 18-23 d after operation respectively.The animals were sacrificed and their brains were removed for determination of the expression of ChAT in CA3 of hippocampal neuron.ResultsCompared with group C,the latency was significantly shortened and number of errors increased in groups I/R1 and I/R2 at 4-7 d after operation and in group I/R3 at 4-9 d after operation,the expression of ChAT in hippocampal neuron down-regulated in groups I/R1,I/R2 and I/R3 at 9 d after operation( P <0.05 or 0.01).There was no significant difference in the latency and number of errors at 18-23 d after operation and the expression of ChAT in hippocampal neuron at 23 d after operation among groups C,I/R1,I/R2 and I/R3 ( P > 0.05).Compared with group I/R1,the number of errors was significantly increased at 4 and 5 d after operation in group I/R2,the latency shortened at 4-6 d after operation and number of errors increased at 4-9 d after operation in group I/R3,and the expression of ChAT in hippocampal neuron down-regulated at 9 d after operation in groups I/R2 and I/R3 ( P < 0.05 or 0.01 ).There was no significant difference in the latency and number of errors at 18-23 d after operation and the expresson of ChAT in hippocampal neuron at 23 d after operation among groups I/R1,I/R2 and I/R3 ( P > 0.05).ConclusionPartial hepatic I/R can result in transient cognitive impairment in mice by down-regulating the expression of ChAT in hippocampal neuron.

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