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1.
Chinese Journal of Anesthesiology ; (12): 414-417, 2016.
Article in Chinese | WPRIM | ID: wpr-496932

ABSTRACT

Objective To investigate the effect of theanine pretreatment on DNA repair function in neurons during brain ischemia-reperfusion (I/R) injury in rats.Methods One hundred and eight male Sprague-Dawley rats,weighing 290-310 g,aged 15 weeks,were randomly divided into 3 groups (n =36 each) using a random number table:sham operation group (S group),I/R group and theanine pretreatment group (T group).Global cerebral I/R was produced by 4-vessel occlusion method.Bilateral vertebral arteries were electrically cauterized,and bilateral common carotid arteries were clamped for 6 min.Theanine 1 g/kg was injected intravenously at 4 h before clamping bilateral common carotid arteries in T group,and the equal volume of normal saline was given in the other two groups.At 2,6,12,24,48 and 72 h of reperfusion,6 rats were selected in each group and sacrificed,the brains were removed,and the hippocampus was isolated for determination of the number of viable neurons in the hippocampal CA1 region (with a light microscope),apoptosis in neurons in the hippocampal CA1 region (by TUNEL),and expression of DNA repair protein X-ray repair cross-complementing group 1 (XRCC1) and Ku70 (by immunohistochemistry).The apoptotic index was calculated.Results Compared with S group,the number of viable neurons was significantly decreased,and the apoptotic index was significantly increased at 6,12,24,48 and 72 h of reperfusion,and the expression of XRCC1 and Ku70 was significantly down-regulated at 2,6,12,24,48 and 72 h of reperfusion in I/R group (P<0.01).Compared with I/R group,the number of viable neurons was significantly increased at 12,24,48 and 72 h of reperfusion,the apoptotic index was significantly decreased at 6,12,24,48 and 72 h of reperfusion,and the expression of XRCC1 and Ku70 was significantly up-regulated at 2,6,12,24,48 and 72 h of reperfusion in T group (P < 0.01).Conclusion The mechanism by which theanine pretreatment attenuates brain I/R injury is related to enhancement of DNA repair function and reduction of neuronal apoptosis in rats.

2.
Chinese Journal of Anesthesiology ; (12): 951-954, 2013.
Article in Chinese | WPRIM | ID: wpr-442852

ABSTRACT

Objective To investigate the effect of dexmedetomidine on the stress responses during wakeup test in patients undergoing cerebral functional area operation performed under propofol combined with remifentanil anesthesia.Methods Thirty-six ASA physical status Ⅰ or Ⅱ patients,undergoing cerebral functional area operation requiring wake-up test,aged 18-60 yr,weighing 50-70kg,were randomly divided into control group (group C) or dexmedetomidine group (group D) with 18 cases in each group.Dexmedetomidine 0.8 μg/kg was infused over 10 min before induction of anesthesia followed by infusion at 0.4 μg·kg-1 · h-1 in group D,while the equal volume of normal saline was infused in group C.Anesthesia was induced with target-controlled infusion of propofol and remifentanil and iv injection of cisatracurium.At 30 min prior to wake-up test,target-controlled infusion of propofol and application of mulscle relaxants were stopped,the target plasma concentration of remifentanil was decreased to 1 ng/ml,and in group D the infusion rate of dexmedetomidine was decreased to 0.1 μg·kg 1· h-1.Anesthesia time and consumption of anesthetics before wake-up test,wake-up time,and development of complications and intraoperative awareness during wake-up test were recorded.At 30 min prior to wake-up test (T1),immediately after wake-up (T2),at 5 min after wake-up (T3),and at 10 min after the anesthetic depth was deepened (T4),HR,mean arterial pressure and BIS value were recorded and blood samples were taken for determination of plasma concentrations of epinephrine (E) and norepinephrine (NE).Results Compared with group C,the consumption of propofol and remifentanil was significantly reduced before wake-up,the incidence of hypertension was decreased during wake-up test,and HR and plasma E and NE concentrations were decreased at each time point (P < 0.05),and no significant difference in mean arterial pressure and BIS value was found in group D (P > 0.05).Tachycardia,restlessness,bucking and awareness were not observed during wake-up test in group D.Conclusion Dexmedetomidine can inhibit the stress responses during wake-up test and raise the quality of wake-up test in patients undergoing cerebral functional area operation performed under propofol combined with remifentanil anesthesia.

3.
Chinese Journal of Tissue Engineering Research ; (53): 187-189,封三, 2006.
Article in Chinese | WPRIM | ID: wpr-592486

ABSTRACT

BACKGROUND: Focal cerebral ischemia model in rats should be established under drugged state by surgery operation, but anaesthetic drug may influence the outcome of focal cerebral ischemia.OBJECTIVE: To observe the effects of ketamine anesthesia on the pathological outcome of focal cerebral ischemia model in rats, and perform control with pentobarbital.DESIGN: Randomized controlled animal experiment.SETTING: Center of Experimental Animal and Department of Pathology of Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University.MATERIALS: The experiment was performed in the Center of Experimental Animal and Department of Pathology of Second Affiliated Hospital,School of Medicine, Xi'an Jiaotong University from May 2004 to March 2005. Thirty male SD rats were randomly assigned into pentobarbital group and ketamine group with 15 rats in each group.METHODS: The rats in the pentobarbital group and ketamine group were subjected to 40 mg/kg pentobarbital and 60 mg/kg ketamine by abdominal anaesthesia, respectively. The permanent middle cerebral artery occlusion (MCAO) was performed in rats by thread embolism in cavity in order to induce cerebral ischemia after abolition of righting reflex.MAIN OUTCOME MEASURES: ①A modified Bederson's scoring system was adopted to determine the neurological functional deficit at hour 4 after the MCAO. ②Five rats from each group were selected at hour 24 after MCAO. They were killed and their brain was stained with 20 g/L 2,-3,-5-triphenyltetrazolium hydrochloride (TTC). The infarct volume was determined. ③ MCAO was performed for 72 hours and mortality rate of two groups were recorded. Four rats in each group were re-anesthetized. They were killed and their brain was gained. Survival neurons were detected with toluidine blue staining.RESULTS: Totally 30 rats were involved in the result analysis. ①There was no significant difference in neurological score 4 hours after MCAO between pentobarbital group and ketamine group (1.46±0.98,1.38±0.68 ,P>0.05). ②The infarct volume in the ketamine group was less than that in the pentobarbital group at hour 24 after MCAO [(28.1±4.11)%,37.8±4.95]%, P<0.05]. ③The mortality rate 72 hours after ischemia was not significantly different between pentobarbital group and ketamine group (42% vs 33%,P>0.05). But neuron density in penumbra in the ketamine group was higher than that in the pentobarbital group [(836±15),(740±24) numbers/mm2, P<0.05].CONCLUSION: ①The ketamine anesthesia induces minor brain injury in setting of the focal cerebral ischemia model in rats. ②When neuroprotective effects of procedures or drugs being studied are evaluated in this focal cerebral ischemia model, they might provide no additional advantage to cerebral ischemia.

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