Objective To investigate the protective effect of propofol on the brain against ischemia-reperfusion (I/R) injury. Methods Ninety healthy SD rats weighing 290-310g were randomly divided into 3 groups: Ⅰ propofol group (P) (n =42); Ⅱ normal saline group (NS) (n =42) and Ⅲ sham operation group (S) (n = 6). The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.3 ml?100 g-1. Right external, internal and common carotid arteries were exposed. A nylon thread (0.25 mm in diameter) with rounded tip was inserted at the bifurcation into internal carotid artery and threaded cranially until resistance was felt. The distance from the bifurcation to the tip of the thread was about 17.5-18.5 mm. Middle cerebral artery occlusion (MCAO) was confirmed by ipsilateral Horner's sign and contralateral hemiplegia when the animals were awake after anesthesia. In group P propofol 10 mg?100 g-1 was given intraperitoneally (i .p. ) 10 min before MCAO which was maintained for 1 hour. In group NS, NS was given instead of propofol. In group S the carotid arteries were exposed but MCAO was not performed. Reperfusion was produced by withdrawal of the nylon thread. The animals were killed at 0,2, 5, 11, 23, 71 h and 1 week after reperfusion was started (6 animals at each time-point) . Brains were immediately removed and sliced. The infarct size was analyzed quantitatively by Kontron IBAS 2.5 image auto-analysis system. The glucose transporter-1 (GLUT-1) mRNA was assessed by RT-PCR. The expression of GLUT-1 protein was determined by immuno-histochemistry. Results The infarct size was significantly smaller in P group than in NS group. In P group GLUT-1 mRNA began to increase at Oh, peaked at 23 h and remained higher than normal at 1 week after reperfusion was started and was significantly higher than that in NS group at 0, 2, 5, 11, 23, 71 h and 1 week. The changes in expression of GLUT-1 protein corresponded with the changes in GLUT-1 mRNA.Conclusion Propofol can protect the brain from I/R injury to some extent when given before ischemia. Upregulation of GLUT-1 expression is involved in the mechanism.

Objective To investigate the effects of different afferent nerve injury on development of neuropathic pain and its relationship with brain-derived neurotrophic factor (BDNF) in spinal cord and dorsal root ganglion (DRG) in rats. Methods Twenty-four male SD rats aged 2 months weighing 200-250 g were randomly divided into 3 groups:group Ⅰ sham operation (group S); group Ⅱ sural nerve injury (group SUR) and group Ⅲ gastrocnemius-soleus nerve injury (group GS). Sural nerve and gastrocnemius-soleus nerve were transected in group SUR and GS respectively. Paw withdrawal threshold to von Frey filament stimulation was measured the day before and at day 3 and 7 after operation. The animals were killed at postoperative day 7 after the measurement of paw withdrawal threshold. The ipsllateral L5 DRG and L5 segment of the spinal cord were removed. BDNF expression in the spinal dorsal horn was determined. The percentage of BDNF positive neurons and ATF-3 positive neurons in the total DRG neurons and the percentage of BDNF positive neurons in the damaged neurons (ATF-3 positive) were calculated. Results Mechanical hyperalgesia developed after transection of gastrocnemius-soleus muscle in group GS. Mechanical pain threshold was sinificantly lower, while BDNF expression in the spinal dorsal horn and the percentage of BDNF positive neurons in total DRG neurons were significantly higher in group GS than in group S and SUR (P ＜ 0.01). There was no significant difference in all variables between group SUR and S (P＞0.05). There was no significant difference in the percentage of ATF-3 positive neurons in the total DRG neurons between group GS and SUR (P ＞ 0.05), but the percentage of BDNF positive neurons in the damaged neurons (ATF-3 positive) was significantly higher in group GS than in group SUR (P ＜ 0.05). Conclusion Transection of the afferent nerve innervating muscle can produce neuropathic pain through up-regulation of BDNF expression in spinal dorsal horn and DRG in rats, while transection of the afferent nerve innervating skin can not.

Objective To observe the clinical efficacy and safety of 2 differentdoses of dexmedetomidine combined with low-concentration ropivacaine during lumbar plexus block for elderly patients. Methods Ninety elderly patients were randomly divided into group A,B and C with 30 cases in each group. All patients were performed lumbar plexus block guided by ultrasound and nerve stimulator.35 mL of 0.25% ropivacaine was injected in group A,35ml of 0.25% ropivacaine plus dexmedetomidine 0.5 μg/kg in group B,and 35 mL of 0.25% ropiva-caine plus dexmedetomidine 1 ug·kg-1in group C. Onset time,duration,blocking extent and the occurrence of adverse events wererecordedafter lumbar plexus block.Ramssay sedation score,blood pressure,heart rate and res-piration were monitored intraoperatively,and the dosage of analgesic within 24 hours after operation was measured. Results Group C witnessed the shortest onset time of sensory and motor block and the longest duration,followed by group B and A(P<0.01).The Ramssay sedation score of group C was higher than that of group A and B(P<0.05),but no significant difference was found between group A and B. Group C witnessed the lowest blood pres-sure and heart rate(P < 0.05),followed by group A and B(P < 0.05). The dosage of analgesics in group C was less than thatof group A and B(P<0.05),withthe lest in group B(P<0.05).All patients in group B and C com-pleted the surgery only under nerve blockade.However,there were6 patients in group Arequiring additional intrave-nous anesthesia to complete the surgery for poor outcome of nerve blockade. Conclusions The mixture of 0.5~1 μg·kg-1dexmedetomidine and 0.25% ropivacaine in lumbar plexus block can achieve good anesthetic outcome for elderly patients,with moderate sedation,stable respiration and circulation,and less adverse events.