ABSTRACT
Objective To evaluate the efficacy of dezocine for prevention of postoperative cognitive dysfunction (POCD) in elderly patients undergoing total knee arthroplasty under remifentanil-based anesthesia.Methods Sixty-eight patients of both sexes, aged 65-85 yr, weighing 48-78 kg, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ , undergoing elective unilateral total knee arthroplasty under general anesthesia, were randomly divided into 2 groups (n =34 each) using a random number table: control group (group C) and dezocine group (group D).After induction of anesthesia, the patients were tracheally intubated and mechanically ventilated.Anesthesia was maintained with iv infusion of propofol 0.05-0.06 mg · kg-1 · min-1 and remifentanil 0.05-0.10 μg · kg-1 · min-1, and intermittent iv boluses of vecuronium 0.04 mg/kg.Dezocine 0.1 mg/kg was injected intravenously at 30 min before skin incision in group D.At 1 day before operation (T0) , and 1, 3, 5, 7 days after operation (T1 , T2, T3 , T4) , the blood samples from the central vein were collected for determination of serum cortisol (Cor), neuron specific enolase (NSE) and S-100β protein concentrations.Before operation, and 5 and 7 days after operation, the patients' cognitive function was assessed using Mini-Mental State Examination, and the occurrence of POCD was recorded.Results Compared with the baseline value at T0, the serum Cor, NSE and S-100β protein concentrations were significantly increased at T1-3, and MMSE scores were decreased at T3,4 in the two groups.Compared with group C, the serum Cot, NSE and S-100β protein concentrations were significantly decreased at T1-4, and Mini-Mental State Examination scores were increased at 5 and 7 days after operation, and the incidence of POCD was decreased in group D.Conclusion Dezocine 0.1 mg/kg intravenously injected at 30 min before skin incision can prevent the occurrence of POCD in elderly patients undergoing total knee arthroplasty under remifentanil-based anesthesia.
ABSTRACT
Objective To investigate the role of astrocytes activation in post herpetic neuralgia (PHN). Methods The kunming mice (20-25 g) were used in this study. Resiniferatoxin was injected into the peritoneal cavity.Immunofuorescence was used to detect the activation of astrocytes , mechanical paw withdrawal threshold (MWT)and thermal withdrawal latency (TWL) were used to assay the mechanical allodynia and thermal hyperalgesia, respectively. Fluorocitrate, an inhibitor of astrocytes was intrathecally (i.t.) or intraperitonealy (i. p.) injected into the mice. Results Compared with the vehicle group, MWT was decreased, and TWL was increased significantly in the RTX group. Pre-treatments of fluorocitrate (Fc, i.t.,or i.p.) inhibited the decrease of MWT. Conclusion The activation of astrocytes mediates the post herpetic neuralgia.
ABSTRACT
Objective To investigate the effects of brain-derived neurotrophic factor (BDNF) pretreatment on neuron apoptosis and the expression of Bcl-2 and Bax protein following global cerebral ischemia-reperfusion (I/R) injury in gerbils. Method Forty-eight mongolian gerbils were randomly divided into six groups in equal number (n = 8): normal control group (group C), ischemia-reperfusion group (group I/R) and four BDNF pretreatment groups according to various lengths of time from BDNF pretreatment to ischemia-reperfusion. The BDNF pretreat-ment was carried out in gerbils with lateral ventricular injection of BDNF 0.5μg 6 h, 12 h,24 h and 48 hours be-fore cerebral ischemia, and those gerbils assigned into PR6, PR12, PR24 and PR48 groups. The global cerebral is-chemia-reperfusion was induced by occlusion of bilateral common carotid arteries for 20 minutes and then the arter-ies were released for 24 hours reperfusion. The confirmation of global cerebra ischemia was evidenced by the ap-pearance of mydriasis and disappearance of light reflex and righting reflex. Twenty-four hours later, all gerbils including those of control group were sacrificed and a piece of tissue was taken from frontal cortex just behind the optic chiasma 1～4 millimeter for making paraffin sections. Neuron apoptosis was identified by using TUNEL and immunohischemistry was used to detect the expression of Bcl-2 and Bax protein in cerebral cortex. The data were analyzed by using analysis of variance. Results There were no apoptotic cells, and expression of Bcl-2 and Bax protein positive cells found in group C. Neuron apoptosis in brain cortex was detected in I/R group and BDNF pre-treatment groups. The indexes of neuron apoptosis in BDNF pretreatment groups were markedly lower than those in group I/R (P < 0.01). Compared with group I/R, the index of expression of Bcl-2 protein positive cells was in-creased significantly in BDNF pretreatment groups (P = 0.005), while the index of expression of Bax protein posi-tive cells were decreased significantly (P < 0.01 in all groups). Among 4 BDNF pretreatment group, the lowest apoptosis index and lowest of expression of Bax protein positive cells were found in PR6 and PR12 BDNF pretreat-ment groups (P = 0.0056 and 0.001, respectively). Conclusions Different time windows of BDNF pretreatment can decrease the neuron apoptosis in different degree, and protect brain against cerebral ischemia-reperfusion injury significantly. Among BDNF pretreatment time windows, pretreatment of 6 hours and 12 hours are the better ones.The mechanism of protection of BDNF pretreatment may be attributed to inducing Bcl-2 protein expressions and in-hibiting Bax protein expressions, and thereby inhibiting neuron apoptosis.