RESUMO
Objective:To evaluate the effect of dexmedetomidine on perioperative neurocognitive disorders in elderly frail patients undergoing hip joint surgery.Methods:Sixty elderly patients of either sex, aged≥ 60 yr, weighing 40-100 kg, of American Society of Anesthesiologists Physical Status classification Ⅰ-Ⅲ, with the Frail Scale score 3-5 points, scheduled for elective hip surgery under spinal-epidural anesthesia, were divided into 2 groups ( n=30 each) using the random number table method: control group (group C) and dexmedetomidine group (group D). Dexmedetomidine was intravenously infused at a dose of 0.5 μg/kg at 10 min before anesthesia followed by a continuous infusion of 0.2 μg·kg -1·h -1 until 10 min before the end of surgery in group D. The equal volume of 0.9% sodium chloride solution was given at the corresponding time point in group C. Blood samples from the median cubital vein were collected before surgery (T 1) and at 1 and 3 days after surgery (T 2, 3) for determination of concentrations of serum S100β and neuron-specific enolase by enzyme-related immunosorbent assay. Postoperative delirium was assessed within 3 days after surgery using the Confusion Assessment Method. Cognitive function was evaluated by Mini-Mental State Examination at T 1 and 30 days after surgery. Results:Compared with the baseline at T 1, the concentrations of serum S100β and NSE were significantly increased at T 2 and T 3 in two groups ( P<0.05). Compared with group C, the concentrations of serum S100β and neuron-specific enolase and incidence of postoperative delirium and postoperative cognitive dysfunction were significantly decreased at T 2 and T 3 in group D( P<0.05). Conclusions:Dexmedetomidine can effectively decrease the occurrence of perioperative neurocognitive disorders in elderly frail patients undergoing hip joint surgery.
RESUMO
Objective To evaluate the role of extracellular signal-regulated kinase (ERK) signaling pathway in intrathecal dexmedetomidine-induced reduction of spinal cord ischemia-reperfusion (I/R)injury in rats.Methods Eighty clean-grade male Sprague-Dawley rats,aged 9-10 weeks,weighing 300-350 g,were divided into 4 groups (n =20 each) using a random number table method:sham operation group (group S),spinal cord I/R group (group I/R),dexmedetomidine group (group D),and dexmedetomidine plus ERK signaling pathway blocker PD98059 group (group P).Spinal cord ischemia was produced by cross-clamping of the abdominal aorta distal to the left renal artery for 25 min followed by reperfusion to establish the model of spinal cord I/R injury.Dexmedetomidine 1 μg/kg was intrathecally injected at 20 min before establishing the model in D and P groups,PD98059 2 mg/kg was given via the tail vein at the same time in group P,and the equal volume of normal saline was given instead in S and I/R groups.Five rats were selected at 6,8,10 and 12 h of reperfusion,and the modified Basso,Beattie,Bresnahan (BBB) scale was used to assess the hindlimb locomotor function.Five rats were sacrificed after assessing the locomotor function at 6 h of reperfusion,and the L3-5 segments of the spinal cord were taken for determination of cell apoptosis (by TUNEL) and expression of phosphorylated ERK (p-ERK) (by Western blot).The apoptosis index was calculated.Results Compared with group S,the BBB scores were significantly decreased at each time point of reperfusion,the apoptosis index was increased,and the expression of pERK was up-regulated in the other three groups (P＜0.05).Compared with I/R group,the BBB scores were significantly increased at each time point of reperfusion,the apoptosis index was increased,and the expression of p-ERK was up-regulated in group D,and no significant change was found in the apoptosis index or p-ERK expression in group P (P＞0.05).Compared with group D,the BBB scores were significantly decreased at each time point of reperfusion,the apoptosis index was increased,and the expression of pERK was down-regulated in group P (P＜0.05).Conclusion The mechanism by which intrathecal dexmedetomidine reduces spinal cord I/R injury is related to activating ERK signaling pathway in rats.
RESUMO
Objective@#To evaluate the role of extracellular signal-regulated kinase (ERK) signaling pathway in intrathecal dexmedetomidine-induced reduction of spinal cord ischemia-reperfusion (I/R) injury in rats.@*Methods@#Eighty clean-grade male Sprague-Dawley rats, aged 9-10 weeks, weighing 300-350 g, were divided into 4 groups (n=20 each) using a random number table method: sham operation group (group S), spinal cord I/R group (group I/R), dexmedetomidine group (group D), and dexmedetomidine plus ERK signaling pathway blocker PD98059 group (group P). Spinal cord ischemia was produced by cross-clamping of the abdominal aorta distal to the left renal artery for 25 min followed by reperfusion to establish the model of spinal cord I/R injury.Dexmedetomidine 1 μg/kg was intrathecally injected at 20 min before establishing the model in D and P groups, PD98059 2 mg/kg was given via the tail vein at the same time in group P, and the equal volume of normal saline was given instead in S and I/R groups.Five rats were selected at 6, 8, 10 and 12 h of reperfusion, and the modified Basso, Beattie, Bresnahan (BBB) scale was used to assess the hindlimb locomotor function.Five rats were sacrificed after assessing the locomotor function at 6 h of reperfusion, and the L3-5 segments of the spinal cord were taken for determination of cell apoptosis (by TUNEL) and expression of phosphorylated ERK (p-ERK) (by Western blot). The apoptosis index was calculated.@*Results@#Compared with group S, the BBB scores were significantly decreased at each time point of reperfusion, the apoptosis index was increased, and the expression of p-ERK was up-regulated in the other three groups (P<0.05). Compared with I/R group, the BBB scores were significantly increased at each time point of reperfusion, the apoptosis index was increased, and the expression of p-ERK was up-regulated in group D, and no significant change was found in the apoptosis index or p-ERK expression in group P (P>0.05). Compared with group D, the BBB scores were significantly decreased at each time point of reperfusion, the apoptosis index was increased, and the expression of p-ERK was down-regulated in group P (P<0.05).@*Conclusion@#The mechanism by which intrathecal dexmedetomidine reduces spinal cord I/R injury is related to activating ERK signaling pathway in rats.
RESUMO
Objective To evaluate the effects of combination of dexmedetomidine and mild hypothermia on global cerebral ischemia-reperfusion (I/R) injury in neonatal rats.Methods Ninety-six neonatal Sprague-Dawley rats,aged 6-7 days,weighing 18-22 g,were randomly divided into 4 groups (n=24 each) using a random number table:I/R group,mild hypothermia group (group H),dexmedetomidine group (group D) and combination of dexmedetomidine and mild hypothermia group (group DH).Global cerebral ischemia was induced in rats anaesthetized with chloral hydrate by bilateral common carotid artery clamping (for 15 min) combined with hypotension followed by reperfusion.Dexmedetomidine 75 pg/kg was given intraperitoneally at 30 min before ischemia in D and DH groups,while the equal volume of normal saline was given in I/R and H groups.The temperature in the temporal muscle was maintained at 36.7-37.2℃ in I/R and D groups,and at 34.8-35.3℃ in H and DH groups.At 12,24 and 72 h of reperfusion,8 rats were randomly chosen in each group,and neurological deficit score (NDS) was determined.The animals were then sacrificed,and their brains were removed for determination of myeloperoxidase (MPO) activity (by spectrophotometry) and contents of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in brain tissues (using ELISA).Results Compared with I/R group,the NDS,MPO activity and contents of TNF-α and IL-6 were significantly decreased in the other three groups.The NDS,MPO activity and contents of TNF-α and IL-6 were significantly lower in DH group than in H or D group.Conclusion Dexmedetomidine can optimize cerebral protection providedby mild hypothermia against global cerebral I/R injury through inhibiting inflammatory responses in brain tissues of neonatal rats.