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Objective To investigate the effects of different doses of dexmedetomidine on perioperative inflammatory responses in patients undergoing one-lung ventilation (OLV).Methods Thirty-six ASA T or Ⅱ patients (aged 43-72 years and weighing 50-78 kg) scheduled for esophagectomy were randomly divided into three groups (n =12 each):control group (group C),low dose dexmedetomidine group (group D1) and high dose dexmedetomidine group (group D2).Dexmedetomidine 1 μg/kg was infused intravenously 10 minutes before anesthesia induction,then infused at a rate of 0.2 μg· kg-1 · h-1 (group D1) or 0.5 μg· kg-1· h-1 (group D2) until 30 minutes before the end of operation.Group C received the equal volume of normal saline.Blood samples were collected before anesthesia induction (T0),immediately before OLV (T1),30 minutes after OLV (T2),90 minutes after OLV (T3),30 minutes after lung inflation (T4) and 2 hours after operation (T5) for monitoring serumlevels of tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8).Results Compared with T0,serum levels of TNF-α and IL-8 significantly increased at T3 and T5 in all the three groups (P ＜ 0.05).Compared with group C,serum levels of TNF-α and IL-8 significantly decreased at T3 and T5 in group D2 (P ＜ 0.05).There was no significant difference in the indexes mentioned above between group C and group D1 (P ＞ 0.05).Conclusion Dexmedetomidine 1 μg/kg given before anesthesia induction and then infused at the rate of 0.5 μg· kg-1 ·h-1 during operation can reduce inflammatory responses in patients undergoing OLV.
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Objective To evaluate the role of mitochondrial ATP-sensitive potassium (mito-KATP) channels in attenuation of renal ischemia-reperfusion (I/R) injury by lidocaine pretreatment in rats.Methods Sixty healthy male Wistar rats,weighing 300-350 g,were randomly assigned into 5 groups (n =12 each) using a random number table:sham operation group (group S); renal I/R group (group I/R); lidocaine pretreatment group (group L) ; 5-HD (a specific blocker of the mito-KATP channel) group and 5-HD + lidocaine pretreatment group (group 5-HD + L).Renal ischemia was induced by occlusion of bilateral renal arteries for 60 min with atraumatic microclips followed by 4 h reperfusion.At 60 min before renal ischemia,lidocaine 5 mg/kg was intravenously injected followed by continuous infusion at 2 mg· kg-1 · h-1 in group L.5-HD 10 mg/kg was injected intraperitoneally at 65 min before ischemia in group 5-HD.In 5-HD + L groups,5-HD 10 mg/kg was injected intraperitoneally at 65 min before ischemia and the other procedures were similar to those previously described in group L.In S and I/R groups,the animals received equal volumes of normal saline instead of lidocaine.Blood samples were obtained at 6 h of reperfusion for determination of serum creatinine (Cr) and urea mitrogen (BUN) concentrations.Bilateral kidneys were removed for determination of mitochondrial membrane potential in the renal tubular epidural cells,malondialdehyde (MDA) content,and superoxide dismutase (SOD) activity and for microscopic examination.Results Compared with group S,the serum Cr and BUN concentrations and MDA content were significantly increased,and SOD activity and mitochondrial membrane potential were decreased in I/R,L,5-HD and 5-HD + L groups (P ＜ 0.05).Compared with group I/R,the serum Cr and BUN concentrations and MDA content were significantly decreased,and SOD activity and mitochondrial membrane potential were increased in L and 5-HD + L groups (P ＜ 0.05),and no significant changes were found in the serum Cr and BUN concentrations,MDA content,SOD activity and mitochondrial membrane potential in group 5-HD (P ＞ 0.05).Compared with group L,the serum Cr and BUN concentrations and MDA content were significantly increased,and SOD activity and mitochondrial membrane potential were decreased in 5-HD + L group (P ＜ 0.05).The pathological changes were significantly reduced in group L as compared with I/R and 5-HD + L groups.Conclusion Mito-KATp channels are involved in reduction of I/R-induced renal injury by lidocaine pretreatment in rats.
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Objective To investigate the effect of lidocaine pretreatment on renal HMGB1 expression during renal ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Wistar rats weighing 300-350 g were randomly divided into 3 groups ( n=12 each):sham operation group (group S),I/R group and lidocaine pretreatment group (group L).Renal I/R was induced by occlusion of bilateral renal arteries for 60 min followed by 4 or 24 h reperfusion.Lidocaine 5 mg/kg was injected iv at 60 min prior to ischemia followed by 2 mg· kg- 1· h- 1 infusion iv for 60 min in group L.Equal volume of normal saline was given in group I/R.Six rats in each group were sacrificed at 4 or 24 h of reperfusionand their kidneys were removed for microscopic examination and for determination of SOD activity,MDA content and the expression of HMGB1 mRNA and protein.Results Compared with group S,renal HMGB1 mRNA and protein expression,MDA content were significantly increased,while SOD activity were significantly decreased in groups I/R and L( P ＜ 0.05).Compared with group I/R,renal HMGB1 mRNA and protein expression,and MDA content were significantly decreased,while SOD activity were significantly increased in group L ( P ＜ 0.05 ).Conclusion Lidocaine pretreatment can attenuate renal I/R injury in rats by down-regulating HMGB1 expression
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Objective To investigate the role of astroglial glutamate-glutamine shuttle in the development of neuropathic pain (NP) in rats. Methods Forty-eight adult male SD rats weighing 200-230 g were randomly divided into 8 groups (n =6 each): Ⅰ control group (group C);Ⅱ sham operation group (group S);group ⅢNP;Ⅳ-Ⅶ 0.01, 0.03, 0.05 and 0.10 mmol/L methionine sulfoximine (MSO, an inhibitor of glutamine synthetase (GS)) group (group M1-4 );Ⅷ MSO + glutaminate group (group MG). In group C no operation was performed. In group S the sciatic nerve was only exposed but not ligated. NP was induced by ligation of the tibial nerve and commom peroneal nerve according to the technique described by Dixon. After the establishment of the model, intrathecal PBS 50 μl was injected in group NP, IT 0.01, 0.03, 0.05 and 0.10 mmol/L MSO 50 μl was injected intrathecally in group M1-4, and 0.05 mmol/L MSO 50 μl was injected intrathecally and then 0.25 mmol/L glutamine 50 μl was injected intrathecally 15 min later in group MG. Mechanical pain threshold was measured 1 week before ligation (T0 , baseline), 1 week after ligation (T1) and 15, 30, 45 and 60 min after injection of MSO (T2-5). Then rats were killed and the lumbar segment of the spinal cord was removed for determination of the expression of glial fibrillary acidic protein (GFAP) and GS and the co-expression (GFAP/GS) in the dorsal horn.Results Mechanical pain threshold was significantly lower at T1-5 in group MG and NP and at T2-4 in group M3.4 ,and the expression of GFAP, GS and GFAP/GS was significantly higher in group MG,NP and M3 than in group S and C ( P ＜ 0.05) .Conclusion Astroglial glutamate-glutamine shuttle in the spinal cord is involved in the development of neuropathic pain in rats.
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To examine the aging-related changes of microglia and astrocytes in hypothalamus of rats after intraperitoneal injection of hypertonic saline in rats, old- and young-aged rats were injected with hypertonic saline solution into peritoneal cavity. Lectin histochemical techniques using Ricinus communis agglutinin-1 (RCA-1) and immunocytochemical method employing antibody against glial fibrillary acidic protein (GFAP) were used to demonstrate microglia and astrocytes in the hypothalamus of the rats, and the positively-stained cells were analyzed by computer-assisted image analysis system. Our results showed that the numbers of microglia and astrocytes were significantly increased in the hypothalamus of old-aged rats. After intraperitoneal injection of hypertonic saline, the number of microglia was significantly decreased in the hypothalamus of both young- and old-aged groups. After introperitoneal injection of hypertonic saline, the number of GFAP positive cells was significantly increased in the hypothalamus of young rats, but the number of GFAP positive cells did not show significant change in the hypothalamus of old rats. It is concluded that in the hypothalamus of old-aged rats, the increase of microglia may be related with the aging or degeneration of neurons, and the increase of astrocytes may provide more nourishment required by the aged neurons. The microglia and astrocytes in the hypothalamus of the two group rats may be affected by hypertonic saline, and the response of these cells to the stimuli is characterized by some aging-related changes.
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To examine the aging-related changes of microglia and astrocytes in hypothalamus of rats after intraperitoneal injection of hypertonic saline in rats, old- and young-aged rats were injected with hypertonic saline solution into peritoneal cavity. Lectin histochemical techniques using Ricinus communis agglutinin-1 (RCA-1) and immunocytochemical method employing antibody against glial fibrillary acidic protein (GFAP) were used to demonstrate microglia and astrocytes in the hypothalamus of the rats, and the positively-stained cells were analyzed by computer-assisted image analysis system. Our results showed that the numbers of microglia and astrocytes were significantly increased in the hypothalamus of old-aged rats. After intraperitoneal injection of hypertonic saline,the number of microglia was significantly decreased in the hypothalamus of both young- and oldaged groups. After introperitoneal injection of hypertonic saline, the number of GFAP positive cells was significantly increased in the hypothalamus of young rats, but the number of GFAP positive cells did not show significant change in the hypothalamus of old rats. It is concluded that in the hypothalamus of old-aged rats, the increase of microglia may be related with the aging or degeneration of neurons, and the increase of astrocytes may provide more nourishment required by the aged neurons. The microglia and astrocytes in the hypothalamus of the two group rats may be affected by hypertonic saline, and the response of these cells to the stimuli is characterized by some aging-related changes.
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To study the effect of Buyang Huanwu Decoction (BHD) on neural cell apoptosis after cerebral ischemia in gerbils and its mechanism, gerbil model with cerebral ischemia was established by clamping of bilateral carotid arteries and then reperfusion. Neural cell apoptosis of hippocampal gyrus slides was observed under electron microscope 120 hours after reperfusion. The activities of Na + -K + ATPase , Ca 2+ ATPase , Mg 2+ ATPase and NOS, and the contents of lactic acid, NO and amino acid in cerebral tissues were detected 120 hours after reperfusion. The results showed that BHD can reduce the incidence of neural cell apoptosis of hippocampal gyrus, prevent the decrease of Na + -K + ATPase and Ca 2+ ATPase activities, increase NO content and NOS activity, and reduce cerebral glucose content. It is indicated that BHD can counteract neural cell apoptosis after cerebral ischemia in gerbils and its mechanism may be related to the improvement of cerebral energy metabolism, regulation of NO synthesis and antagonism of toxic effect of excitatory amino acid.