切口痛大鼠脑干嘴端腹内侧髓质谷氨酸和γ-氨基丁酸释放的动态变化

目的 探讨切口痛大鼠脑干嘴端腹内侧髓质谷氨酸和γ-氨基丁酸释放的动态变化.方法 雄性SD大鼠,体重250～300 g,麻醉下于右侧脑干嘴端腹内侧髓质内置入微透析导引管.恢复5 d后,选择12只无神经行为学障碍的大鼠,随机分为2组(n=6):A组仅吸入1.2%异氟醚5 min;B组吸入1.2%异氟醚5 min,同时制备右足底切口痛模型.分别于术前(基础状态)、术后3 h、1 d、2 d、3 d时收集微透析液20 μl,采用高压液相法测定微透析液内谷氨酸和γ-氨基丁酸浓度,各神经递质的释放水平以各时点测定值与基础值的百分数表示.结果 与基础值比较,B组术后1 d时谷氨酸的释放水平升高(P<0.01),术后2.3 d时谷氨酸的释放水平差异无统计学意义(P>0.05),术后3 h、1 d、2 d.3 d时7.氨基丁酸的释放水平升高(P<0.01);与A组比较,B组术后1 d时谷氨酸的释放水平升高,术后3 h、1 d.2 d.3 d时γ-氨基丁酸的释放水平升高(P<0.01).结论 大鼠术后脑干嘴端腹内侧髓质谷氨酸和γ-氨基丁酸的释放增加,可能改变了下行疼痛调控通路的功能.     

异丙酚对大鼠不同脑区兴奋性和抑制性氨基酸类神经递质释放的影响

目的 评价异丙酚对大鼠皮质区、丘脑区、海马区和纹状体区兴奋性和抑制性氨基酸类神经递质释放的影响,探讨异丙酚麻醉的中枢机制.方法 Wistar大鼠12只,雌雄各半,体重300～350 g,麻醉后参照Paxinos和Waston定位图谱按照不同脑区坐标预埋微透析探针套管,恢复4 d后,随机分为2组(n=6):对照组和异丙酚组,分别尾静脉输注生理盐水6 ml/kg和异丙酚120 mg·kg-1·h-1,1 h后收集微透析液,采用高效液相色谱-电化学法测定微透析液中氨基酸类神经递质(谷氨酸、天冬氨酸、γ-氨基丁酸和甘氨酸)浓度.结果 与对照组比较,异丙酚组各脑区谷氨酸、天冬氨酸水平降低,γ-氨基丁酸、甘氨酸水平升高(P<0.05或0.01).结论 异丙酚抑制大鼠不同脑区(皮质区、丘脑区、海马区和纹状体区)兴奋性氨基酸类神经递质释放而增强抑制性氨基酸类神经递质释放,可能是其麻醉的中枢机制之一.     

曲马多预先给药对切口痛大鼠背根神经节神经生长因子表达的影响

目的 探讨曲马多预先给药对切口痛大鼠背根神经节神经生长因子(NGF)表达的影响.方法 雄性SD大鼠24只,体重200～250 g,随机分为4组(n=6),对照组(C组)仅给予麻醉及腹腔注射生理盐水5 ml;切口痛组(I组)于术前30 min腹腔注射生理盐水5 ml;曲马多1 mg/kg预先给药组(T1组)和曲马多10 mg/kg预先给药组(T10组)分别于术前30 min腹腔注射曲马多1、10 mg/kg.制备大鼠右后爪切口痛模型,T1组和T10组大鼠苏醒后采用累积疼痛评分法评定痛行为学,于术前30 min和术后2 h测定大鼠机械痛阈、热痛阈及右侧背根神经节NGF的表达水平.结果 与C组比较,I组、T1组术后2 h机械痛阈和热痛阈降低,累积疼痛评分升高,背根神经节NGF表达上调,T10组背根神经节NGF表达上调(P＜0.05或0.01);与I组比较,T1组和T10组术后2 h机械痛阈和热痛阈升高,累积疼痛评分降低,背根神经节NGF表达下调(P＜0.05);与T1组比较,T10组术后2 h机械痛阚和热痛阈升高,累积疼痛评分降低(P＜0.05或0.01),背根神经节NGF表达差异无统计学意义(P＞0.05).结论 曲马多1、10 mg/kg腹腔内预先给药均可下调切口痛大鼠背根神经节NGF表达水平.     

丙泊酚对大鼠不同脑区氨基酸类递质的影响

目的 观察丙泊酚麻醉下大鼠不同脑区氨基酸类神经递质水平的变化,探讨丙泊酚麻醉中枢作用的可能机制.方法 12只大鼠随机分为丙泊酚组和对照组,按照不同的坐标预埋微透析探针,分别持续静注丙泊酚和生理盐水60 min.收集微透析液样品,用高效液相色谱-电化学法测定氨基酸类递质含量.结果 实验大鼠各脑区谷氨酸(Glu)、天冬氨酸(Asp)、γ-氨基丁酸(GABA)、甘氨酸(Gly)的分布存在较大差异,丙泊酚组皮质、海马、丘脑Glu、Asp含量较对照组显著下降(P<0.01),纹状体区也下降明显(P<0.05);而皮质、海马、丘脑、纹状体GABA、Gly含量则明显升高(P<0.01).结论 丙泊酚对大鼠中枢神经系统氨基酸类递质有不同程度的影响,抑制兴奋性氨基酸突触传递而增强抑制性氨幕酸突触传递可能是其中枢作用的机制之一.     

Stargazin在切口痛大鼠脊髓背角GluR1-AMPA受体胞浆至胞膜转运中的作用

目的 评价Stargazin在切口痛大鼠脊髓背角含谷氨酸受体1亚基的使君子酸(GluR1-AMPA)受体胞浆至胞膜转运中的作用.方法 成年雄性清洁级SD大鼠45只,体重280 ～ 300 g,6～8周龄,采用随机数字表法,将其分为5组:正常对照组(C组)、假手术组(S组)、切口痛+生理盐水组(P组)、切口痛+ Stargazin小干扰RNA(siRNA)组(I组)和切口痛+Stargazin无意义siRNA组(N组).P组、I组和N组分别鞘内注射生理盐水10μl、20 μmol/L siRNA、20μmol/L无意义siRNA 10μl,2次/d,连续3d,4d后制备右足底切口痛模型.切口痛术后3h时测定大鼠累计痛评分(CPS)和机械缩足阈(PWT).然后处死大鼠,取L3-6节段脊髓背角,采用Westem blot法检测胞浆和胞膜GluR1和GluR2亚基表达,采用免疫共沉淀技术检测脊髓背角Stargazin与GluR1或GluR2亚基的共表达.结果 与C组比较,P组和N组CPS评分升高,PWT降低,脊髓背角胞浆GluR1表达下调,脊髓背角胞膜GluR1表达上调,I组CPS评分升高(P＜0.05或0.01);与P组比较,I组CPS评分降低,PWT升高,脊髓背角胞浆GluR1表达上调,脊髓背角胞膜GluR1表达下调,脊髓背角Stargazin和Stargazin与GluR1共表达下调(P＜ 0.05或0.01).结论 Stargazin介导了切口痛大鼠GluR1-AMPA受体从胞浆至胞膜转运.     

黑皮质素4型受体在大鼠脊髓星形胶质细胞释放兴奋性氨基酸中的作用

目的 探讨黑皮质素4型受体(MC4R)在大鼠脊髓星形胶质细胞释放兴奋性氨基酸中的作用.方法 原代培养大鼠脊髓星形胶质细胞,随机分为3组,每组6孔:正常白对照组(C组)、T组和TH组.C组未作任何处理,T组加入终浓度为10μg/L的TNF-α;TH组同时加入终浓度为10μg/L的TNF-α和终浓度为1 μmol/L的MC4R特异性阻断剂HS014.各组孵育3 h后采用高效液相-串联四级杆质谱法检测上清液谷氨酸(Glu)和天门冬氨酸(Asp)的浓度.结果 与C组比较,T组Glu和Asp浓度升高(P＜0.01),TH组Glu和Asp浓度差异无统计学意义(P＞0.05);与T组比较,TH组Glu和Asp浓度降低(P＜0.01).结论 MC4R介导了大鼠脊髓星形胶质细胞释放兴奋性氨基酸的作用.     

持续性术后痛大鼠脊髓星形胶质细胞的活化

目的 探讨持续性术后痛大鼠脊髓背角星形胶质细胞的活化.方法 成年雄性SD大鼠48只,体重200～250 g,随机分为2组(n=24):假手术组和模型组.模型组采用皮肤肌肉切口牵拉术制备持续性术后痛模型,假手术组仅暴露内收肌,不牵拉皮肤肌肉组织.分别于模型制备前(基础状态)、制备后1、3、12、22和32 d时测定大鼠机械缩足阈值(MWT).各时点MWT测定结束后随机取4只大鼠,处死后采用免疫组织荧光法测定脊髓胶质纤维酸性蛋白(GFAP)的表达水平.结果 与基础值比较,假手术组各时点MWT和脊髓GFAP表达水平差异无统计学意义(P＞0.05),模型组模型制备后1～22 d MWT降低,12 d时最低,模型制备后3～22 d脊髓GFAP表达上调,12 d时达峰值(P＜0.05或0.01);与假手术组比较,模型组MWT降低,脊髓GFAP表达上调(P＜0.05).结论 大鼠持续性术后痛与脊髓星形胶质细胞的活化有关.     

脊髓NF-κB信号通路在大鼠持续性术后痛中的作用

目的 评价脊髓NF-κB信号通路在大鼠持续性术后痛中的作用.方法 选择鞘内置管成功的成年雄性SD大鼠90只,体重200～250 g,采用随机数字表法,将其随机分为3组(n=30):假手术组(S组)、持续性术后痛组(SMIR组)和吡咯烷二硫代氨基甲酸盐组(PDTC组).SMIR组和PDTC组采用皮肤/肌肉切口牵拉法制备大鼠持续性术后痛模型;S组仅分离暴露肌肉,未牵拉.术后1d时开始,PDTC组于30s内鞘内注射NF-KB抑制剂PDTC 10 ng,S组和SMIR组鞘内注射等容量生理盐水,1次/d,连续7d.于术前1 d(T0)、术后1 d(T1)、3 d(T2)、7 d(T3)、12 d(T4)和22 d(T5)时,测定机械缩足反应阈值(MWT);各时点MWT测定结束后,随机取5只大鼠,断头处死后取脊髓组织,采用ELISA法测定TNF-α含量.结果 与S组比较,T1-5时SMIR组MWT降低,T2时PDTC组MWT降低,T3-5时SMIR组和PDTC组脊髓TNF-α含量升高(P＜0.05或0.01);与SMIR组比较,T2-5时PDTC组MWT升高,T3.4时脊髓TNF-α含量降低(P＜0.05或0.01).结论 脊髓NF-κB信号通路参与了大鼠持续性术后痛的发生发展.     

鞘内吗啡对切口疼痛模型大鼠脊髓背角P物质的影响

目的研究鞘内(IT)吗啡对切口疼痛模型大鼠脊髓背角P物质(SP)的影响.方法雄性SD大鼠16只,随机分为四组(每组4只)假手术组(组Ⅰ)、术前30min IT 0.9%氯化钠20μl组(对照组,组Ⅱ)、术后30min IT吗啡5μg组(组Ⅲ)和术前30min IT吗啡5μg组(组Ⅳ).按Brennan法制成切口疼痛模型,以累积疼痛评分确定疼痛行为.免疫组织化学方法观察脊髓背角SP免疫反应(SP-LI).结果组Ⅲ和组Ⅳ大鼠的累积疼痛评分均明显低于组Ⅱ(P＜0.01).组Ⅱ大鼠术侧脊髓背角浅层SP-LI物质积分光密度明显高于组Ⅰ及对侧(对照组0.62±0.07,假手术组0.40±0.09,P＜0.01);与组Ⅱ比较,组Ⅳ的大鼠术侧脊髓背角浅层SP-LI物质积分光密度(0.37±0.06)明显降低(P＜0.01),但两用药组间比较无显著差别.结论在大鼠切口疼痛模型中,术前IT吗啡的抗伤害作用与其抑制SP在脊髓背角的释放有关.     

一氧化氮在神经病理性痛大鼠脊髓敏化中的作用

目的 评价一氧化氮(NO)在神经病理性痛大鼠脊髓敏化中的作用.方法 成年雄性Wistar大鼠32只,体重200～300 g,随机分为4组(n=8):假手术组(S组)、假手术预先给药组(S-N组)、坐骨神经慢性压迫性损伤(CCI)组和CCI预先给药组(CCI-N组).建立CCI致神经病理性痛模型,S-N组和CCI-N组分别于模型制备前鞘内注射10 μl(250 μg)NC-硝基-L-精氨酸-甲基酯,分别于术前和术后3 d测定热痛阈,于术后4、7 d各处死4只大鼠,取L4,5脊髓,测定脊髓背角磷酸化环磷酸腺苷反应元件结合蛋白(pCREB)表达水平.结果 各组术后3 d热痛阈较基础值均降低(P＜0.05);与S组和S-N组比较,CCI组热痛阈降低,脊髓背角pCREB表达上调(P＜0.05),CCI-N组上述指标差异无统计学意义(P＞0.05);与CCI组比较,CCI-N组热痛阈升高,脊髓背角pCREB表达下调(P＜0.05).结论 NO参与神经病理性痛大鼠脊髓敏化,其作用机制与促进脊髓背角pCREB释放有关.     

Activity of the descending noradrenergic pathway after surgery in rats

Background: Previous studies have shown that activation of the descending noradrenergic inhibition pathway results in analgesia after surgery. However, the time course of activity of the descending noradrenergic pathway after surgery has not been examined previously. Here, we investigated the spinal release of noradrenaline (NA) in the post‐operative period in a freely moving rat model of incisional pain. Methods: Loop microdialysis catheters were implanted subarachnoidally via the atlanto‐occipital membrane in Sprague–Dawley rats. Twelve healthy rats without neural deficits were divided into two groups, Group A and Group B, following 5 days of recovery. A plantar incision in the right hind paws of rats in Group A was performed under 1.2% isoflurane. All rats in Group B were only anesthetized by 1.2% isoflurane for the same duration. The microdialysate samples for NA determination were collected before anesthesia, 3 h and 1, 2 and 3 days after incision (or isoflurane anesthesia in Group B) in both groups. The cumulative pain scores were assessed at the above time points. Results: The spinal release of NA increased gradually, peaked at 2 days after the incision and remained at the peak level up to the third day after the incision. The cumulative pain scores peaked 3 h after the incision, and gradually decreased afterwards and returned to the baseline values 3 days after the incision. Conclusions: The descending NA tone might be apparently more active in the post‐operative period. The descending noradrenergic inhibitory pathway plays an important role in post‐operative neuroplasticity.     

右美托咪啶对切口痛大鼠中脑导水管去甲肾上腺素释放的影响

目的 探讨右美托咪啶对切口痛大鼠中脑导水管去甲肾上腺素(NE)释放的影响.方法 成功植入微透析系统的雄性Wistar大鼠24只,采用随机数字表法,将大鼠随机分为4组(n=6),对照组(C组):腹腔注射0.9%生理盐水2 ml,15 min后吸入2%异氟醚;切口痛组(IP组):腹腔注射0.9%生理盐水2 ml,15 min后制备切口痛模型;D组:腹腔注射右美托咪啶30 μg/kg,15 min后制备切口痛模型;拮抗组(DY组):腹腔注射右美托咪啶30 μg/kg和育亨宾0.5 mg/kg,15 min后制备切口痛模型.除DY组外,其余各组于术前30 min(基础状态)、术后4 h内每30 min收集微透析液10μl,DY组于术前30 min、术后30、60 min时收集微透析液,采用高效液相色谱仪和电化学检测器测定微透析液NE浓度;DY组于术前30 min(基础状态)、术后1 h,其余各组于术前30 min(基础状态)、术后1、2、3、4h时测定机械缩足反应阈值(MWT).结果 与C组比较,IP组和DY组术后MWT降低,微透析液NE浓度升高,D组术后微透析液NE浓度升高(P＜0.05),MWT差异无统计学意义(P＞0.05);与IP组比较,D组和DY组术后MWT升高,微透析液NE浓度降低(P＜0.05);与D组比较,DY组术后MWT降低,微透析液NE浓度升高(P＜0.05).结论 右美托咪啶可抑制切口痛大鼠中脑导水管NE的释放,从而产生中枢镇痛作用.

Abstract：

Objective To investigate the effect of dexmedetomidine on norepinephrine(NE)release in midbrain periaqueductal gray(PAG)in a rat model of incisional pain.Methods Twenty-four male Wistar rats in which microdialvsis catheter was successfully placed in the ventrolateral region of PAG without complications were randomly divided into 4 groups(n=6 each):group control(group C);group incisional pain(group IP);group dexmetomidine(group D)and group dexmedetomidine+yohimbine(group DY).Incisional pain was induced by an incision made into the plantar surface of left hindpaw in IP,D,DY groups.Dexmedetomidine 30 μg/kg and dexmedetomidine 30 μg/kg+yohimbine 0.5 mg/kg were given intraperitoneally at 15 min before plantar incision in group D and group DY respectively.Mechanical paw withdrawal threshold(MWT)to von Frey filament stimulation was measured at 30 min before(baseline)and 1,2,3,4 h after operation in C,IP,D groups,and at 30 min before(baseline),and 1 h after operation in group DY.Dialysate samples were collected at 30 min before(baseline)and at evcry 30 min after operation for 4 h via cerebral microdialysis catheter for determination of the NE concentration in C,IP,D groups,and at 30 min before(baseline),30,60 min after operation in group DY.Results Incisional pain significantly decreased MWT and increased the NE concentration in dialysate in group IP.Dexmedetomidine premedication significantly inhibited mechanical hyperalgesia and attenuated incisional pain-induced increase in the NE concentration in dialysate in group D.Yohimbine counteracted effects of dexmedetomidine.Conclusion Dexmedetomidine has analgesic effect though inhibition of NE release from PAG.     

异氟烷对大鼠皮层、海马及脊髓氨基酸类递质的影响

目的 通过观察异氟烷对大鼠皮层、海马及脊髓氨基酸类递质含量的影响，从在体水平探讨异氟烷麻醉作用的可能机制。方法 16只SD大鼠随机分2组，A组吸入1MAC异氟烷30min后，取皮质、海马及脊髓并测定其递质含量。B组除不吸异氟烷外均同A组。结果 与B组比，A组皮层、海马的Asp、Glu含量降低；而海马、脊髓的Gly含量则增高。结论 异氟烷可能通过抑制中枢系统兴奋性氨基酸突触传递增强抑制性氨基酸突触传导而产生麻醉应用。     

Effect of pretreatment with intrathecal excitatory amino acid receptor antagonists on the development of pain behavior caused by plantar incision

BACKGROUND: Drugs that block spinal excitatory amino acid receptor activation may prevent pain after surgery. The authors previously studied the effect of excitatory amino acid receptor antagonists after incision. In the present study, we examined the role of N-methyl-d-aspartate (NMDA), non-NMDA, and metabotropic glutamate receptors (mGluRs) on the development of pain behavior after plantar incision. METHODS: Rats with lumbar intrathecal catheters were anesthetized with halothane. Fifteen minutes before an incision was made, drug [40 nmol MK-801; 20 nmol NBQX; or 200 nmol (+)-MCPG] or vehicle was injected intrathecally followed by an infusion of the same drug for 75 min. Withdrawal thresholds to calibrated von Frey filaments applied adjacent to the wound and response frequencies to a blunt mechanical stimulus applied directly to the wound were measured before incision and 1, 2, 4, and 6 h after incision and then once daily for 6 days. RESULTS: Preincision treatments with antagonists against the NMDA (MK-801) and group I and II metabotropic receptors [(+)-MCPG] did not inhibit the development of mechanical hyperalgesia caused by incision. Preincision treatment with the non-NMDA receptor antagonist NBQX increased withdrawal thresholds at 1 and 2 h and on postoperative day 1 compared with the vehicle group; response frequencies were reduced 1 and 2 h after incision and on postoperative day 2 (P < 0.05). In an additional group, postincision treatment with NBQX was similar to preincision treatment. CONCLUSION: Spinal NMDA and mGluR antagonists may not be useful for preventing postsurgical pain. Spinal non-NMDA receptor antagonists reduced pain behaviors, but a preventive effect using preincision treatment was not apparent.     

Effects of mild hypothermia on the cortical release of excitatory amino acids and nitric oxide synthesis following hypoxia

Studies concerning neurotransmitter release following cerebral hypoxia are scarce, and the effects of mild hypothermia on hypoxia-induced neurotransmitter release are unknown. The purpose of this study was to investigate changes in excitatory amino acid (EAA) concentrations and nitric oxide (NO) synthesis following cerebral hypoxia in rats, and the effects of mild hypothermia on both. Cerebral hypoxia (PaO2, 30-40 mm Hg) was induced in each rat for 60 min. Cerebral blood flow (CBF) was measured by laser-Doppler flowmetry, and the extracellular concentrations of EAAs and NO end-products (nitrite and nitrate) were measured by in vivo microdialysis in normothermic (37 degrees C) and hypothermic (32 degrees C) rats. In both groups, CBF showed modest increases during hypoxia and returned to baseline during reoxygenation. The EAA levels of the normothermic rats increased markedly after hypoxia induction and returned to baseline levels during reoxygenation. Hypothermia abolished these increases completely. The NO end-product levels under normothermic conditions declined slightly during hypoxia, and then increased transiently during reoxygenation. Hypothermia appeared to attenuate the NO end-product level and to delay the peak. When the relationship between glutamate and the NO end-products was examined on an individual-animal basis, glutamate release did not parallel NO synthesis. The results indicate that hypothermic neuroprotection during cerebral hypoxia may be attributable to the amelioration of damage by reduction of presynaptic EAA release. Although it is unclear from the present results alone whether endothelial NO synthase, neuronal NO synthase or both caused the elevation of the NO end-products during reoxygenation, it is possible that the attenuation and delay of the peak of the NO end-product level plays a role in protection from NO-induced neuronal damage.     

Nerve Growth Factor Expression after Plantar Incision in the Rat

Background: Postoperative pain control remains a significant problem. Advances will proceed if we can further reveal the underlying mechanisms of incisional pain and its mediators. Previous studies have demonstrated that nerve growth factor (NGF) is released in incised tissue and contributes to hyperalgesia in incisional pain. The purpose of this study is to examine the expression of NGF in skin after planter incision.

Methods: Adult Sprague-Dawley rats underwent incision at the plantar aspect of hind paw. The NGF messenger RNA (mRNA) was measured at various times after incision by polymerase chain reaction. NGF protein expression was detected by Western blot and immunohistochemistry in incisions.

Results: NGF mRNA increased from 2 to 4 h after incision and was the same as control by postoperative day 1. A large-molecular-weight form of NGF, approximately 75 kd, was found in normal skin. The large-molecular-weight NGF protein increased 4 h after incision and returned to baseline on postoperative day 7. The skin immediately adjacent to the incision had the greatest NGF expression. Immunohistochemical staining for NGF was present adjacent to the incision and localized in Schwann cells and axons.     

术中静脉输注氨基酸对犬糖代谢的影响

目的 探讨术中静脉输注氨基酸对犬糖代谢的影响.方法 健康成年杂种犬36只,雌雄不拘,体重12～16 kg,全麻下行小肠部分切除术,随机分为4组(n=9):对照组(C组)静脉输注0.9%生理盐水,A1组、A2组和A3组分别于切皮前即刻至术毕静脉输注2.85%、5.70%、11.4%18-氨基酸溶液12 ml·kg-1·h-1.于麻醉前、麻醉诱导后15 min、手术15 min、30 min、1 h、关腹即刻、术后1、2、4、8、24 h时分别抽右股静脉血3 ml,测定血糖、乳酸、胰岛素和胰高血糖素浓度;于麻醉诱导后15 min、关腹即刻、术后24 h时行左后下肢外侧近端肌肉活检,测定肌糖原含量;于关腹即刻、术后24 h时行肝活检,测定肝糖原含量,采用Homa指数估计胰岛素抵抗程度.结果 与麻醉前比较,各组麻醉诱导后15 min至术后24 h时血糖升高,C组术后1 h至24 h时血胰岛素浓度升高,A1组、A2组和A3组手术15 min至术后24 h时血胰岛素浓度升高(P<0.05);与C组比较,A3组麻醉诱导后15 min至术后24 h时血糖升高,A1组关腹即刻、A2组手术15 min及关腹即刻、A3组手术15 min至术后4 h时血胰岛素浓度升高,A2组关腹即刻、A3组手术15 min至术后2 h时Homa指数升高(P<0.05).各组血乳酸浓度及胰高血糖素浓度比较差异无统计学意义(P0.05);组间比较肝糖原、肌糖原含量差异无统计学意义(P0.05).结论 术中静脉输注氨基酸可升高犬血胰岛素浓度,但不抑制糖原分解;低、中剂量氨基酸对血糖无明显影响,术中静脉输注高剂量氨基酸后胰岛素抵抗程度加重,血糖升高.     

Nerve growth factor expression after plantar incision in the rat

BACKGROUND: Postoperative pain control remains a significant problem. Advances will proceed if we can further reveal the underlying mechanisms of incisional pain and its mediators. Previous studies have demonstrated that nerve growth factor (NGF) is released in incised tissue and contributes to hyperalgesia in incisional pain. The purpose of this study is to examine the expression of NGF in skin after planter incision. METHODS: Adult Sprague-Dawley rats underwent incision at the plantar aspect of hind paw. The NGF messenger RNA (mRNA) was measured at various times after incision by polymerase chain reaction. NGF protein expression was detected by Western blot and immunohistochemistry in incisions. RESULTS: NGF mRNA increased from 2 to 4 h after incision and was the same as control by postoperative day 1. A large-molecular-weight form of NGF, approximately 75 kd, was found in normal skin. The large-molecular-weight NGF protein increased 4 h after incision and returned to baseline on postoperative day 7. The skin immediately adjacent to the incision had the greatest NGF expression. Immunohistochemical staining for NGF was present adjacent to the incision and localized in Schwann cells and axons. CONCLUSION: NGF mRNA is increased and a large-molecular-weight form of NGF protein is expressed in the region adjacent to the incision. NGF immunoreactivity is present in nerve bundles; both Schwann cells and axons are labeled. Immunoreactive NGF in axons is likely taken up into cut axons. This study suggests some common mechanisms for neuropathic and incisional pain.