中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
2期
174-177
,共4页
白惠萍%彭云水%王倩%吴川%刘飞飞%刘朋%郭跃先%王秀丽
白惠萍%彭雲水%王倩%吳川%劉飛飛%劉朋%郭躍先%王秀麗
백혜평%팽운수%왕천%오천%류비비%류붕%곽약선%왕수려
糖尿病%巴氯芬%神经痛%谷氨酸%兴奋性突触后电位%脊髓%神经元
糖尿病%巴氯芬%神經痛%穀氨痠%興奮性突觸後電位%脊髓%神經元
당뇨병%파록분%신경통%곡안산%흥강성돌촉후전위%척수%신경원
Diabetes mellitus%Baclofen%Neuralgia%Glutamic acid%Excitatory postsynaptic potentials%Spinal cord%Neurons
目的 评价糖尿病因素对巴氯芬抑制神经痛大鼠脊髓谷氨酸能神经元突触后电流(mEPSCs)的影响.方法 雄性SD大鼠30只,4周龄,体重150 ~ 170 g,采用随机数字表法,将其分为2组(n=15):对照组(C组)和糖尿病神经痛组(D组).D组腹腔注射链脲佐菌素50 mg/kg制备大鼠糖尿病神经痛模型,C组腹腔注射等容量生理盐水.腹腔注射后28 d时空腹血糖>16.7 mmol/L且机械痛阈<4g为模型制备成功.随后处死大鼠取脊髓,制备脊髓薄片,采用全细胞膜片钳技术记录脊髓神经元谷氨酸能mEPSCs,每组分别记录20个神经元.细胞封接后稳定5 min,灌流液中通过微量泵加入巴氯芬,终浓度分别为1、10、20、50 μmol/L,每两个浓度间隔5 min.于给药前、给药后即刻和洗脱后5 min分别记录神经元谷氨酸能mEPSCs的频率和强度,计算巴氯芬对神经元谷氨酸能mEPSCs的抑制率.结果 与C组比较,D组各浓度下神经元谷氨酸能mEPSCs频率增加,抑制率降低(P<0.05),强度差异无统计学意义(P>0.05).结论 糖尿病因素降低了巴氯芬对大鼠神经痛的镇痛效应,与抑制脊髓谷氨酸能神经元mEPSCs有关.
目的 評價糖尿病因素對巴氯芬抑製神經痛大鼠脊髓穀氨痠能神經元突觸後電流(mEPSCs)的影響.方法 雄性SD大鼠30隻,4週齡,體重150 ~ 170 g,採用隨機數字錶法,將其分為2組(n=15):對照組(C組)和糖尿病神經痛組(D組).D組腹腔註射鏈脲佐菌素50 mg/kg製備大鼠糖尿病神經痛模型,C組腹腔註射等容量生理鹽水.腹腔註射後28 d時空腹血糖>16.7 mmol/L且機械痛閾<4g為模型製備成功.隨後處死大鼠取脊髓,製備脊髓薄片,採用全細胞膜片鉗技術記錄脊髓神經元穀氨痠能mEPSCs,每組分彆記錄20箇神經元.細胞封接後穩定5 min,灌流液中通過微量泵加入巴氯芬,終濃度分彆為1、10、20、50 μmol/L,每兩箇濃度間隔5 min.于給藥前、給藥後即刻和洗脫後5 min分彆記錄神經元穀氨痠能mEPSCs的頻率和彊度,計算巴氯芬對神經元穀氨痠能mEPSCs的抑製率.結果 與C組比較,D組各濃度下神經元穀氨痠能mEPSCs頻率增加,抑製率降低(P<0.05),彊度差異無統計學意義(P>0.05).結論 糖尿病因素降低瞭巴氯芬對大鼠神經痛的鎮痛效應,與抑製脊髓穀氨痠能神經元mEPSCs有關.
목적 평개당뇨병인소대파록분억제신경통대서척수곡안산능신경원돌촉후전류(mEPSCs)적영향.방법 웅성SD대서30지,4주령,체중150 ~ 170 g,채용수궤수자표법,장기분위2조(n=15):대조조(C조)화당뇨병신경통조(D조).D조복강주사련뇨좌균소50 mg/kg제비대서당뇨병신경통모형,C조복강주사등용량생리염수.복강주사후28 d시공복혈당>16.7 mmol/L차궤계통역<4g위모형제비성공.수후처사대서취척수,제비척수박편,채용전세포막편겸기술기록척수신경원곡안산능mEPSCs,매조분별기록20개신경원.세포봉접후은정5 min,관류액중통과미량빙가입파록분,종농도분별위1、10、20、50 μmol/L,매량개농도간격5 min.우급약전、급약후즉각화세탈후5 min분별기록신경원곡안산능mEPSCs적빈솔화강도,계산파록분대신경원곡안산능mEPSCs적억제솔.결과 여C조비교,D조각농도하신경원곡안산능mEPSCs빈솔증가,억제솔강저(P<0.05),강도차이무통계학의의(P>0.05).결론 당뇨병인소강저료파록분대대서신경통적진통효응,여억제척수곡안산능신경원mEPSCs유관.
Objective To evaluate the effect of diabetes on baclofen-induced inhibition of miniature excitatory postsynaptic currents (mEPSCs) in spinal glutamatergic neurons in rats with neuropathic pain.Methods Thirty male Sprague-Dawley rats,aged 4 weeks,weighing 150-170 g,were randomly divided into 2 groups (n=15 each group):control group (C group) and diabetic neuropathic pain group (D group).Diabetic neuropathic pain was induced by intraperitoneal injection of streptozotocin 50 mg/kg and confirmed 28 days later by blood glucose > 16.7 mmol/L and pain threshold < 4 g in group D,while the rats received the equal volume of normal saline in C group.The animals were anesthetized with intraperitoneal 10% chloral hydrate 50 mg/kg.The rats were then sacrificed and lumbar segments (L1.5) of the spinal cord were removed for slice preparations.Glutamatergic mEPSCs in lamina Ⅱ neurons were recorded by using whole-cell patch-clamp technique and 20 neurons located in lamina Ⅱ of the spinal cord were recorded in each group.The cells stabilized for 30 min after sealing,and then baclofen with the final concentrations of 1,10,20,50 μmol/L was added to the perfusion solution at 5 min intervals followed by washout.The frequency and intensity of glutamatergic mEPSCs were recorded immediately before and after administration and at 5 min after washout.The inhibitory effect of baclofen on glutamatergic mEPSCs was measured and the inhibitory rate was calculated.Results Compared with group C,the frequency of glutamatergic mEPSCs was significantly increased and the inhibitory rate was decreased under each concentration (P < 0.05),and no significant change was found in the intensity of mEPSCs under each concentration in D group (P > 0.05).Conclusion Diabetes decreases baclofen-induced analgesic effect in rats with neuropathic pain,which is related to inhibition of mEPSCs in spinal glutamatergic neurons.