中国临床药理学杂志
中國臨床藥理學雜誌
중국림상약이학잡지
THE CHINESE JOURNAL OF CLINICAL PHARMACOLOGY
2014年
7期
611-614
,共4页
于婵娟%蒋晖%黄春阳%刘亚华
于嬋娟%蔣暉%黃春暘%劉亞華
우선연%장휘%황춘양%류아화
依托咪酯%海马%动作电位%离子通道%全细胞电流钳技术
依託咪酯%海馬%動作電位%離子通道%全細胞電流鉗技術
의탁미지%해마%동작전위%리자통도%전세포전류겸기술
etomidate%hippocampus%action potential%ion channel%current clamp technique
目的:研究依托咪酯对大鼠海马CA1区胞体动作电位及配体门控离子通道的影响。方法40只雄性大鼠快速断头,取出海马组织并用切片机切出400μm厚度的海马脑片,随机平分为4组:脂肪乳剂组(空白组)、依托咪酯组(对照组)和2个实验组(依托咪酯+DIDS组与依托咪酯+四乙铵组)。用全细胞电流钳技术给予不同强度的刺激,记录各组在不同刺激强度下对大鼠海马CA1区神经元动作电位发放的情况。结果脂肪乳剂不影响胞体动作电位的频率和幅值。10μmol· L-1依托咪酯脂肪乳剂能明显减少胞体动作电位的数目,同时动作电位的幅值也减小;逐渐增大刺激的强度,胞体动作电位产生的个数会相应地增加,但幅值无明显变化。 DIDS+依托咪酯组在20 min后减少动作电位数目,且随着刺激强度的增加,动作电位衰减的时间逐渐延长。加入K+通道阻滞剂(四乙胺)后,不影响依托咪酯对动作电位产生的抑制。结论依托咪酯脂肪乳剂抑制神经元动作电位发放的作用,可能主要通过开放氯通道、增加氯离子内流来实现;而钾通道对依托咪酯的抑制作用影响轻微。
目的:研究依託咪酯對大鼠海馬CA1區胞體動作電位及配體門控離子通道的影響。方法40隻雄性大鼠快速斷頭,取齣海馬組織併用切片機切齣400μm厚度的海馬腦片,隨機平分為4組:脂肪乳劑組(空白組)、依託咪酯組(對照組)和2箇實驗組(依託咪酯+DIDS組與依託咪酯+四乙銨組)。用全細胞電流鉗技術給予不同彊度的刺激,記錄各組在不同刺激彊度下對大鼠海馬CA1區神經元動作電位髮放的情況。結果脂肪乳劑不影響胞體動作電位的頻率和幅值。10μmol· L-1依託咪酯脂肪乳劑能明顯減少胞體動作電位的數目,同時動作電位的幅值也減小;逐漸增大刺激的彊度,胞體動作電位產生的箇數會相應地增加,但幅值無明顯變化。 DIDS+依託咪酯組在20 min後減少動作電位數目,且隨著刺激彊度的增加,動作電位衰減的時間逐漸延長。加入K+通道阻滯劑(四乙胺)後,不影響依託咪酯對動作電位產生的抑製。結論依託咪酯脂肪乳劑抑製神經元動作電位髮放的作用,可能主要通過開放氯通道、增加氯離子內流來實現;而鉀通道對依託咪酯的抑製作用影響輕微。
목적:연구의탁미지대대서해마CA1구포체동작전위급배체문공리자통도적영향。방법40지웅성대서쾌속단두,취출해마조직병용절편궤절출400μm후도적해마뇌편,수궤평분위4조:지방유제조(공백조)、의탁미지조(대조조)화2개실험조(의탁미지+DIDS조여의탁미지+사을안조)。용전세포전류겸기술급여불동강도적자격,기록각조재불동자격강도하대대서해마CA1구신경원동작전위발방적정황。결과지방유제불영향포체동작전위적빈솔화폭치。10μmol· L-1의탁미지지방유제능명현감소포체동작전위적수목,동시동작전위적폭치야감소;축점증대자격적강도,포체동작전위산생적개수회상응지증가,단폭치무명현변화。 DIDS+의탁미지조재20 min후감소동작전위수목,차수착자격강도적증가,동작전위쇠감적시간축점연장。가입K+통도조체제(사을알)후,불영향의탁미지대동작전위산생적억제。결론의탁미지지방유제억제신경원동작전위발방적작용,가능주요통과개방록통도、증가록리자내류래실현;이갑통도대의탁미지적억제작용영향경미。
Objective To study the effect of etomidate emulsion on ac-tion potential and ligand -gated ion channel of hippocampal CA 1.Methods Forty male rats were decollated quickly , and then the hippo-campus were taken out and cut into 400 μm thickness of hippocampus slices using the slicing machine.The slices were divided into 4 groups randomly:lipid emulsion group ( n =10 ); etomidate group ( n =10 );etomidate+DIDS(4,4′-diisothiocyanato-2,2′-stilbenedisulfonic acid disodium salt hydrate ) group ( n=10 ) and etomidate+TEA ( tetraethyl-ammonium) group (n=10).The 4 groups were given lipid emulsion ,eto-midate,etomidate +DIDS ( Cl - channel blocker ) and etomidate +TEA ( K +channel blocker ) , respectively.Different stimulus intensities were give by current clamp technique and the impact of action potential firing were recorded.Results Intralipid did not change the number or ampli-tude of action potential.As the time incubated by etomidate was post-poned , the sum and amplitude of action potential in the soma of the hipp-ocampal CA1 neurons obviously reduced.When the stimulus intensity was augmented little by little , the sum of action potential firing should be notably increased but the amplitude of action potential had not obviouslychanged.DIDS plus etomidate reduced the sum of action potential after 20 min.With the stimulus intensity increasing , the degenerative time of action potential increased gradually.The last group joined with TEA which blocks potassium ion channel did not affect the suppression function of etomidate.Conclusion Etomidate emulsion may finally inhibit action potential through opening Cl -channel in order to increase Cl -internal flow to achieve general anesthesia.K+channel may have few effects on this process.