田麗,程焱△,張哲成,劉娜,朱炬
糖尿病大鼠運(yùn)動(dòng)神經(jīng)纖維損害的MUNE檢測(cè)
田麗1,程焱1△,張哲成2,劉娜2,朱炬2
目的通過(guò)運(yùn)動(dòng)單位數(shù)目估計(jì)(MUNE)技術(shù)對(duì)糖尿病大鼠運(yùn)動(dòng)神經(jīng)纖維功能狀況進(jìn)行評(píng)價(jià),探討MUNE對(duì)糖尿病周圍神經(jīng)?。―PN)的早期診斷價(jià)值。方法鏈脲佐菌素誘導(dǎo)糖尿病大鼠模型(DM組),在造模后第4、8、12周對(duì)DM組及對(duì)照組(正常SD大鼠)進(jìn)行腓腸肌MUNE及坐骨神經(jīng)常規(guī)運(yùn)動(dòng)神經(jīng)傳導(dǎo)速度(MCV)及波幅(CMAP)檢測(cè),電鏡觀察坐骨神經(jīng)的超微結(jié)構(gòu)。結(jié)果造模后第4周,DM組腓腸肌MUNE低于對(duì)照組(275.88±87.87 vs 369.71±75.64,P<0.05),而坐骨神經(jīng)MCV及CMAP較對(duì)照組差異無(wú)統(tǒng)計(jì)學(xué)意義;電鏡觀察顯示DM組坐骨神經(jīng)大部分神經(jīng)纖維尚正常,少量軸索萎縮,神經(jīng)髓鞘板層分離。第8周,與對(duì)照組相比,DM組腓腸肌MUNE降低(357.49±72.68 vs 221.26±92.41,P<0.01),而MCV、CMAP仍較對(duì)照組差異無(wú)統(tǒng)計(jì)學(xué)意義;電鏡觀察顯示尚有較正常神經(jīng)纖維,髓鞘局灶性板層松散、分離,軸索萎縮,軸索膜與髓鞘內(nèi)層分離,出現(xiàn)大的間隙。第12周,DM組腓腸肌MUNE(127.87±19.80 vs 366.85±51.25)、坐骨神經(jīng)MCV[(35.06±4.33)m/s vs(50.47±6.07)m/s]、CMAP[(2.91±1.37)mV vs(5.98±2.14)mV]低于對(duì)照組(P<0.01);電鏡顯示神經(jīng)髓鞘折曲,軸索受擠壓等受損嚴(yán)重。結(jié)論MUNE較常規(guī)運(yùn)動(dòng)神經(jīng)傳導(dǎo)檢測(cè)易于早期發(fā)現(xiàn)DPN軸索功能異常。
糖尿病神經(jīng)病變;運(yùn)動(dòng)神經(jīng)元;神經(jīng)傳導(dǎo);坐骨神經(jīng);顯微鏡檢查,電子,透射;運(yùn)動(dòng)單位數(shù)目估計(jì)
近年關(guān)于糖尿病周圍神經(jīng)?。╠iabetic peripheral neuropathy,DPN)的研究多集中于DPN的發(fā)病機(jī)制,以及疼痛、麻木等感覺障礙的治療方面,對(duì)運(yùn)動(dòng)神經(jīng)纖維損害的關(guān)注較少。運(yùn)動(dòng)單位數(shù)目估計(jì)(motor unit number estimation,MUNE)檢測(cè)對(duì)運(yùn)動(dòng)單位的評(píng)價(jià)不受神經(jīng)再生補(bǔ)償?shù)挠绊?,因此,在臨床以及傳統(tǒng)的電診斷參數(shù)正常情況下,MUNE可能發(fā)現(xiàn)運(yùn)動(dòng)神經(jīng)纖維軸索的早期損害[1-2]。本研究通過(guò)電鏡觀察糖尿病大鼠坐骨神經(jīng)超微結(jié)構(gòu)的改變,以此為客觀依據(jù),探討MUNE對(duì)糖尿病運(yùn)動(dòng)神經(jīng)纖維損害的早期診斷價(jià)值。
1.1 材料清潔級(jí)Sprague-Dawley(SD)雄性大鼠,體質(zhì)量為180~220 g,購(gòu)自北京大學(xué)醫(yī)學(xué)部動(dòng)物中心。鏈脲佐菌素(美國(guó)Sigma公司),Medtronic Keypoint 4.NET肌電誘發(fā)電位儀(美敦力),HITACHI-7500透射電鏡(日立)。
1.2 方法
1.2.1 糖尿病大鼠模型的建立及分組采用隨機(jī)數(shù)字表法將健康雄性SD大鼠37只分為2組,對(duì)照組19只、DM組18只。鏈脲佐菌素以0.1 mol/L,pH 4.2的無(wú)菌檸檬酸-檸檬酸鈉緩沖液配制成濃度為2%的溶液,DM組按照60 mg/kg體質(zhì)量一次性腹腔注射鏈脲佐菌素制備糖尿病模型。給藥l周后測(cè)定大鼠尾靜脈血糖,血糖大于16.7 mmol/L判定為糖尿病造模成功。對(duì)照組大鼠僅給予腹腔注射等體積的檸檬酸-檸檬酸鈉緩沖液。
于第4周末兩組各處死1只大鼠取坐骨神經(jīng)電鏡觀察,各取8只行右下肢神經(jīng)電生理檢測(cè);為避免重復(fù)測(cè)量對(duì)實(shí)驗(yàn)結(jié)果造成影響,在第8周末對(duì)其進(jìn)行左下肢神經(jīng)電生理檢測(cè)后處死,并各取1只大鼠坐骨神經(jīng)電鏡觀察;于第12周末取各組內(nèi)剩余大鼠(對(duì)照組10只,DM組9只)進(jìn)行右下肢神經(jīng)電生理檢測(cè),并各送檢1只大鼠坐骨神經(jīng)電鏡觀察。
1.2.2 神經(jīng)電生理檢測(cè)檢測(cè)項(xiàng)目包括腓腸肌MUNE、坐骨神經(jīng)常規(guī)運(yùn)動(dòng)傳導(dǎo)速度(motor nerve conduction velocity,MCV)、復(fù)合肌肉動(dòng)作電位(compound motor active potential,CMAP)波幅。將大鼠用10%水合氯醛350 mg/kg體質(zhì)量腹腔注射麻醉后,俯臥固定于平板上。應(yīng)用肌電誘發(fā)電位儀進(jìn)行神經(jīng)電生理檢測(cè)。環(huán)境溫度約22~25℃。
常規(guī)運(yùn)動(dòng)神經(jīng)傳導(dǎo)檢測(cè)方法:采用單極針經(jīng)皮插入作為刺激電極;第一刺激點(diǎn)陰極置于坐骨切跡,陽(yáng)極旁開5 mm;第二刺激點(diǎn)陰極置于同側(cè)內(nèi)踝后方,陽(yáng)極旁開5 mm,用方形波(5~15 mA)刺激神經(jīng)。另將一對(duì)單極針電極作為記錄電極,陰極插入同側(cè)足底骨間肌,陽(yáng)極插入同側(cè)足底皮下。接地電極置于尾部皮下。分別測(cè)量潛伏期和CMAP波幅,MCV(m/s)=兩刺激部位之間的距離/兩刺激部位的潛伏期差。儀器設(shè)置:帶通2~100 kHz,掃描速度5 ms/D,靈敏度5 mV/D,刺激脈沖時(shí)限0.2 ms。見圖1A。
MUNE檢測(cè)方法:刺激電極及記錄電極均為單極針電極,刺激電極陰極放置于坐骨切跡,陽(yáng)極旁開5 mm。記錄電極陰極插入腓腸肌,陽(yáng)極置于內(nèi)踝后方皮下。地線置于刺激電極和記錄電極之間皮下。以超強(qiáng)刺激誘發(fā)最大波幅M波,再以閾刺激強(qiáng)度獲最小M波,逐漸增大刺激強(qiáng)度并記錄10個(gè)階梯遞增的M波。肌電誘發(fā)電位儀(Keypoint 5.06)軟件輸出MUNE。儀器設(shè)置:帶通20 Hz~10 kHz,掃描速度5 ms/D,靈敏度5 mV/D,刺激脈沖時(shí)限0.1 ms,見圖1B。
Fig.1The electrophysiological test of rats圖1 大鼠神經(jīng)電生理檢測(cè)
1.2.3 坐骨神經(jīng)電鏡觀察標(biāo)本經(jīng)2.5%戊二醛固定液、1%四氧化鋨后固定,上升梯度乙醇脫水,環(huán)氧丙烷過(guò)渡,Epon812環(huán)氧樹脂包埋,經(jīng)半薄切片定位后,超薄切片,醋酸鈾及檸檬酸鉛雙重染色,HITACHI-7500透射電鏡觀察。
1.3 統(tǒng)計(jì)學(xué)方法采用SPSS 17.0統(tǒng)計(jì)軟件包進(jìn)行分析,計(jì)量資料用均數(shù)±標(biāo)準(zhǔn)差表示,組間比較采用2組獨(dú)立樣本t檢驗(yàn),P<0.05為差異有統(tǒng)計(jì)學(xué)意義。
2.1 造模后第4周2組大鼠血糖、神經(jīng)電生理、電鏡檢測(cè)結(jié)果的比較DM組大鼠血糖高于對(duì)照組(P<0.01),右側(cè)腓腸肌MUNE明顯低于對(duì)照組(P<0.05),右側(cè)坐骨神經(jīng)CMAP、MCV與對(duì)照組比較差異無(wú)統(tǒng)計(jì)學(xué)意義,見表1。
對(duì)照組大鼠坐骨神經(jīng)軸索、髓鞘形態(tài)正常,內(nèi)可見微管微絲排列有序,可見線粒體,見圖2A;DM組
大鼠可見輕微損傷,大部分神經(jīng)纖維尚正常,少量軸索萎縮、線粒體結(jié)構(gòu)欠清晰,部分神經(jīng)髓鞘局灶板層分離,見圖2B、C。
Tab.1Comparison of the blood glucose and electrophysiological parameters at the 4th week of modeling between two groups表1 造模后4周大鼠血糖、神經(jīng)電生理檢測(cè)結(jié)果的比較(n=8,)
Tab.1Comparison of the blood glucose and electrophysiological parameters at the 4th week of modeling between two groups表1 造模后4周大鼠血糖、神經(jīng)電生理檢測(cè)結(jié)果的比較(n=8,)
*P<0.05,**P<0.01,表2、3同
組別對(duì)照組D M組t血糖(m m o l / L)5 . 0 0 ± 0 . 5 3 2 7 . 6 4 ± 3 . 5 6 1 7 . 7 9 6**M U N E 3 6 9 . 7 1 ± 7 5 . 6 4 2 7 5 . 8 8 ± 8 7 . 8 7 2 . 2 8 9*C M A P(m V)6 . 1 6 ± 2 . 2 0 6 . 0 8 ± 2 . 0 2 0 . 0 8 3 M C V(m / s)5 1 . 4 5 ± 6 . 2 6 4 9 . 6 1 ± 6 . 0 6 0 . 5 9 6
Fig.2The ultrastructure of sciatic nerve under electron microscope at 4th week of modeling圖2 造模后4周坐骨神經(jīng)超微結(jié)構(gòu)(電鏡)
2.2 造模后第8周2組大鼠血糖、神經(jīng)電生理、電鏡檢測(cè)結(jié)果的比較DM組大鼠血糖高于對(duì)照組(P<0.01),左側(cè)腓腸肌MUNE明顯低于對(duì)照組(P<0.01),左側(cè)坐骨神經(jīng)CMAP、MCV與對(duì)照組比較差異無(wú)統(tǒng)計(jì)學(xué)意義,見表2。
Tab.2Comparison of the blood glucose and electrophysiological parameters at the 8th week of modeling between two groups表2 造模后8周大鼠血糖、神經(jīng)電生理檢測(cè)結(jié)果的比較(n=8,)
Tab.2Comparison of the blood glucose and electrophysiological parameters at the 8th week of modeling between two groups表2 造模后8周大鼠血糖、神經(jīng)電生理檢測(cè)結(jié)果的比較(n=8,)
組別對(duì)照組D M組t血糖(m m o l / L)5 . 0 1 ± 0 . 5 8 2 2 . 2 5 ± 4 . 1 3 1 1 . 6 9 3**M U N E 3 5 7 . 4 9 ± 7 2 . 6 8 2 2 1 . 2 6 ± 9 2 . 4 1 3 . 2 7 7**C M A P(m V)6 . 1 1 ± 1 . 8 2 5 . 6 0 ± 1 . 5 5 0 . 6 0 6 M C V(m / s)5 1 . 0 3 ± 5 . 1 1 4 6 . 1 9 ± 6 . 3 6 1 . 6 7 8
對(duì)照組大鼠坐骨神經(jīng)組織結(jié)構(gòu)正常,見圖3A;DM組大鼠坐骨神經(jīng)尚有較正常神經(jīng)纖維,但存在較多髓鞘局灶性板層松散、分離,軸索萎縮,軸索膜與髓鞘內(nèi)層分離,出現(xiàn)大的間隙。髓鞘板層分為內(nèi)外兩部分,外側(cè)部分有熔融灶,亦有髓鞘完全熔融,板層結(jié)構(gòu)不清,微絲微管受損,見圖3B、C。
Fig.3The ultrastructure of sciatic nerve under electron microscope at 8th week of modeling圖3 造模后8周坐骨神經(jīng)超微結(jié)構(gòu)(電鏡)
2.3 造模后第12周2組大鼠神經(jīng)電生理、血糖、電鏡檢測(cè)結(jié)果的比較DM組大鼠血糖高于對(duì)照組(P<0.01),右側(cè)腓腸肌MUNE、坐骨神經(jīng)CMAP、MCV均較對(duì)照組明顯減低(P<0.01),見表3。
Tab.3Comparison of the blood glucose and electrophysiological parameters at the 12th week of modeling between two groups表3 造模后12周大鼠血糖、神經(jīng)電生理檢測(cè)結(jié)果的比較
Tab.3Comparison of the blood glucose and electrophysiological parameters at the 12th week of modeling between two groups表3 造模后12周大鼠血糖、神經(jīng)電生理檢測(cè)結(jié)果的比較
組別對(duì)照組D M組t n 1 0 9血糖(m m o l / L)5 . 3 9 ± 0 . 7 0 2 3 . 2 3 ± 3 . 5 9 1 4 . 6 5 8**M U N E 3 6 6 . 8 5 ± 5 1 . 2 5 1 2 7 . 8 7 ± 1 9 . 8 0 1 3 . 6 5 7**C M A P(m V)5 . 9 8 ± 2 . 1 4 2 . 9 1 ± 1 . 3 7 3 . 6 7 1**M C V(m / s)5 0 . 4 7 ± 6 . 0 7 3 5 . 0 6 ± 4 . 3 3 6 . 3 0 5**
對(duì)照組大鼠坐骨神經(jīng)組織結(jié)構(gòu)正常,見圖4A;DM組大鼠坐骨神經(jīng)受損嚴(yán)重,直徑大的神經(jīng)較直徑小的嚴(yán)重。髓鞘折曲,軸索受擠壓。同一有髓神經(jīng)纖維髓鞘壁厚薄不同,髓鞘板層松散,蓬松變厚,有折疊、熔融,見圖4B、C。
DPN可累及周圍神經(jīng)的感覺及運(yùn)動(dòng)纖維,運(yùn)動(dòng)神經(jīng)纖維的損害可以導(dǎo)致患者行動(dòng)緩慢、步態(tài)不穩(wěn)以及頻繁的跌倒,并增加了足潰瘍及截肢的風(fēng)險(xiǎn)[3]。MUNE是一項(xiàng)能早期定量發(fā)現(xiàn)運(yùn)動(dòng)單位異常的神經(jīng)電生理技術(shù)[4],Paramanathan等[5]研究發(fā)現(xiàn)累及運(yùn)動(dòng)軸索變性的疾病常存在運(yùn)動(dòng)單位數(shù)目的減少,且出現(xiàn)在運(yùn)動(dòng)神經(jīng)傳導(dǎo)異常之前,提示MUNE可能較常規(guī)電生理更易發(fā)現(xiàn)運(yùn)動(dòng)神經(jīng)軸索變性。
Fig.4The ultrastructure of sciatic nerve under electron microscope at 12th week of modeling圖4 造模后12周坐骨神經(jīng)超微結(jié)構(gòu)(電鏡)
傳統(tǒng)的神經(jīng)電生理檢測(cè)方法(包括運(yùn)動(dòng)神經(jīng)傳導(dǎo)、針極肌電圖等)對(duì)于評(píng)價(jià)疾病的進(jìn)展程度及輕度的軸索損害敏感性不佳,這是由于側(cè)支芽生的存在掩蓋了輕度的神經(jīng)損傷[6]。MCV反映的是最快神經(jīng)纖維的傳導(dǎo)速度,只有在大量神經(jīng)纖維損害時(shí)才出現(xiàn)MCV的下降[7],因此MCV敏感度較低;CMAP波幅反映的是所測(cè)神經(jīng)纖維的數(shù)量和同步興奮的程度,運(yùn)動(dòng)神經(jīng)軸突損害和功能障礙時(shí),神經(jīng)纖維同步化興奮的程度降低,CMAP波幅下降。
Souayah等[1]利用環(huán)狀電極對(duì)鼠下肢肌肉運(yùn)動(dòng)單位數(shù)目進(jìn)行估計(jì),發(fā)現(xiàn)高血糖后2周即可出現(xiàn)MUNE的下降,并觀察到神經(jīng)纖維損害及末端側(cè)支芽生,提示MUNE檢測(cè)可在糖尿病的早期階段發(fā)現(xiàn)運(yùn)動(dòng)神經(jīng)纖維異常,而高血糖后6周,MUNE繼續(xù)下降,MCV及CMAP仍為正常,但該研究未繼續(xù)觀察至運(yùn)動(dòng)神經(jīng)損害嚴(yán)重(MCV及CMAP下降)。本研究利用單極針電極對(duì)糖尿病大鼠腓腸肌MUNE及坐骨神經(jīng)MCV及CMAP進(jìn)行檢測(cè),發(fā)現(xiàn)高血糖后4周MUNE較對(duì)照組明顯下降,且電鏡觀察到坐骨神經(jīng)軸索、髓鞘超微結(jié)構(gòu)的損害,與Souayah等[1]的研究結(jié)果一致。本研究進(jìn)一步觀察至第12周糖尿病大鼠坐骨神經(jīng)結(jié)構(gòu)嚴(yán)重?fù)p害時(shí),MCV、CMAP較對(duì)照組出現(xiàn)下降。Albrecht等[8]報(bào)道CMAP波幅下降時(shí),運(yùn)動(dòng)單位已經(jīng)丟失80%~90%。本研究結(jié)果顯示在第12周運(yùn)動(dòng)神經(jīng)傳導(dǎo)檢測(cè)(MCV、CMAP)異常時(shí),DM組大鼠MUNE較對(duì)照組下降65%,提示與常規(guī)運(yùn)動(dòng)神經(jīng)傳導(dǎo)檢測(cè)相比,MUNE可早期發(fā)現(xiàn)運(yùn)動(dòng)神經(jīng)軸索損害。
在DPN等慢性神經(jīng)病變的發(fā)展過(guò)程中,軸突損害的同時(shí)伴隨著側(cè)支芽生再生,病變運(yùn)動(dòng)單位中的肌纖維因接受正常神經(jīng)纖維的再生支配,從而殘存運(yùn)動(dòng)單位所支配范圍增加,在一定程度上彌補(bǔ)了軸突喪失對(duì)CMAP波幅的影響,因此DPN早期總的運(yùn)動(dòng)單位數(shù)目減少,但CMAP波幅可以正常[2],隨著疾病的進(jìn)展,由于失神經(jīng)支配的速度超過(guò)側(cè)支芽生的速度,不僅運(yùn)動(dòng)單位減少,也導(dǎo)致MCV下降、CMAP波幅減低、肌肉萎縮和肌肉無(wú)力[6]。因此一旦出現(xiàn)MCV、CMAP異常,往往病變已經(jīng)較重。
綜上,本研究發(fā)現(xiàn)MUNE較常規(guī)運(yùn)動(dòng)神經(jīng)傳導(dǎo)檢測(cè)易于早期發(fā)現(xiàn)DPN大鼠運(yùn)動(dòng)軸索功能異常,為利用MUNE技術(shù)早期發(fā)現(xiàn)糖尿病患者周圍神經(jīng)病變提供了實(shí)驗(yàn)依據(jù)。
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(2015-04-16收稿 2015-06-25修回)
(本文編輯 李國(guó)琪)
The detection of motor nerve injury by MUNE in an animal model of diabetes
TIAN Li1,CHENG Yan1△,ZHANG Zhecheng2,LIU Na2,ZHU Ju2
1 Department of Neurology,Tianjin Medical University General Hospital,Tianjin 300052,China;2 Department of Neurology,Tianjin Third Central Hospital△
ObjectiveTo investigate motor nerve function status in rats with diabetes mellitus by motor unit number estimation(MUNE),and discuss it′s early diagnostic value in diabetic peripheral neuropathy(DPN).MethodsDiabetic rat model(DM group)was induced by streptozotocin.The MUNE of gastrocnemius muscle and motor nerve conduction(MCV,CMAP)of the sciatic nerve were measured at the 4th,8th and 12thweek after onset of hyperglycemia in the DM group and the control group(normal SD rats).The ultrastructure of sciatic nerve was observed by electron microscope.ResultsAt the 4th week,MUNE of gastrocnemius muscle was significantly decreased in DM group compared to that of the control group(275.88±87.87 vs 369.71±75.64,P<0.05).There were no significant differences in MCV and CMAP of sciatic nerve between two groups.The electron microscopy observation showed that most nerve fibers were normal;a small amount of axonal atrophy,and myelin lamellar structure was separated in DM group.At the 8th week,compared with the control group,MUNE were reduced in gastrocnemius muscle in DM group(357.49±72.68 vs 221.26±92.41,P<0.01).There were no significant differences in MCV and CMAP of the sciatic nerve between DM group and control group.The electron microscope observation showed that part of nerve fibers were normal,the myelin focal plate layer was loose and separated,axonal atrophy,the axonal membrane and myelin sheath inner layer was separated with big gap.At the 12th week,MUNE of gastrocnemius muscle(127.87±19.80 vs 366.85±51.25),sciatic nerve MCV[(35.06±4.43)m/s vs(50.47±6.07)m/s]and CMAP[(2.91±1.37)mV vs(5.98±2.14)mV]were significantly decreased in DM group than those of control group(P<0.01).The electron microscopy observation showed severely damaged myelin flex and axonal squeeze.ConclusionMUNE is much earlier in detecting early motor nerve dysfunction in DM than conventional motor nerve conduction test.
diabetic neuropathies;motor neurons;neural conduction;sciatic nerve;microscopy,electron,transmission;motor unit number estimation
R741.044
A
10.11958/j.issn.0253-9896.2015.12.012
天津市衛(wèi)生局科技基金資助項(xiàng)目(2012KY04);天津市衛(wèi)生行業(yè)重點(diǎn)攻關(guān)項(xiàng)目(14KJ110)
1天津醫(yī)科大學(xué)總醫(yī)院神經(jīng)內(nèi)科(郵編300052);2天津市第三中心醫(yī)院神經(jīng)內(nèi)科
田麗(1982),女,主治醫(yī)師,博士在讀,主要從事神經(jīng)電生理研究
△通訊作者E-mail:cylfl@sohu.com