本文選題：急性低血壓　切入點(diǎn)：前庭內(nèi)側(cè)核　出處：《延邊大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：實(shí)驗(yàn)?zāi)康?1998年就有學(xué)者提出,前庭交感反射的中樞通路。它們是前庭神經(jīng)-前庭神經(jīng)核(nucleivestibularis,VN)-延髓外側(cè)網(wǎng)狀結(jié)構(gòu)-延髓頭端腹外側(cè)區(qū)-脊髓灰質(zhì)側(cè)角-交感神經(jīng)。本研究室用免疫組織化學(xué)法又發(fā)現(xiàn),前庭內(nèi)側(cè)核(medial vestibular nucleus,MVN)區(qū)的 N-甲基-D-門冬氨酸受體(N-methy1-D-aspartic acid receptor,NMDA)和α-氨基-3-羥基-5-甲基-4-異惡唑丙酸受體(amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor,AMPA)參與由急性低血壓誘發(fā)的前庭性血壓調(diào)控過程,也能增加血清腎上腺素的濃度明顯增加。機(jī)體血液中腎上腺素的來源主要是腎上腺髓質(zhì),而去甲腎上腺素則由腎上腺髓質(zhì)和交感神經(jīng)節(jié)后神經(jīng)元的末梢分泌。血液中的去甲腎上腺素可以反應(yīng)交感神經(jīng)的興奮狀態(tài)。至于急性低血壓經(jīng)外周前庭器官影響血壓的調(diào)控中是否有交感神經(jīng)參與,未見相關(guān)研究報(bào)道。本研究的目的在于探討急性低血壓誘發(fā)前庭性血壓調(diào)控過程中,MVN區(qū)谷氨酸的部分離子型受體對(duì)血清去甲腎上腺素含量的影響。同時(shí)采用蛋白印跡分析法進(jìn)一步證實(shí)硝普鈉誘發(fā)急性低血壓時(shí),MVN區(qū)給予谷氨酸的離子型受體激動(dòng)劑和阻斷劑對(duì)脊髓胸段內(nèi)c-Fos和p-ERK1/2蛋白表達(dá)的影響。以證明急性低血壓時(shí)MVN區(qū)的谷氨酸離子型受體經(jīng)過脊髓-交感神經(jīng)參與由急性低血壓誘發(fā)的前庭性血壓調(diào)控機(jī)制。實(shí)驗(yàn)方法:實(shí)驗(yàn)為了排除血壓的變化經(jīng)過壓力感受器對(duì)中樞神經(jīng)核團(tuán)功能的影響,用手術(shù)方法摘除動(dòng)物的頸動(dòng)脈竇和主動(dòng)脈弓壓力感受器。用多通道生理記錄儀監(jiān)測(cè)該模型大鼠壓力感受性反射的敏感性,確定模型制備成功48h后,再進(jìn)行MVN區(qū)核團(tuán)定位,將36只SD大鼠隨機(jī)分為阻斷劑組(Antagonist)和激動(dòng)劑組(Agonist)。阻斷劑組中分為MVN區(qū)注射人工腦脊液(ACSF)的對(duì)照組以及阻斷劑MK-801、CNQX,核團(tuán)給藥10min后靜脈注射硝普鈉(Sodiumnitroprusside,SNP)誘發(fā)低血壓。激動(dòng)劑組又分為注射人工腦脊液(ACSF)的對(duì)照組以及受體激動(dòng)劑NMDA組和AMPA組3個(gè)小組。激動(dòng)劑組不誘發(fā)急性低血壓。用微量泵以1.5μl/min的速度向核團(tuán)注射藥品。30min后開胸心室腔內(nèi)取血離心獲得血清后,用ELASA法檢測(cè)血清去甲腎上腺素的含量。取T5-7段脊髓,用蛋白印跡分析法(Western-Blot)對(duì)該段脊髓內(nèi)c-Fos和p-ERK1/2蛋白表達(dá)進(jìn)行檢測(cè)。實(shí)驗(yàn)結(jié)果:1.將谷氨酸(Glu)離子型受體阻斷劑(CNQX、MK-801)經(jīng)過定位針注射到前庭內(nèi)側(cè)核(MVN)區(qū)后,再用硝普鈉(SNP)誘發(fā)急性低血壓,發(fā)現(xiàn)胸髓T5-7段中的c-Fos蛋白的表達(dá)以及p-ERK1/2蛋白含量明顯低于對(duì)照組(ACSF)(P0.05)。2.前庭內(nèi)側(cè)核區(qū)注射谷氨酸(Glu)離子型受體激動(dòng)劑(NMDA、AMPA),使胸髓T5-7段中的c-Fos和p-ERK1/2蛋白的表達(dá)含量明顯高于注射人工腦脊液的對(duì)照組(P0.05)。3.把谷氨酸(Glu)的兩種離子型受體阻斷劑(CNQX、MK-801)注射到前庭內(nèi)側(cè)核(MVN)區(qū)后,再用硝普鈉(SNP)誘發(fā)急性低血壓,發(fā)現(xiàn)血清中去甲腎上腺素(NE)的含量明顯低于對(duì)照組(ACSF)(P0.05)。4.前庭內(nèi)側(cè)核區(qū)的谷氨酸(Glu)離子型受體激動(dòng)劑(NMDA、AMPA),明顯提高血清中去甲腎上腺素(NE)的含量,與對(duì)照組(ACSF)比較差異顯著(P0.05)。結(jié)論:誘發(fā)急性低血壓可以使MVN區(qū)谷氨酸離子型受體興奮再通過興奮交感神經(jīng)參與血壓的調(diào)節(jié)。
[Abstract]:Objective: to 1998, some scholars have suggested that the central pathway of vestibular sympathetic reflex. They are vestibular nerve vestibular nucleus (nucleivestibularis, VN) - lateral medullary reticular formation - rostral ventrolateral medulla - spinal cord lateral horn - sympathetic nerve. This study by immunohistochemical method and found that the medial vestibular nucleus (medial vestibular nucleus, MVN) N- methyl -D- aspartate receptor region (N-methy1-D-aspartic acid receptor, NMDA -3-) and alpha amino hydroxy -5- methyl -4- isoxazole propionate receptor (amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor, AMPA) involved in the regulation of blood pressure by vestibular evoked acute hypotension, can also increase the concentration of serum epinephrine increased significantly the source of adrenaline in the blood. The body is mainly the adrenal medulla, and norepinephrine from the adrenal medulla and sympathetic postganglionic nerve The peripheral blood in the secretion of norepinephrine can response to sympathetic nerve stimulation. As for acute hypotension by peripheral vestibular organs influence whether blood pressure regulation of sympathetic nerve involvement, no reports about. The purpose of this study is to investigate the acute hypotension induced by vestibular blood pressure regulation process, part of the ion receptor MVN the excitatory glutamate effect of norepinephrine on the content of serum. At the same time using Western blot analysis further confirmed that acute hypotension induced by sodium nitroprusside, ionic MVN administration of glutamate receptor agonists and blocking agents on the expression of c-Fos and p-ERK1/2 protein in the spinal cord. The ionotropic glutamate proved acute hypotension MVN region of the receptor after spinal cord - sympathetic nerve involvement by the vestibular blood pressure regulation mechanism of induced acute hypotension. Methods: experiments in order to exclude The change of blood pressure after effects on the central nervous nuclei baroreceptor function, carotid sinus and aortic arch baroreceptors with surgical removal of the animal. The feeling reflected by the pressure sensitivity of rat multi channel physiological recorder monitoring the model, determine the model preparation work after 48h, and then MVN nuclei, 36 SD rats were randomly divided into blocker group (Antagonist) and agonist group (Agonist). The blocker group divided into injection of artificial cerebrospinal fluid (ACSF) in the MVN region of the control group and the blocking agent MK-801, CNQX, nucleus after administration of 10min intravenous injection of sodium nitroprusside (Sodiumnitroprusside, SNP) agonist induced hypotension. Group was divided into injection of artificial cerebrospinal fluid (ACSF) excited control group and receptor agent NMDA group and AMPA group. Group 3 agonist group did not induce acute hypotension. Using micro pump at the rate of 1.5 l/min to the nucleus after.30min injection of drugs Open chest ventricular cavity blood serum after centrifugation, the content of serum norepinephrine by ELASA method. The T5-7 segment of the spinal cord by Western blotting analysis method (Western-Blot) was used to detect the expression of c-Fos in spinal cord and p-ERK1/2 protein. Results: 1. glutamic acid (Glu) ion receptor blocker (CNQX MK-801), after positioning needle injected into the medial vestibular nucleus (MVN) area, and sodium nitroprusside (SNP) induced acute hypotension, found expression in thoracic spinal cord of T5-7 segment of c-Fos protein and p-ERK1/2 protein content was significantly lower than the control group (ACSF) (P0.05).2. injection in the medial vestibular nucleus (Glu) glutamate ionotropic receptors agonist (NMDA, AMPA), the control group the expression content of thoracic spinal cord of T5-7 segment of c-Fos and p-ERK1/2 protein was significantly higher than that of the injection of artificial cerebrospinal fluid (P0.05) to.3. (Glu) two glutamate ion receptor blocker (CNQX, MK-801) was injected into the vestibule The medial nucleus (MVN) area, and sodium nitroprusside (SNP) acute hypotension induced by norepinephrine, found in serum (NE) were significantly lower than the control group (ACSF) (P0.05) glutamate.4. medial vestibular nucleus (Glu) of the ionotropic agonists (NMDA, AMPA), significantly increased norepinephrine the content of serum (NE), and the control group (ACSF) and there was significant difference (P0.05). Conclusion: acute hypotension induced by MVN can make the ionotropic glutamate receptor stimulation through regulating region of sympathetic nerve involved in blood pressure.

【學(xué)位授予單位】：延邊大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R544.2

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 楊愛萍;張道宮;呂亞峰;李亞偉;徐繼良;劉賢峰;李遠(yuǎn)令;樊兆民;;前庭自旋轉(zhuǎn)試驗(yàn)在耳源性眩暈疾病診斷中的應(yīng)用價(jià)值[J];臨床耳鼻咽喉頭頸外科雜志;2016年08期

2 王建智;王臨生;趙昱;梁立權(quán);葛澤松;王東培;張作明;王小成;;民航飛行人員視眼動(dòng)功能試驗(yàn)和前庭眼動(dòng)反射試驗(yàn)結(jié)果分析[J];現(xiàn)代生物醫(yī)學(xué)進(jìn)展;2013年17期

3 寇佳;蔡廣研;張雪光;吳杰;陳仆;劉述文;張巖;尹忠;師鎖柱;陳香美;;良性高血壓腎小動(dòng)脈硬化癥患者的臨床病理特點(diǎn)分析[J];中華腎病研究電子雜志;2012年02期

4 王文;林曙光;朱鼎良;趙連友;吳兆蘇;;推廣《中國(guó)血壓測(cè)量指南》,規(guī)范化測(cè)量血壓[J];中華高血壓雜志;2012年03期

5 景改萍;唐建良;;眩暈的病因及臨床表現(xiàn)分析[J];中國(guó)全科醫(yī)學(xué);2009年05期

6 姜海英;金正元;邴艷華;金清華;崔勛;金元哲;;急性低血壓時(shí)孤束核內(nèi)谷氨酸和�；撬岷孔兓痆J];中國(guó)現(xiàn)代醫(yī)學(xué)雜志;2007年16期

7 吳子明;李新民;張慶泉;;169例急性前庭性眩暈的臨床研究[J];中國(guó)聽力語言康復(fù)科學(xué)雜志;2007年02期

8 于海玲;安英;姜海英;金清華;金元哲;;單側(cè)迷路破壞后大鼠前庭神經(jīng)內(nèi)側(cè)核區(qū)氨基酸含量的變化(英文)[J];生理學(xué)報(bào);2007年01期

9 馬明信;;低血壓的危害和防治[J];保健醫(yī)苑;2006年12期

10 趙喜慶,張崇智,何仲義;前庭脊髓束的研究進(jìn)展[J];華北煤炭醫(yī)學(xué)院學(xué)報(bào);2003年02期

相關(guān)博士學(xué)位論文 前1條

1 蔡懿靈;谷氨酸能前庭—內(nèi)臟投射通路在暈動(dòng)癥大鼠植物神經(jīng)反應(yīng)中的作用[D];第二軍醫(yī)大學(xué);2007年

相關(guān)碩士學(xué)位論文 前2條

1 李美至;脊髓灰質(zhì)側(cè)角離子型谷氨酸受體參與急性低血壓誘發(fā)的前庭性血壓調(diào)控機(jī)制[D];延邊大學(xué);2016年

2 楊艷召;前庭性血壓調(diào)控中MVN和RVLM的功能聯(lián)系[D];延邊大學(xué);2014年

，

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