MVN區(qū)Glu離子型受體參與血清NE含量的調(diào)節(jié)
本文選題:急性低血壓 切入點:前庭內(nèi)側核 出處:《延邊大學》2017年碩士論文 論文類型:學位論文
【摘要】:實驗目的:1998年就有學者提出,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)-延髓外側網(wǎng)狀結構-延髓頭端腹外側區(qū)-脊髓灰質側角-交感神經(jīng)。本研究室用免疫組織化學法又發(fā)現(xiàn),前庭內(nèi)側核(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。機體血液中腎上腺素的來源主要是腎上腺髓質,而去甲腎上腺素則由腎上腺髓質和交感神經(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,未見相關研究報道。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血清去甲腎上腺素含量的影響。同時采用蛋白印跡分析法進一步證實硝普鈉誘發(fā)急性低血壓時,MVN區(qū)給予谷氨酸的離子型受體激動劑和阻斷劑對脊髓胸段內(nèi)c-Fos和p-ERK1/2蛋白表達的影響。以證明急性低血壓時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)控機制。實驗方法:實驗為了排除血壓的變化經(jīng)過壓力感受器對中樞神經(jīng)核團功能的影響,用手術方法摘除動物的頸動脈竇和主動脈弓壓力感受器。用多通道生理記錄儀監(jiān)測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,再進行MVN區(qū)核團定位,將36只SD大鼠隨機分為阻斷劑組(Antagonist)和激動劑組(Agonist)。阻斷劑組中分為MVN區(qū)注射人工腦脊液(ACSF)的對照組以及阻斷劑MK-801、CNQX,核團給藥10min后靜脈注射硝普鈉(Sodiumnitroprusside,SNP)誘發(fā)低血壓。激動劑組又分為注射人工腦脊液(ACSF)的對照組以及受體激動劑NMDA組和AMPA組3個小組。激動劑組不誘發(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)對該段脊髓內(nèi)c-Fos和p-ERK1/2蛋白表達進行檢測。實驗結果: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蛋白的表達以及p-ERK1/2蛋白含量明顯低于對照組(ACSF)(P0.05)。2.前庭內(nèi)側核區(qū)注射谷氨酸(Glu)離子型受體激動劑(NMDA、AMPA),使胸髓T5-7段中的c-Fos和p-ERK1/2蛋白的表達含量明顯高于注射人工腦脊液的對照組(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)的含量明顯低于對照組(ACSF)(P0.05)。4.前庭內(nèi)側核區(qū)的谷氨酸(Glu)離子型受體激動劑(NMDA、AMPA),明顯提高血清中去甲腎上腺素(NE)的含量,與對照組(ACSF)比較差異顯著(P0.05)。結論: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.
【學位授予單位】:延邊大學
【學位級別】:碩士
【學位授予年份】:2017
【分類號】:R544.2
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