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  • 學位論文

血管加壓素對大白鼠顏面神經呼吸活動的影響

The effect of arginine vasopressin on respiratory-related facial nerve activity in rats

指導教授 : 黃基礎
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摘要


本研究的主要目的是要探討血管加壓素 (arginine vasopressin; AVP) 作用在延腦腹外側 (ventrolateral medulla;VLM) 對膈神經及顏面神經呼吸活動的影響,並且探討這樣的影響是否藉由AVP V1A接受器所達成。 實驗動物為250-350 g雄性Wistar品系大鼠,以urethane (1.2 g/kg)腹腔麻醉,進行氣管及股動、靜脈插管,切斷兩側迷走神經後,將大鼠以臥姿安置在腦定位儀上,給予gallamine triethiodide (i.v.) 痲痹,接上人工呼吸器,分離並紀錄膈神經及顏面神經的呼吸活動,調整混合氣體使呼氣末二氧化碳濃度分別為正常 (0.04-0.05) 及二氧化碳濃度增加 (0.07-0.08) 的情形下進行實驗。 利用微量注射技術以麩胺酸鈉 (glutamate;Glu) 確定VLM的位置並區分為升壓區與降壓區,待確定後,注射1.5x10-8 IU及3.0x10-8 IU劑量的AVP至VLM,觀察膈神經活動、顏面神經呼吸活動與血壓的反應;此外,在同一區域分別以0.3及0.6 ng的AVP V1A接受器拮抗劑預處理,立即再注射同劑量的AVP,觀察膈神經、顏面神經與血壓有無改變。 結果顯示AVP注射在VLM內側,血壓不變,膈神經及顏面神經的呼吸活動受到抑制,稱為第一型反應 (Type I response);而AVP作用在VLM外側,血壓上升,膈神經與顏面神經的呼吸活動同樣受到抑制,稱為第二型反應 (Type II response);呼氣末二氧化碳濃度增加,會減弱AVP對於膈神經呼吸活動的抑制作用,AVP對於顏面神經的抑制卻不會因為呼氣末二氧化碳濃度增加而減弱;以AVP V1A接受器拮抗劑預處理會抵消AVP對膈神經與顏面神經呼吸活動的抑制作用;若以phentolamine預處理,AVP對呼吸的抑制作用仍在,顯示AVP對呼吸的抑制作用不是升壓引起感壓反射所造成的。這些結果暗示內生性AVP神經纖維可能經由VLM區域神經元上的V1A接受器而調控心肺功能,並可能藉由影響顏面神經而影響上呼吸道的暢通。

並列摘要


The aim of the present study was to examine the effects of Arg8-vasopressin (AVP) which was microinjected into ventrolateral medulla (VLM) on phrenic nerve activity and respiratory-related facial nerve discharge. In addition, we further identified whether these effects of AVP on cardiopulmonary functions were mediated by AVP V1A receptor. Adult male Wistar rats (250-350 g) were used. Under urethane (1.2g/kg i.p.) anesthesia, tracheotomy was performed and femoral artery and vein were catheterized. The animal was placed in a prone position on a stereotaxic instrument. The phrenic and facial nerves on one side was isolated and cut distally. Activities of both nerves were recorded via an amplifier and then integrated. Ends-tidal fractional concentration of gas was maintained at normncapnia or hypercapnia in hyperoxia. AVP and AVP V1A antagonist were microinjected into the VLM to observe the responses of phrenic and facial nerve activity. The results revealed that:(1) AVP microinjected into the medial portion of the VLM produced apnea, decreases in phrenic and facial nerve activities without change in blood pressure (Type I response). (2) AVP microinjected into the lateral portion of the VLM produced apnea, decrease in phrenic and facial nerve activities and concomitant pressor effect (Type II response). (3) These inhibitions of AVP upon phrenic and respiratory-related facial nerves were partially attenuated by hypercapnia. (4) These cardiopulmonary responses could be totally abolished by treatment of vasopressin V1A antagonist ([β-Mercapto-β, β-cyclopentamethyl enepropionyl1,-O-Me-Tyr2-Arg8]-vasopressin). (5) Pretreatment with phentolamine could abolish the pressor effect but not affect the inhibitory action on PNA evoked by AVP. These results implied that the modulatory effects of an endogenous vasopressinergic pathway on cardiopulmonary functions were mediated by vasopressin V1A receptor located on the neurons within the VLM. In addition, this pathway may also influence upper airway patency by the modulation on respiratory-related facial nerve.

參考文獻


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