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研究生:鄭季媛
研究生(外文):Cheng, Chi-Yuan
論文名稱:自發性高血壓大白鼠具較強clonidine止痛作用機轉之研究
論文名稱(外文):Enhanced clonidine-induced antinociception in spontaneously hypertensive rats involved presynaptic noradrenergic mechanism
指導教授:王昀王昀引用關係
指導教授(外文):Wang Yun
學位類別:碩士
校院名稱:國防醫學院
系所名稱:藥理學研究所
學門:醫藥衛生學門
學類:藥學學類
論文種類:學術論文
論文出版年:1995
畢業學年度:83
語文別:中文
論文頁數:94
外文關鍵詞:clonidine自發性高血壓大白鼠藍斑核clonidineSHRlocus coeruleous
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Clonidine 為臨床上常用的中樞降血壓及止痛藥物。在我們以往的研究發
現clonidine對高血壓動物(如SHR和WKY 相比)有較強的止痛作用。而此較
強的止痛作用可能與血壓沒有直接的關係。在本研究中腹腔注射 DSP4 破
壞無甲基腎上腺素神經元後,以熱板試驗測量clonidine的止痛作用,我
們發現WKY與SHR 仍可產生明顯的止痛作用,其中WKY的 clonidine 止痛
程度可因 DSP4 處理而提高。此外,皮下注射 methamphetamine後再投予
clonidine,可降低 WKY 與SHR 的clonidine止痛程度。這些結果顯示突
觸前無甲基腎上腺素神經元可能與 SHR 較強之 clonidine止痛作用的發
生有關。在HPLC-ECD的實驗,我們發現clonidine可明顯地提高SHR 藍斑
核中無甲基腎上腺素的組織濃度,但對WKY 並無影響。而以離體藍斑核腦
切片伏安電化學技術測量細胞外液無甲基腎上腺素濃度時,我們發現在
SHR,clonidine可抑制KCl 溶液引發之無甲基腎上腺素的釋放,但對WKY
並無影響。因此我們推論SHR產生較強的clonidine 止痛作用,可能與
clonidine調控其突觸前無甲基腎上腺素的釋放有關。綜合以上結果,
SHR 產生較強的 clonidine 止痛作用機轉,可能是由於 clonidine對SHR
具有較強之抑制無甲基腎上腺素釋放的作用,使突觸前內生性的無甲基腎
上腺素釋放較少,進而對clonidine 作用於突觸後受體產生之止痛作用的
抑制程度較少所造成。
Clonidine, an ( alpha2 adrenergic agonist, produces potent
anti- nociceptive and hypotensive actions in various
animals. We previously reported that clonidine-induced
antinociceptive effect was greater in spontaneously
hypertensive rats (SHR) than Wistar-Kyoto rats (WKY). The
enhanced antinociceptive effect of clonidine in SHR was not
directly related to the high blood pressure. In the present
study, we found that clonidine-induced anti- nociception,
measured by hot plate method, was increased after
pretreatment with N-(2-chloroethyl)-N-ethyl-2-
bromobenzylamine ( DSP4 ) in WKY. The clonidine-induced
antinociception was decreased in SHR and WKY after
pretreatment with methamphetamine. These data suggest that
presynaptic noradrenergic mechanism is involved in the
supersensitivity of clonidine in SHR. To further investigate
the difference of clonidine effects on presynaptic
noradrenergic neurons in SHR and WKY, we measured the
con- centration of norepinephrine(NE) in locus coeruleus (L.C.)
using HPLC-ECD. We found that the concentration of NE in L.
C. was increased in SHR, but not in WKY. We also examined
the inter- actions of clonidine and K+-evoked NE release
from L.C. brain slices using nafion-coated carbon fiber
electrodes and chrono- amperometric recording techniques. We
found that clonidine, at the dose of 1 micromolar, inhibited K+-
evoked NE release in the L.C.is more sensitive to this
clonidine-mediated inhibition, as compared with WKY. These
data suggest that the supersensitivity of clonidine in SHR may
be regulated by releasing NE from pre- synaptic noradrenergic
neurons. In conclusion , our data suggest that the
enhanced anti- nociceptive effect of clonidine in SHR may be
derived from the presynaptic noradrenergic mechanism in the CNS.

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