臺灣博碩士論文加值系統

先前我們許多的研究，將麩胺酸鈉(sodium glutamate, Glu) 微量注射於
橋腦的藍斑核旁肱區(LC-PBN)和巨大細胞蓋區(FTG)、 延腦的背區( DM)
及吻端腹外側區(CVLM)等區域都能引發升壓反應,微量注射於延腦尾端腹
外側區則引發降血壓反應,證明在這些神經機構中,都有引發心臟血管反應
的細胞存在。近年,我們期望進一步了解在上述這些區域中,麩胺酸鈉究竟
激發一類接受器引發血壓反應。本實驗使用以尿酯(urethane,400 mg/kg
)及氯醛醣(alpha-chloralose,40 mg/kg) 麻醉的貓為材料,記錄血壓(
SAP) , 平均血壓(MSAP)及心跳(HR), 亦同時記錄兩交感神經的活性,一條
是記錄來星狀神經節之椎神經(VNA)另一條是腎神經(RNA), 探討它們在血
壓反應中之異同實驗利用不同亞型的麩胺酸鹽接受器拮抗劑glutamate
acid diethyl ester (GDEE,0.5 M,50 nl) 來拮抗Quisqualate接受器,
D-2-amino-5-phos-phonovaleric acid (D-AP5,0.025 M,50 nl)來拮抗
N-methyl-D-aspartate 接受器(NMDA receptor), 分別探討Quisqualate
及 NMDA接受器在腦幹各心臟血管反區細胞, 接受Glu微量注射 (0.1M,50
nl)後引發血壓反應的重要性, 除此之外, 為了要探討各心臟血管反應區
能對Glu反應的細胞是否也對血管收縮素II(AngII)反應, 在另一組的實驗
，我們在上述反應區同一點, 分別微量注射 Glu(0.1 M,50 nl)及 Ang
II(0.16 mM, 50 nl)。 結果顯示,在各升壓區中, Glu引發血壓上升及神
經活性增加的反應皆能被GDEE拮抗, 而D-AP5對Glu的拮抗作用則視反應區
之不同而稍有差異。 在CVLM降血壓區, Glu引發之血壓下降及神經活性減
低作用皆不能被 GDEE及D-AP5所拮抗。同時, 在血壓反應過程中對兩交感
神經之相關性加以比較, 發現椎神經與腎神經的活性變化並不一定一致。
一般來說, 貓的椎神經活性與升血壓反應相關性較腎神經的高。大部分
Glu 刺激能引發血壓反應的刺激點, 給予 AngII亦可引發同樣的血壓反應
。綜合上述實驗的結果, 可歸納成以下三點結論：1.腦幹各心血管反應區
的細胞, 引發血壓上升主要是透過Quisqualate接受器, NMDA接受器並不
重要。Glu在CVLM所產生的降壓作用，既非透過NMDA, 也非透過
Quisqualate接受器, 究竟為何,尚待進一步研究。 2. 腦幹各心臟血管
反應區, 應用不同的神經細胞及不同機制來達成不同的交感神經調控, 而
以透過椎神經的, 似較腎神經的為高。3. 大部分心臟血管區的細胞, 能
接受Glu引發反應的, 同時也能接受 Ang II引發相似的反應。

In our previous studies, using sodium glutamate (Glu) as a
tool, we have demonstrated the existence of pressor neurons in
the locus ceruleus-parabrachial nucleus (LC-PBN), giganto-
cellular tegmental field (FTG), rostral ventrolateral medulla
(RVLM) and dorsal medulla (DM). In the present study attempt
was made to examine the role of glutamate receptors in the
neurons of above pressor or depressor areas that responded to
Glu. 55 cats anesthetized with mixture of urethane and .alpha.-
chloralose. The following responses were recorded: systemic
arterial pressure , mean systemic arterial pressure, heart rate
and sympathetic nerve activities. The later included those of
the vertebral nerve (VNA), and renal nerve (RNA). In order to
determine the nature of receptor responsible for Glu actions,
GDEE was microinjected into the cardiovascular-reactive areas
to block the action of quisqualate receptors, while D-AP5 to
blockthe NMDA receptors. Also, microinjection of angiotensin II
(Ang II) into the same areas, which responded to Glu, was
performed to examine whether they could produce the same or
different actions. Our results showed that the above mentioned
pressor areas, GDEE completely blocked pressor response of SAP
increase and augmentation of nerve activities induced by Glu,
while D-AP5 was effective only for SAP action but not nerves
action. In CVLM, neither GDEE and D-AP5 could block the
depressor responses, either SAP or nerves, elicited by Glu.
AngII produced similar effects as the same pressor or depressor
areas responded to Glu. Our results suggest that: (1) the
pressor responses elicited by Glu are primarily mediated by
quisqualate receptors, while the depressor responses are not
mediated by quisqualate and NMDA receptors, (2) VNA is more
closely related with the SAP change than RNA, (3) Glu-sensitive
neurons areas are sensitive to Ang II , highly suggested the
coexistence of Glu and Ang II receptors in the same neurons.