臺灣博碩士論文加值系統

一氧化氮為最近十年內所發現之一種重要的血管舒張物質。它具有調整血
管張力的功用。我們將大白鼠養於 90% 氧氣的容器中二天觀察高氧對於
其肺臟生成一氧化氮之影響以及一氧化氮在肺血管缺氧收縮反應中所扮演
之角色。本實驗是以一氧化氮監測器、壓力感應器並利用動物原位離體肺
之模型，監測大白鼠肺臟一氧化氮之生成以及肺動脈壓之變化。體外實驗
中︰我們取出大白鼠全血或血漿加入 0.05 M L- arginine(生成ㄧ氧化
氮之先驅物)溶液中，結果呼吸高氧之大白鼠(高氧組)所生成的一氧化氮
明顯大於呼吸正常氧之大白鼠(對照組)。體內的實驗中：以緩衝溶液灌流
動物離體肺時，在高氧組所生成的一氧化氮明顯地大於對照組；加入了
L-arginine 1 mM 後，可見高氧組所生成之一氧化氮的量，明顯地大於對
照組。而加入一氧化氮合成■競爭性抑制劑 L-NAME(Nw-nitro-L-
arginine methyl ester) 1 mM 後，則可見高氧組之一氧化氮含量的減少
，顯著地大於對照組。於缺氧誘發肺血管收縮(HPV)反應中，以稀釋過之
全血溶液灌流動物時，結果是高氧組明顯地大於對照組，且缺氧誘發一氧
化氮之生成亦明顯地大於對照組；但是加入 1 mM L-NAME 作用三十分鐘
後則以上之反應與對照組無異。然而以誘發型一氧化氮合成■抑制劑
dexamethasone(10 mg/kg/day, 二天)處理之吸高氧大白鼠，則其缺氧誘
發肺血管收縮反應與吸正常氧大白鼠無明顯差別，但卻明顯地大於吸高氧
的大白鼠﹔用 diltiazem (2 mg/kg/day, 二天) 處理吸高氧的大白鼠，
以抑制構成型一氧化氮合成■，則其 HPV 反應與高氧組之大白鼠無異，
但是明顯地小於吸正常氧的大白鼠。綜合以上結果，我們認為大白鼠置於
高氧環境下確實會增加肺臟一氧化氮的生成，以致於減少了缺氧誘發之肺
血管收縮反應，其中誘發型一氧化氮合成■之活化可能佔重要角色。

Nitric Oxide (NO) has been found for about 10 years and many
studies indicate that NO is a potent vessel dilator and a major
physiological regulator of basal blood vessel tone. The rats
were put in an oxygen enriched (90% O2) environment for 2 days
to know the effects of hyperoxia on the NO synthesis in the rat
lungs and the role of NO involved in hypoxic pulmonary
vasoconstriction. We used the isolated perfusion lung models
with physiological salt solution (PSS) as perfusate and
employed a NO meter to measure the NO changes. The pulmonary
pressure was detected. In vitro, the whole blood or plasma from
the hyperoxic rats (HOR) and normoxic rats (NOR) were added
into the solution containing L-arginine (NO precuror; 0.05 M).
The results showed that the NO response in the HOR was
significantly higher than the NOR. In the isolated PSS perfused
rat lungs, the release of the NO gained from the HOR was
markedly higher than which gained from the NOR. After the
conditions were stable, we added 1 mM L- arginine into the
perfusate, and the NO response in the HOR was notedly higher
than the NOR. When the NOS inhibitor, L-NAME, 1 mM was applied,
the reverse of NO curve was prominently in the HOR than in the
NOR. The hypoxic pulmonary vasoconstriction (HPV) response was
blunted and hypoxic-induced NO synthesis was higher in the HOR.
L-NAME 1mM was applied for 30 mins after the 1st hypoxic
challenge, then the HPV response and NO synthesis in the 2nd
hypoxic challenge between the two groups were similar. While we
treated the HOR with dexamethasone (inducible NOS inhibitor) 10
mg/kg/day for 2 days, the HPV response restored to the normoxic
condition. When the HOR pretreated with diltiazem (constitutive
NOS inhibitor, 2 mg/kg/day for 2 days), the HPV response didn't
restore to the normoxic condition. We suggest that NO synthase
was activated under the hyperoxic condition, so that the HPV
response was attenuated. Activation of inducible NOS in rat
lungs might play a major role.