睡眠障礙為一顯著之壓力來源，常伴隨交感神經系統活性上升並增加罹患心血管疾病之機率。先前研究顯示，一氧化氮(nitric oxide, NO) 於調控交感神經系統活性功能中扮演相當重要的角色；緣此，本實驗目的即在偵測嚴重睡眠剝奪後，負責心血管訊息初級傳遞之結狀神經節(nodose ganglion, NG) 內，一氧化氮合成(nitric oxide synthase,NOS) 之活性表現情形。睡眠剝奪之實驗模式採用水上轉盤法(disc on water, DOW method)。成年大鼠置於水上轉盤並接受五日睡眠剝奪後，將結狀神經節取下並進行一氧化氮合成免疫組織化學反應(NOS immunohistochemistry)。實驗結果顯示，在正常大鼠結狀神經節內，約有43% 之神經元具一氧化氮合成免疫組織化學反應正向標誌。電腦影像分析結果亦發現，具一氧化氮合成正向標誌神經元之染色相對視密度值(relative optical density, ROD) 為143 ？b3%。然而，經睡眠剝奪處理後，結狀神經節內具一氧化氮合成正向標誌之神經元數目從43% 劇降至20%，其染色相對視密度值亦從143 ？b3% 驟降至109 ？b2%。一氧化氮為重要之交感神經活性抑制物質，本研究證明睡眠剝奪將導致一氧化氮合成活性顯著降低，此一變化將嚴重干擾一氧化氮之生合成過程，並引發交感神經系統過度興奮，繼而可能致使心血管疾病發生之機率大增。
Sleep disorder is a prevalent stress associated with increased sympathetic activity and potentiates the occurrence of cardiovascular disease. Since nitric oxide (NO) may play an important role in the regulation of sympathetic activity, the present study is aimed to determine the NO synthase (NOS) expression in the nodose ganglion (NG), which carrying the primary cardiovascular afferents to the lower brainstem, after total sleep deprivation (TSD). The TSD was performed by the disc on water (DOW) method. Adult rats subjected to five days of TSD were processed for quantitative nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d, a co-factor of NOS) histochemistry and neuronal NOS immunohistochemistry. The present results indicated that in the untreated and control rats, about 43% of the nodose neurons were positively stained for NADPH-d/NOS reactivity. Quantitative image analysis revealed that the staining intensity [relative optical density (ROD)] of NADPH-d/NOS positive neurons were 143 3%. However, following TSD, both the percentage and ROD of NADPH-d/NOS reactive neurons were drastically decreased from nearly 43% to 20% as well as from 143 3% to 109 2%, respectively. Considering that NO could serve as an important messenger in the sympatho-inhibition response, a decrease of NOS expression in the NG following TSD would impair the NO production, which might serve as a potential mechanism responsible for the development of neuropathogenesis in TSD relevant cardiovascular disturbances.
