• 作者： 吳錦楨; 顏茂雄
• 作者服務機構： 國防醫學院藥理學科
• 中文摘要： 本論文研究dexamethasone（DEX，一種誘導型一氧化氮合成酵素生成抑制劑）合併aminoguanidine（AG，一種誘導性一氧化氮合成酵素活性抑制劑）對大鼠經內毒素處理後各種症狀之療效。同時也檢視假如完全抑制一氧化氮的形成是否具有改善內毒素所引起的低血壓、血管低反應性和存活率。實驗結果顯示，大鼠經內毒素處理後會引起血壓下降、心跳增快和血管的低反應性，而且血中一氧化氮的濃度持續性上升。DEX與AG前後給予的混合療法可以完全抑制因內毒素所引起的一氧化氮過量生成，並改善遲緩性低血壓，但卻會加強心跳過快的現象；然而對內毒素所引起的血管低反應性只有部份改善。最後整體的結果顯現出此種混合療法可以提高動物的存活率。這些結果暗示著（1）這種混合療法可改善內毒素所引起的部份致命作用；（2）一氧化氮只是引起敗血性休克時血管低反應性的因素之一。
• 英文摘要： The effects of a combination of dexamethasone (DEX, an inhibitor of inducible nitric oxide synthase(iNOS) synthesis) and aminoguanidine (AG, an inhibitor of iNOS activity) on the anesthetized rat treatedwith endotoxin (lipopolysaccharide, LPS) were examined. In addition, we investigated whether a completeinhibition of nitric oxide (NO) formation caused by LPS prevents the hypotension, restores the vascularhyporeactivity to normal and improves the survival rate. The combination of DEX (3 mg/kg at 30 min priorto LPS) plus AG (15 mg/kg at 2 h after LPS) inhibited the overproduction of nitrate (an indicator of NO)and prevented the development of delayed hypotension, but further enhanced tachycardia in rats treatedwith LPS for 6 h. In addition, the vascular hyporeactivity to norepinephrine (NE) was, however, only partiallyrestored in endotoxemic rats treated with DEX plus AG. During the experimental period, the survival rateof LPS-rats treated with DEX plus AG was also improved when compared to that of rats treated with LPSonly. The beneficial effects of the combined therapy with DEX plus AG on rats with endotoxemia, suggest-ing that (i) combined treatment of animals with DEX plus AG may reduce some of the detrimental effects ofLPS and (ii) NO only partially contributes to the vascular hyporeactivity in endotoxic shock.
• 中文關鍵字： dexamethasone; aminoguanidine; nitric oxide; lipopolysaccharide; endotoxic shock.
• 英文關鍵字： --