• 沒有找到結果。

創傷出血性休克誘發血液及肝臟葡萄糖-六-磷酸去氫酶的反應及 調節;不過血液與肝臟的反應並不相同。創傷出血性休克後從 1.5 小時 時間點, 大白鼠血液中葡萄糖-六-磷酸去氫酶活性明顯上升; 林格氏 液復甦介入未抑制血中葡萄糖-六-磷酸去氫酶活性上升反應。肝臟葡 萄糖-六-磷酸去氫酶在創傷出血休克後從 1.5 小時時間點即明顯增加;

但創傷出血休克後 4 小時點向上調節反應情形消失。林格氏液復甦液 給抑制大白鼠肝臟葡萄糖-六-磷酸去氫酶在休克後向上調節反應。

創傷出血休克後肝臟與血液氧化壓力的變化有所不同。創傷出血 性休克誘發血液及肝臟氧化壓力的改變可由血液中還原型麩氨基硫與 氧化型麩氨基硫的比值( GSH/GSSG ratio ) 的曲線變化看出。休克後 血液氧化壓力的改變在非常早期即發生;在 1.5 小時時間點即明顯增 加。而復甦介入可改善血液中部份氧化壓力。而創傷出血性休克後肝 臟氧化壓力先明顯增加; 在 4 小時時間點達到尖峰;之後在 8-12 小時時 間點後下降(創傷出血休克後肝臟組織的還原型麩氨基硫在休克後 8-12 小時時間點觀察到明顯上升)。林格氏液復甦介入明顯降低創傷出血休

克後肝臟的氧化壓力 (跟控制組比較,復甦介入並無明顯改變休克初 期 12 小時肝臟組織的還原型麩氨基硫)。

休克初期的數小時內,血液中發炎細胞激素 IL6 和抗發炎細胞激 素 IL10 顯著增加; 但 12-hour 後消失。林格氏液復甦介入抑制 IL6 增 加。但休克後經林格氏液復甦初期幾小時, IL-10 仍然增加,但是低 於休克組。所以林格氏液復甦介入無法完全,只部份抑制血液中 IL-10 上升。

創傷出血性休克改變並增加血液及肝臟氧化壓力; 同時改變並調 節血液及肝臟葡萄糖-六-磷酸去氫酶。但是兩者在創傷出血休克後之 調節反應是有所不同。創傷出血休克後, 肝臟氧化壓力先增加而後下 降; 肝臟葡萄糖-六-磷酸去氫酶也是先增後降。復甦介入降低肝臟氧 化壓力;也抑制肝臟葡萄糖-六-磷酸去氫酶休克後之增加;甚至轉而下 降。這是否暗示肝臟葡萄糖-六-磷酸去氫酶面對創傷出血休克後之反 應與發炎反應較有關係? 然而本實驗缺乏直接證據可以直接說明。創 傷出血休克後, 血液氧化壓力大增;同時血液葡萄糖-六-磷酸去氫酶 活性增加; 血液發炎細胞激素 IL-6 及抗發炎細胞激素 IL-10 也增加。

復甦介入抑制血液 IL-6 上升及抑制部份血液 IL-10 上升; 降低血液部 份氧化壓力。但是復甦介入並未明顯降低血液葡萄糖-六-磷酸去氫酶

活性之增加。是否血液葡萄糖-六-磷酸去氫酶面對創傷出血休克後之 調節反應與肝臟葡萄糖-六-磷酸去氫酶有所不同? 需進一步實驗釐 清。

圖表

圖一 動物實驗

圖二 實驗不同時序時間點測定之血液 G6PD 比較曲線

圖四 實驗不同時序時間點西方點墨法測定肝臟之 G6PD 曲線圖

圖五 實驗不同時序時間點測定血液 GSH 比較曲線圖

圖六 實驗不同時序時間點測定血液 GSH/GSSG Ratio 比較曲線圖

圖七 實驗不同時序時間點測定肝臟 GSH 比較曲線圖

圖八 實驗不同時序時間點測定肝臟 GSH/GSSG Ratio 比較曲線圖

圖九 實驗不同時序時間點測定血液細胞激素 IL-6 比較曲線圖

圖十 實驗不同時序時間點測定血液細胞激素 IL-10 比較曲線

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