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題 名 | Acute Hyperglycemia Impairs Norepinephrine Vasoconstriction through the Formation of Thromboxane A[feaf]=急性高血糖透過形成血栓形成素而破壞新腎上腺素對血管的收縮作用 |
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作 者 | 吳家兆; 羅時鴻; 林石化; 林裕峰; 蔡建松; 金忠孝; | 書刊名 | 醫學研究 |
卷 期 | 20:8 2000.10[民89.10] |
頁 次 | 頁397-407 |
分類號 | 415.147 |
關鍵詞 | 小腸; 新腎上腺素; 高血糖; 血栓形成素; Intestine; Norepinephrine; Hyperglycemia; Thromboxane; |
語 文 | 英文(English) |
中文摘要 | 大白鼠腸系膜微動脈暴露在高血糖(300 mg/dl)的環境中一小時或過氧化鉀(1μM)的環境中一分鐘後,高血糖及過氧化鉀都使血管內皮細胞對乙醯膽鹼所引起的內皮細胞依賴性血管擴張作用減少了百分之六十至七十。暴露於高血糖後的微動脈對新腎上腺素的收縮作用減少了一半。在另一組實驗動物中,暴露於過氧化鉀後的微動脈對新腎上腺素的收縮作用卻不改變。以藥物來抑制花生四烯酸的代謝或抑制血栓形成素之接受器後,都可保護微動脈對新腎上腺素的收縮作用(不受到高血糖的破壞)。急性高血糖損傷微動脈對新腎上腺素的收縮作用可能是透過形成血栓形成素,此損傷機轉和氧游離基無關。 |
英文摘要 | The in vivo intestinal microvasculature of normal rats was exposed to 300 mg/dl glucose (isotonicity maintained) for one hour or intravascular potassium superoxide at approximately 1 μM for one minute. Both hyperglycemia and superoxide reduced endothelial dependent dilation to acetylcholine by 60-70%. The constrictor responses to norepinephrine following glucose exposure were reduced by about half. In separate animals, superoxide exposure had no effect on constrictor responses to norepinephrine. Blockade of eicosanoid production by ETYA or pretreatment with a thromboxane A₂ receptor blocker (SQ-29548) fully protected norepinephrine responses during hyperglycemia. Acute hyperglycemia impairs vasoconstrictor responses of mesenteric arterioles to norepinephrine through production of eicosanoids, particularily thromboxane A₂, but not the associated formation of oxygen radicals. |
本系統中英文摘要資訊取自各篇刊載內容。