Acute Hyperglycemia Impairs Norepinephrine Vasoconstriction through the Formation of Thromboxane A2

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。

關鍵字

小腸；新腎上腺素；高血糖；血栓形成素

並列摘要

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 seperate 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.

並列關鍵字

intestine ； norepinephrine ； hyperglycemia ； thromboxane

國際替代計量

Acute Hyperglycemia Impairs Norepinephrine Vasoconstriction through the Formation of Thromboxane A2

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