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[辅酶A(COA)对链脲佐菌素诱导的糖尿病大鼠主动脉6-酮-前列腺素F1α含量的影响。其对人类微循环障碍有益作用的潜在作用机制]

[Effect of coenzyme A (COA) on the 6-keto-prostaglandin F1 alpha content of the aorta of rats made diabetic with streptozotocin. Potential mechanism of action of its favorable effect on microcirculatory disorders in man].

作者信息

Kirsch F, Cloarec M

机构信息

Laboratoire de physiologie biochimique, Faculté de Médecine Saint-Antoine, Paris.

出版信息

J Mal Vasc. 1988;13(3):201-4.

PMID:3049877
Abstract

The production of 6-keto-prostaglandin F1 alpha, a stable metabolite of the vasodilator prostacyclin (PGI2), by fragments of the thoracic aorta of rats made diabetic by streptozotocin, was evaluated by radio-immunological assay. The level of production was found to be statistically higher (p less than or equal to 0.01) in the group treated with Coenzyme A (CoA) than in the placebo group. The authors suggest that the mode of action of CoA 1000 much greater than in microcirculatory pathology could involve an increased production of vasodilator prostacyclin.

摘要

通过放射免疫分析法评估了链脲佐菌素诱导糖尿病大鼠胸主动脉片段产生6-酮-前列腺素F1α(血管舒张剂前列环素(PGI2)的稳定代谢产物)的情况。发现辅酶A(CoA)治疗组的产生水平在统计学上高于安慰剂组(p≤0.01)。作者认为,CoA的作用方式(比在微循环病理中的作用大得多)可能涉及血管舒张剂前列环素产量的增加。

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