地塞米松对清醒大鼠冠状动脉结扎所致猝死的保护作用可能机制。
The possible mechanism of protection induced by dexamethasone against sudden death due to coronary ligation in conscious rats.
作者信息
Koltai M, Leprán I, Nemecz G, Szekeres L
出版信息
Br J Pharmacol. 1983 Jun;79(2):327-9. doi: 10.1111/j.1476-5381.1983.tb11003.x.
Abstract
Rat isolated peritoneal cells (10(7) cells ml-1) incubated in the presence of dexamethasone (3 X 10(-9) M, for 90 min) were shown to release some factor(s), having a mol. wt. of 15 k, as determined by size exclusion chromatography, which inhibited phospholipase A2 activity and offered significant protection against sudden death due to post-infarction arrhythmias in conscious rats pretreated with actinomycin D (0.5 mg kg-1 i.v. 4 h before coronary ligation). This observation suggests that the cardioprotective effect of glucocorticoids in acute myocardial infarction may result from the de novo synthesis of macrocortin, an antiphospholipase protein.
摘要
在存在地塞米松（3×10⁻⁹ M，孵育90分钟）的情况下培养的大鼠分离腹膜细胞（10⁷ 个细胞/毫升）显示会释放某些因子，通过尺寸排阻色谱法测定，这些因子的分子量为15k，它们抑制磷脂酶A2活性，并为在用放线菌素D（冠状动脉结扎前4小时静脉注射0.5毫克/千克）预处理的清醒大鼠中因梗死后心律失常导致猝死提供显著保护。这一观察结果表明，糖皮质激素在急性心肌梗死中的心脏保护作用可能源于抗磷脂酶蛋白巨皮质素的从头合成。
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