几种水杨酸类似物的低钙作用。

Y Kato, K Nishishita, H Sakai, M Tatsumi, K Yamamoto
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引用次数: 1

摘要

本研究旨在探讨阿司匹林致低钙血症的构效关系。几种水杨酸(SA)类似物经胃管口服。一般情况下,药物悬浮在2% CMC溶液中。在治疗后的预定时间,收集60微升血液以测定钙水平。采用阿司匹林、邻羟基苯甲酸钠盐(na -水杨酸钠)、间对羟基苯甲酸钠盐(HBA)、2,5-二羟基苯甲酸钠(DHBA)、PAS二水合钠(PAS- na)、水杨胺(SAM)和2% CMC作为对照。阿司匹林和na -水杨酸可诱导低钙血症,而m-和p- hb - na不能。此外,DHBA和PAS在静脉注射而非口服时引起低钙血症。这些结果表明,羧基必须与苯环上的羟基相邻才能诱导这种类型的低钙血症,并且即使在同一环上存在额外的第三个取代基,SA结构也能够诱导低钙血症。在阿司匹林- dl赖氨酸(水溶性阿司匹林)和SA-DL赖氨酸的比较中,SA-DL赖氨酸对低钙的作用比ASP-DL赖氨酸更有效,因为SA-DL赖氨酸不是PG合成酶的抑制剂。这种现象主要出现在静脉注射后,乙酰基可能更负责乙酰化阿司匹林- dl赖氨酸组的PG合成酶。目前的结果似乎与先前的假设一致,即pg不参与阿司匹林诱导的大鼠低钙血症的过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypocalcemic action of the several types of salicylic acid analogues.

The present study was performed to see the structure-activity relationships on the aspirin-induced hypocalcemia. Several kinds of salicylic acid (SA) analogues administered orally with a stomach tube. In general, the drugs were suspended in the 2% CMC solution. At the scheduled times after the treatment, 60 microliters of the blood was collected to determine the level of calcium. Aspirin, sodium salt of o-hydroxybenzoic acid (Na-salicylate), sodium salt of m- and p-hydroxybenzoic acid (HBA), 2,5-dihydroxybenzoic acid (DHBA), PAS sodium dihydrate (PAS-Na), salicylamide (SAM) and 2% CMC control were used. Hypocalcemia was induced by aspirin and Na-salicylate but not by m- and p-HBA-Na. In addition, DHBA and PAS caused hypocalcemia when they were administered intravenously but not orally. These results suggest that the carboxyl group must be adjacent to the hydroxyl group on the benzene ring to induce this type of hypocalcemia and that the SA structure would be able to induce hypocalcemia, even in the presence of the additional third substituent on the same ring. On the comparison between aspirin-DL lysine (water soluble aspirin) and SA-DL lysine, SA-DL lysine, which is not an inhibitor of PG synthetase, was more effective on the hypocalcemic action than ASP-DL lysine. The phenomenon was observed at the stage especially immediately after intravenous injection, when the acetyl group may be more responsible to acetylate the PG synthetase in the aspirin-DL lysine group. The present results seems to be consistent with the previous hypothesis that PGs are not involved in the process of aspirin-induced hypocalcemia in the rat.

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