ATTENUATION OF ASPIRIN ANALGESIA BY CALCIUM LOADING IN HEALTHY SUBJECTS

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To clarify the mechanism of aspirin analgesia, the relationship among analgesic and hypocalcemic effects and pharmacokinetics of aspirin was investigated in 20 healthy subjects at 20-23 years old. Four experimental groups were made, that is, (1) aspirin 1.0 g, (2) aspirin 1.0 g+calcium gluconate 1.5 g×2,(3) calcium gluconate 1.5 g×2,(4) control (placebo). Calcium gluconate was administered orally twice, that is, 30 and 90 min after oral administration of aspirin. The experiments were carried out under a double blind method. As an analgesic test, the ultrasonic method was used. Aspirin (1.0 g) caused a significant analgesia, the effect reaching the maximum at 90 min and prolonging for about 3 h. Simultaneously, plasma calcium level significantly decreased and kept going down, at least, until 180 min after administration of aspirin. However, when calcium gluconate was loaded at 30 and 90 min after administration of aspirin, both the analgesic and hypocalcemic effects of aspirin were significantly inhibited. The plasma aspirin concentration reached a maximum 30-60 min after administration of aspirin in both groups : aspirin alone and aspirin with calcium gluconate. On the other hand, plasma salicylic acid concentration kept increasing up to 180 min after administration of aspirin in either group. The plasma aspirin and salicylic acid levels in both groups were similar. The above results indicate that the calcium-lowering effect of aspirin is significantly involved in the aspirin analgesia, and that the analgesic effect of aspirin depends on plasma aspirin by itself in terms of inhibition of prostaglandin biosynthesis, but at least in a part, depends on plasma salicylate which may cause the hypocalcemic effect and thus lead to desensitization of a calcium-dependent pain-enhancing mechanism.
社団法人日本薬学会の論文

ATTENUATION OF ASPIRIN ANALGESIA BY CALCIUM LOADING IN HEALTHY SUBJECTS

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