Yanagi Y, Kurokawa H, Nagao Y, Inukai T
Nihon Yakurigaku Zasshi. 1978 Nov;74(8):981-90. doi: 10.1254/fpj.74.981.
Antipyretic activity of SL-573 was not influenced by age and sex difference in rats. The combined effect of other drugs on antipyretic activity of SL-573 was examined, using several drugs which might be clinically applicable. Cefazolin sodium, ampicillin sodium, codeine phosphate, hydrochlorothiazide and haloperidol did not show any significant effect on antipyretic activity of SL-573. Diazepam itself showed antipyretic activity, and its combined use with SL-573 resulted in an additive effect. SL-573 also showed antipyretic activity in mice with fever induced by yeast, as was seen in rats. SL-573 diminished the hyperthermic response to bacterial endotoxin and leucocytic pyrogen in rats, but not to 2, 4-dinitrophenol. Additionally, SL-573 did not inhibit the bacterial endotoxin-induced production of leucocytic pyrogen and its release in saline medium. SL-573, therefore, is considered to be a centrally acting antipyretic. Intraventricular injection of prostaglandin E2 and arachidonic acid induced a hyperthermia in mice. SL-573 clearly inhibited arachidonic acid-induced hyperthermia, but not prostaglandin E2-induced hyperthermia. Since SL-573 is known to inhibit prostaglandin biosynthesis from arachidonic acid, the prostaglandin biosynthesis inhibition may be one of the main mechanisms of antipyretic action of SL-573.
SL - 573的解热活性不受大鼠年龄和性别的影响。使用几种可能在临床上适用的药物，研究了其他药物对SL - 573解热活性的联合作用。头孢唑林钠、氨苄西林钠、磷酸可待因、氢氯噻嗪和氟哌啶醇对SL - 573的解热活性均未显示出任何显著影响。地西泮本身具有解热活性，它与SL - 573联合使用产生相加作用。与在大鼠中观察到的情况一样，SL - 573在酵母诱导发热的小鼠中也显示出解热活性。SL - 573可减轻大鼠对细菌内毒素和白细胞致热原的热反应，但对2,4 - 二硝基苯酚引起的热反应无影响。此外，SL - 573不抑制细菌内毒素诱导的白细胞致热原的产生及其在盐溶液中的释放。因此，SL - 573被认为是一种中枢性解热药。脑室内注射前列腺素E2和花生四烯酸可诱导小鼠发热。SL - 573明显抑制花生四烯酸诱导的发热，但不抑制前列腺素E2诱导的发热。由于已知SL - 573可抑制花生四烯酸合成前列腺素，前列腺素生物合成抑制可能是SL - 573解热作用的主要机制之一。
