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前列腺素在发热中作用的进一步研究。

Further studies on the role of prostaglandin in fever.

作者信息

Dey P K, Feldberg W, Gupta K P, Milton A S, Wendlandt S

出版信息

J Physiol. 1974 Sep;241(3):629-46. doi: 10.1113/jphysiol.1974.sp010675.

Abstract
  1. Experiments were carried out in unanaesthetized cats to find out if a prostaglandin is the mediator (a) for the long lasting fever which often follows injections of phsyiological salt solutions into the cerebral ventricles or into the cisterna magna, as well as their perfusions through the cerebral ventricles, and (b) for the sodium fever which occurs during a perfusion of the cerebral ventricles with calcium-free artificial c.s.f. A fever mediated by prostaglandin should be accompanied by an increase of prostaglandin activity in cisternal c.s.f., and be abolished or prevented by antipyretics like paracetamol or indomethacin which inhibit prostaglandin synthesis. Both criteria were applied.2. The fever which follows injections or perfusions of physiological salt solutions appears to be mediated by a prostaglandin of the E series, probably E(2) (PGE(2)) because it was accompanied by increased prostaglandin E-like activity in the c.s.f. and abolished by paracetamol and indomethacin. During the first few days after pre-treatment of the cats with intramuscular chloramphenicol the injections were rarely followed by fever.3. The fever which occurs during a perfusion with calcium-free artificial c.s.f. appears not to be mediated by prostaglandin, because it was not associated with increased prostaglandin activity in the cisternal effluent, and not prevented by paracetamol or indomethacin, although these antipyretics usually attenuated the fever.4. A perfusion of the cerebral ventricles with artificial c.s.f. containing calcium in an abnormally high concentration (6.25 mM) brought down fever produced by PGE(1), or PGE(2), or bacterial pyrogen.
摘要
  1. 在未麻醉的猫身上进行了实验,以确定前列腺素是否是以下情况的介质:(a) 常在向脑室或小脑延髓池注射生理盐溶液及其通过脑室灌注后出现的持续性发热;(b) 在无钙人工脑脊液灌注脑室期间出现的钠热。由前列腺素介导的发热应伴有小脑延髓池脑脊液中前列腺素活性增加,并可被抑制前列腺素合成的对乙酰氨基酚或吲哚美辛等退热药消除或预防。采用了这两个标准。

  2. 注射或灌注生理盐溶液后出现的发热似乎由E系列前列腺素介导,可能是E(2)(前列腺素E2),因为脑脊液中前列腺素E样活性增加,并被对乙酰氨基酚和吲哚美辛消除。在用肌肉注射氯霉素预处理猫后的头几天,注射后很少出现发热。

  3. 用无钙人工脑脊液灌注期间出现的发热似乎不由前列腺素介导,因为它与小脑延髓池流出液中前列腺素活性增加无关,也不能被对乙酰氨基酚或吲哚美辛预防,尽管这些退热药通常会减轻发热。

  4. 用钙浓度异常高(6.25 mM)的人工脑脊液灌注脑室可降低由前列腺素E1、前列腺素E2或细菌热原引起的发热。

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本文引用的文献

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Effect of pyrogen and antipyretics on prostaglandin acitvity in cisternal c.s.f. of unanaesthetized cats.
J Physiol. 1973 Oct;234(2):279-303. doi: 10.1113/jphysiol.1973.sp010346.
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Pyrogen fever and prostaglandin-like activity in cerebrospinal fluid.
J Physiol. 1973 Jan;228(1):41-53. doi: 10.1113/jphysiol.1973.sp010071.

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