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牛磺酸及其类似物对家兔静脉注射白细胞致热原引起发热的中枢作用。

Central effect of taurine and its analogues on fever caused by intravenous leukocytic pyrogen in the rabbit.

作者信息

Lipton J M, Ticknor C B

出版信息

J Physiol. 1979 Feb;287:535-43. doi: 10.1113/jphysiol.1979.sp012675.

Abstract
  1. Taurine infused I.C.V. after I.V. injection of leukocytic pyrogen (LP) inhibited the initial rise in body temperature and prolonged fever when infusion was stopped. 2. Similar infusion of taurine also inhibited the hypertermic effect of I.C.V. PGE2 (0.5 microgram) but did not cause prolonged hyperthermia. 3. I.C.V. administration of the taurine analogues hypotaurine and beta-alanine, compounds which have been shown previously to compete with taurine for facilitated transport in C.N.S. tissue, also inhibited the initial increase in body temperature and prolonged LP fever. 4. These results suggest that taurine prolongs LP fever by preferentially occupying a carrier system normally required for termination of the effects of endogenous pyrogens or related central mediators of fever. There was no evidence that taurine prolongs fever by blocking inactivation of central PGE2, a substance proposed previously to be a central mediator of fever.
摘要
  1. 静脉注射白细胞致热原(LP)后经脑室内注入牛磺酸,抑制了体温的初始升高,并在停止注入后延长了发热时间。2. 类似的牛磺酸注入也抑制了脑室内注入前列腺素E2(PGE2,0.5微克)引起的体温过高效应,但未导致体温过高的持续时间延长。3. 脑室内给予牛磺酸类似物低牛磺酸和β-丙氨酸,先前已证明这些化合物在中枢神经系统组织中与牛磺酸竞争易化转运,它们也抑制了体温的初始升高并延长了LP发热时间。4. 这些结果表明,牛磺酸通过优先占据内源性致热原或相关发热中枢介质作用终止通常所需的载体系统来延长LP发热时间。没有证据表明牛磺酸通过阻断中枢PGE2的失活来延长发热时间,PGE2先前被认为是发热的中枢介质。

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