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通过向大鼠脑腹侧隔区注射水杨酸钠来阻断前列腺素E1引起的体温过高。

Blockade of prostaglandin E1 hyperthermia by sodium salicylate given into the ventral septal area of the rat brain.

作者信息

Alexander S J, Cooper K E, Veale W L

机构信息

Department of Medical Physiology, Faculty of Medicine, University of Calgary, Alberta, Canada.

出版信息

J Physiol. 1987 Mar;384:223-31. doi: 10.1113/jphysiol.1987.sp016451.

Abstract
  1. Sodium salicylate (30.0 micrograms microliter-1) or artificial cerebrospinal fluid (ACSF) was infused bilaterally into the ventral septal area (v.s.a.) of the unrestrained rat for 1 h before and 1 h after the injection of prostaglandin E1 at a concentration of 20.0 ng microliter-1 into a lateral cerebral ventricle. 2. During control (ACSF) infusions, 200.0 ng of prostaglandin E1 evoked a hyperthermic response (0.95 +/- 0.16 degrees C). During sodium salicylate infusions, the prostaglandin E1-evoked hyperthermia was significantly reduced (P less than 0.025) to 0.31 +/- 0.16 degrees C. 3. The fever index (degrees C h for 1.0 h) during the infusion of sodium salicylate was reduced 66% below that of control infusions (P less than 0.01). 4. These data indicate that sodium salicylate infused in the v.s.a. of rats can antagonize a prostaglandin E-evoked hyperthermia. This suggests that there may be an additional mechanism of action for sodium salicylate antipyresis other than inhibition of prostaglandin E synthesis.
摘要
  1. 在将浓度为20.0纳克/微升的前列腺素E1注入大鼠侧脑室之前1小时和之后1小时,将水杨酸钠(30.0微克/微升)或人工脑脊液(ACSF)双侧注入未束缚大鼠的腹侧隔区(v.s.a.)。2. 在对照(ACSF)输注期间,200.0纳克前列腺素E1引起体温升高反应(0.95±0.16摄氏度)。在水杨酸钠输注期间,前列腺素E1引起的体温过高显著降低(P<0.025)至0.31±0.16摄氏度。3. 水杨酸钠输注期间的发热指数(1.0小时的摄氏度·小时)比对照输注降低了66%(P<0.01)。4. 这些数据表明,注入大鼠腹侧隔区的水杨酸钠可拮抗前列腺素E引起的体温过高。这表明水杨酸钠解热作用可能存在除抑制前列腺素E合成之外的其他作用机制。

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