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24.5摄氏度下β-内啡肽诱导大鼠体温反应的肾上腺与甲状腺相互作用

Adrenal and thyroid interactions of beta-endorphin-induced body temperature responses of rats at 24.5 degrees C.

作者信息

Gwosdow A R, Besch E L

出版信息

Proc Soc Exp Biol Med. 1985 Mar;178(3):412-8. doi: 10.3181/00379727-178-42025.

DOI:10.3181/00379727-178-42025
PMID:3156382
Abstract

The effect of beta-endorphin (beta-END) and the role of the adrenal and thyroid glands on body temperature were examined in male rats in a controlled environment room at 24.5 +/- 0.1 degrees C. Relative humidity of 50 +/- 0.3% and a 12L:12D photoperiod (L = 0900 to 2100 hr) were maintained. Rectal temperature (Tr) was measured using thermistors. Corticosterone and thyroid hormones were determined by radioimmunoassay. Intracerebroventricular (IVT) administration of varying doses (0.05 to 50.0 micrograms) of beta-END resulted in a hyperthermia that began 30 min post-IVT injection and continued for an additional hour. Intravenous injections of the same doses of beta-END resulted in little or no Tr response. The beta-END-induced hyperthermia was antagonized by intraperitoneal injection of naloxone. Pretreatment with propranolol, phenotolamine, or both drugs in combination did not block the hyperthermia caused by beta-END. Adrenalectomized or hypophysectomized rats receiving IVT injections of beta-END did not consistently display an increased Tr. beta-Endorphin administration had no detectable effect on serum corticosterone or thyroxine but serum triiodothyronine was decreased. These data suggest the acute hyperthermic action of beta-END is mediated centrally through opiate receptors and does not involve adrenergic receptors.

摘要

在温度为24.5±0.1摄氏度的可控环境室内,对雄性大鼠体内β-内啡肽(β-END)的作用以及肾上腺和甲状腺对体温的影响进行了研究。维持相对湿度为50±0.3%,光照周期为12小时光照:12小时黑暗(光照时间为09:00至21:00)。使用热敏电阻测量直肠温度(Tr)。通过放射免疫分析法测定皮质酮和甲状腺激素。脑室内(IVT)注射不同剂量(0.05至50.0微克)的β-END会导致体温过高,在IVT注射后30分钟开始,并持续另外一小时。静脉注射相同剂量的β-END导致Tr反应很小或没有反应。腹腔注射纳洛酮可拮抗β-END诱导的体温过高。用普萘洛尔、酚妥拉明或两种药物联合预处理均不能阻断β-END引起的体温过高。接受IVT注射β-END的肾上腺切除或垂体切除大鼠并未持续表现出Tr升高。给予β-内啡肽对血清皮质酮或甲状腺素没有可检测到的影响,但血清三碘甲状腺原氨酸降低。这些数据表明,β-END的急性体温过高作用是通过阿片受体在中枢介导的,不涉及肾上腺素能受体。

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