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脑室内注射拟交感神经药物可抑制大鼠的产热和散热机制。

Intracerebroventricular injection of sympathomimetic drugs inhibits both heat production and heat loss mechanisms in the rat.

作者信息

Lin M T, Chandra A, Chern Y F, Tsay B L

出版信息

Can J Physiol Pharmacol. 1980 Aug;58(8):896-902. doi: 10.1139/y80-137.

Abstract

The effects of intracerebroventricular (i.c.v.) injections of sympathomimetic drugs on thermoregulatory functions in conscious rats maintained at low (8 decrees C), moderate (22 degrees C), and high (30 degrees C) ambient temperatures were assessed. Norepinephrine, tyramine, and ephedrine each produced hypothermia at ambient temperature (Ta) 8 degrees C and hyperthermia at Ta 22 and 30 degrees C. At Ta 8 degrees, the hypothermia in response to norepinephrine, tyramine, and ephedrine was due to decreased metabolic rate (M) whereas at Ta 22 degrees C the hyperthermia was due to cutaneous vasoconstriction. AT Ta 22 degrees C, the hyperthermia in response to norepinephrine and tyramine was due to cutaneous vasoconstriction whereas the hyperthermia in response to ephedrine was brought about by increased M (due to behavioral excitation). Intracerebroventricular injection of epinephrine produced hypothermia followed by hyperthermia at Ta 8 and 22 degrees C. The hypothermia was due to decreased M whereas the hyperthermia was due to cutaneous vasoconstriction and increased M. AT Ta 30 degrees C, epinephrine led to a reduction in cutaneous temperature and hyperthermia. Furthermore, i.c.v. administration of phenylephrine produced a decreased M and hypothermia Ta 8 degrees C and an increased M (due to behavioral excitation) and hyperthermia at Ta 30 degrees C. At Ta 22 degrees C, phenylephrine produced hyperthermia (due to cutaneous vasoconstriction and increased M) preceded by hypothermia (due to decreased M). Moreover, the temperature effects induced by norepinephrine were antagonized by pretreatment with the adrenoceptor antagonist phentolamine. In general, the data indicate that activation of central adrenoceptors with sympathomimetic drugs inhibits both heat production and heat loss mechanisms in the rat.

摘要

评估了脑室内(i.c.v.)注射拟交感神经药物对维持在低温(8摄氏度)、中度(22摄氏度)和高温(30摄氏度)环境温度下的清醒大鼠体温调节功能的影响。去甲肾上腺素、酪胺和麻黄碱在环境温度(Ta)为8摄氏度时均引起体温过低,而在Ta为22和30摄氏度时引起体温过高。在Ta为8摄氏度时,对去甲肾上腺素、酪胺和麻黄碱的体温过低反应是由于代谢率(M)降低,而在Ta为22摄氏度时,体温过高是由于皮肤血管收缩。在Ta为22摄氏度时,对去甲肾上腺素和酪胺的体温过高反应是由于皮肤血管收缩,而对麻黄碱的体温过高反应是由M增加(由于行为兴奋)引起的。脑室内注射肾上腺素在Ta为8和22摄氏度时引起体温过低,随后体温过高。体温过低是由于M降低,而体温过高是由于皮肤血管收缩和M增加。在Ta为30摄氏度时,肾上腺素导致皮肤温度降低和体温过高。此外,脑室内给予去氧肾上腺素在Ta为8摄氏度时导致M降低和体温过低,而在Ta为30摄氏度时导致M增加(由于行为兴奋)和体温过高。在Ta为22摄氏度时,去氧肾上腺素先引起体温过低(由于M降低),随后引起体温过高(由于皮肤血管收缩和M增加)。此外,去甲肾上腺素诱导的温度效应可被肾上腺素能受体拮抗剂酚妥拉明预处理所拮抗。总体而言,数据表明拟交感神经药物激活中枢肾上腺素能受体会抑制大鼠的产热和散热机制。

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