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脑桥前刀切诱导的体温过高:麻醉大鼠非寒战产热存在紧张性抑制的证据

Hyperthermia induced by pre-pontine knife-cut: evidence for a tonic inhibition of non-shivering thermogenesis in anaesthetized rat.

作者信息

Shibata M, Benzi R H, Seydoux J, Girardier L

机构信息

Département de Physiologie, Faculté de Médicine, Centre Médical Universitaire, Genève, Switzerland.

出版信息

Brain Res. 1987 Dec 15;436(2):273-82. doi: 10.1016/0006-8993(87)91671-4.

Abstract

Temperature of colon, interscapular brown adipose tissue (IBAT) and paw skin (index of vasomotor activity) were monitored before and after microwire knife lesions at the pre-pontine or/and the post-mammillary levels in the urethane-anaesthetized rats at room temperature of 23-24 degrees C. Following the pre-pontine, but not the post-mammillary cut, colonic and IBAT temperatures increased by 3-4 degrees C within 90-240 min. IBAT temperature rose faster with a shorter latency and attained a higher steady-state value than colonic temperature; skin temperature, however rose by only 0.8 degrees C. A procaine microinjection into the pre-pontine area transiently increased by more than 1 degree C both colonic and IBAT temperatures, with similar kinetics as for the knife cut. Cardiac output distribution was measured using radiolabelled microspheres. Brown adipose tissue (BAT) was found to be the only organ to which the fractional blood flow increased dramatically (12 times over baseline value) during the development of hyperthermia. Propanolol, injected after the hyperthermia had fully developed, decreased IBAT and then colonic temperatures. Hexamethonium decreased both colonic and IBAT temperatures with a concomitant rise in skin temperature while tubocurarine was without effect. It is concluded that the hyperthermia observed after the pre-pontine lesion results from an increased sympathetic stimulation of BAT thermogenesis triggered by the release of a tonic inhibitory control on its heat production. Such an inhibitory system would be located somewhere between the lower midbrain and the upper pons.

摘要

在23 - 24摄氏度室温下,对氨基甲酸乙酯麻醉的大鼠,在脑桥前或/和乳头体后水平进行微丝刀损伤前后,监测结肠、肩胛间棕色脂肪组织(IBAT)和爪部皮肤温度(血管运动活性指标)。脑桥前切断后(而非乳头体后切断),结肠和IBAT温度在90 - 240分钟内升高3 - 4摄氏度。IBAT温度升高更快,潜伏期更短,且稳态值高于结肠温度;然而,皮肤温度仅升高0.8摄氏度。向脑桥前区域微量注射普鲁卡因可使结肠和IBAT温度短暂升高超过1摄氏度,动力学与刀切相似。使用放射性微球测量心输出量分布。发现在体温升高过程中,棕色脂肪组织(BAT)是唯一血流量分数显著增加(比基线值增加12倍)的器官。在体温升高完全发展后注射普萘洛尔,可降低IBAT温度,随后降低结肠温度。六甲铵可降低结肠和IBAT温度,同时皮肤温度升高,而筒箭毒碱则无作用。结论是,脑桥前损伤后观察到的体温升高是由于对BAT产热的紧张性抑制控制释放,引发交感神经对BAT产热的刺激增加所致。这样一个抑制系统位于中脑下部和脑桥上段之间的某个位置。

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