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发热绵羊对脊髓和下丘脑加热的体温调节反应。

Thermoregulatory responses of febrile sheep to spinal and hypothalamic heating.

作者信息

Blatteis C M, Necker R, Hales J R, Fawcett A A, Hirata K

机构信息

Ian Clunies Ross Animal Research Laboratory, Commonwealth Scientific and Industrial Research Organization, Prospect, New South Wales, Australia.

出版信息

Am J Physiol. 1987 Dec;253(6 Pt 2):R868-76. doi: 10.1152/ajpregu.1987.253.6.R868.

DOI:10.1152/ajpregu.1987.253.6.R868
PMID:3322046
Abstract

Fever was induced by the intravenous injection of 0.25 microgram/kg of lipopolysaccharide (LPS) from Escherichia coli in eight conscious sheep exposed to ambient temperatures adjusted to the lower range of thermoneutrality. Chronic spinal or hypothalamic thermodes were perfused with water of 44 degrees C for 20 min or for most of the rising phase of fever (100 min of the mean 166 min total rise time). The effects of spinal and hypothalamic heating were identical. Thus, before LPS, spinal or hypothalamic heating did not affect the rate of O2 consumption (VO2) but increased skin blood flow (as indicated by skin temperatures) and elicited panting; therefore rectal temperature (Tre) fell. During fever rise, the already reduced skin blood flow and respiratory rate were not affected by spinal or hypothalamic heating, but the increased VO2 was reduced; consequently, the rise in Tre was attenuated. During the plateau phase of fever, all responses were similar to those seen before LPS. In febrilysis, heating strongly enhanced the operating heat loss mechanisms and, hence, augmented the fall in Tre. Thus, although the thermoeffectors activated by spinal or hypothalamic heating were modified during the different stages of fever, the effect on body temperature was nearly the same. Therefore there seems to be no change in spinal or hypothalamic thermosensitivity during fever in sheep.

摘要

在八只清醒的绵羊中,通过静脉注射每千克体重0.25微克的大肠杆菌脂多糖(LPS)来诱发发热,这些绵羊暴露在被调整到热中性较低范围的环境温度下。用44摄氏度的水对慢性脊髓或下丘脑温度传感器灌注20分钟,或在发热上升期的大部分时间(平均总上升时间166分钟中的100分钟)进行灌注。脊髓和下丘脑加热的效果是相同的。因此,在注射LPS之前,脊髓或下丘脑加热并不影响耗氧率(VO2),但会增加皮肤血流量(通过皮肤温度表示)并引发喘气;因此直肠温度(Tre)下降。在发热上升期间,已经减少的皮肤血流量和呼吸频率不受脊髓或下丘脑加热的影响,但增加的VO2会降低;因此,Tre的上升会减弱。在发热的平台期,所有反应与注射LPS之前观察到的相似。在退热期,加热强烈增强了散热机制,因此加剧了Tre的下降。因此,尽管在发热的不同阶段,由脊髓或下丘脑加热激活的热效应器有所改变,但对体温的影响几乎相同。因此,在绵羊发热期间,脊髓或下丘脑的热敏感性似乎没有变化。

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