Riedel W
J Auton Nerv Syst. 1985 Feb-Mar;12(2-3):145-57. doi: 10.1016/0165-1838(85)90057-8.
In conscious rabbits with indwelling intracisternal (i.c.) catheters i.c. injections of 600 micrograms kg-1 6-hydroxydopamine (6-OHDA) elicited with short latencies an increase in metabolic rate followed by cutaneous vasoconstriction and a reduction in renal sympathetic nerve activity; in addition there was depression of respiratory rate, bradycardia and a fall of blood pressure. This differentiated cardiorespiratory activity pattern was fully established about 1 h after i.c. 6-OHDA, when injected at thermoneutrality. At warm ambient temperatures the metabolic and cardiorespiratory responses to i.c. 6-OHDA were considerably diminished and there was tachycardia. Intravenous (i.v.) injection of 4 micrograms kg-1 bacterial endotoxin (LPS) in intact rabbits evoked with short latency an increase in metabolic rate and the typical cardiorespiratory activity pattern normally seen in cold defense, consisting of cutaneous vasoconstriction, a depression of respiratory rate and, as shown in a previous study, a decrease in renal sympathetic nerve activity while heart rate and arterial blood pressure is little altered. When LPS was i.v. injected 2-3 days after i.c. 6-OHDA, the febrile response was attenuated with lesser cutaneous vasoconstriction and respiratory rate depression. There was no early inhibition in renal sympathetic nerve activity but rather marked excitation, with increases in heart rate and arterial blood pressure. The results indicate that the effects on autonomic system activities being produced by transmitter release at noradrenergic terminals acutely following i.c. 6-OHDA are considerably modulated by ambient temperature. Comparison of autonomic system reactions in fever obtained in the intact animal and after i.c. 6-OHDA reveals the important role of central noradrenergic pathways in preserving blood pressure homeostasis and heat conservation. The appearance of cardiorespiratory responses similar to those obtained after i.c. noradrenaline or i.c. 6-OHDA, when non-thermal activation of thyrotropin-releasing hormone (TRH) neurons occurs (as demonstrated in a previous study), suggests the hypothesis that TRH neurons known to be specifically influenced by changes in body temperature, converge onto the central noradrenergic system producing the typical cardiorespiratory pattern of cold defense.
在留置脑池内(i.c.)导管的清醒家兔中,脑池内注射600微克/千克的6-羟基多巴胺(6-OHDA)会在短潜伏期内引发代谢率增加,随后出现皮肤血管收缩和肾交感神经活动降低;此外,呼吸频率降低、心动过缓和血压下降。当在热中性条件下注射时,这种有差异的心肺活动模式在脑池内注射6-OHDA后约1小时完全形成。在温暖的环境温度下,对脑池内注射6-OHDA的代谢和心肺反应明显减弱,并且出现心动过速。在完整家兔中静脉注射(i.v.)4微克/千克细菌内毒素(LPS)会在短潜伏期内引发代谢率增加以及在冷防御中通常出现的典型心肺活动模式,包括皮肤血管收缩、呼吸频率降低,并且如先前研究所示,肾交感神经活动降低,而心率和动脉血压变化不大。当在脑池内注射6-OHDA后2 - 3天静脉注射LPS时,发热反应减弱,皮肤血管收缩和呼吸频率降低程度较小。肾交感神经活动没有早期抑制,而是明显兴奋,同时心率和动脉血压升高。结果表明,脑池内注射6-OHDA后急性地在去甲肾上腺素能神经末梢释放递质对自主神经系统活动产生的影响受到环境温度的显著调节。比较完整动物和脑池内注射6-OHDA后发热时的自主神经系统反应揭示了中枢去甲肾上腺素能通路在维持血压稳态和保存热量方面的重要作用。当促甲状腺激素释放激素(TRH)神经元发生非热激活时(如先前研究所示),出现与脑池内注射去甲肾上腺素或脑池内注射6-OHDA后相似的心肺反应,这提示了一个假说,即已知受体温变化特异性影响的TRH神经元汇聚到中枢去甲肾上腺素能系统,产生冷防御的典型心肺模式。