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脑室内注射前列腺素E2所致发热时交感神经活动的区域差异

Regional differentiation of sympathetic nerve activity during fever caused by intracerebroventricular injection of PGE2.

作者信息

Saigusa T, Iriki M

机构信息

Department of Physiology, Yamanashi Medical College, Japan.

出版信息

Pflugers Arch. 1988 Feb;411(2):121-5. doi: 10.1007/BF00582303.

DOI:10.1007/BF00582303
PMID:3357750
Abstract

In urethane-anesthetized rabbits prostaglandin E2 (PGE2) injected into a lateral cerebral ventricle (icv) produced hyperthermia. During the phase of rising rectal temperature, renal sympathetic activity monitored by multi-unit recording was reduced while the drop of ear skin temperature indicated cutaneous sympathetic activation. These reciprocal changes in activity corresponded to those typical for cold stress as well as for the phase of rising body temperature in fever induced by endotoxic lipopolysaccharides (LPS). However, a slight early stimulation of the heart rate after icv PGE2, contrasted to the initial reductions seen with LPS fever and in the cold. After sino-aortic denervation renal sympathetic inhibition in response to icv PGE2 was reduced but not abolished. After cervical vagotomy the antagonism between cutaneous and visceral sympathetic activity and the increase in heart rate became more prominent. During the phase of subsiding hyperthermia after icv PGE2, renal sympathetic activity returned to its control level, but, unlike LPS fever, did not exceed it. The results of this study indicate that the reciprocal changes in cutaneous and renal sympathetic activity, but not of sympathetic outflow to the heart, are identical during the phase of rising temperature in PGE2 and LPS fever. During the phase of subsiding hyperthermia, renal sympathetic activities change to different extents in PGE2 and LPS fever.

摘要

在氨基甲酸乙酯麻醉的家兔中,向侧脑室注射前列腺素E2(PGE2)会引起体温升高。在直肠温度上升阶段,通过多单位记录监测到的肾交感神经活动降低,而耳皮肤温度下降表明皮肤交感神经激活。这些活动的相互变化与冷应激以及内毒素脂多糖(LPS)诱导的发热中体温上升阶段的典型变化相对应。然而,与LPS发热和寒冷时最初出现的心率降低相反,侧脑室注射PGE2后心率略有早期刺激。在进行窦主动脉去神经支配后,对侧脑室注射PGE2的肾交感神经抑制作用减弱但未消除。在进行颈迷走神经切断术后,皮肤和内脏交感神经活动之间的拮抗作用以及心率增加变得更加明显。在侧脑室注射PGE2后体温下降阶段,肾交感神经活动恢复到对照水平,但与LPS发热不同,并未超过对照水平。本研究结果表明,在PGE2和LPS发热体温上升阶段,皮肤和肾交感神经活动的相互变化相同,但交感神经对心脏的输出变化不同。在体温下降阶段,PGE2和LPS发热时肾交感神经活动的变化程度不同。

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Int J Biometeorol. 1993 Dec;37(4):222-8. doi: 10.1007/BF01387528.
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Participation of interleukin-1 and tumor necrosis factor in the responses of the sympathetic nervous system during lipopolysaccharide-induced fever.白细胞介素-1和肿瘤坏死因子在脂多糖诱导发热期间交感神经系统反应中的作用。
Pflugers Arch. 1990 May;416(3):225-9. doi: 10.1007/BF00392057.
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Comparison of the action of prostaglandin with endotoxin on thermoregulatory response thresholds.前列腺素与内毒素对体温调节反应阈值作用的比较。
Pflugers Arch. 1985 Sep;405(1):1-4. doi: 10.1007/BF00591089.
7
Is prostaglandin E the neural mediator of the febrile response? The case against a proven obligatory role.前列腺素E是发热反应的神经介质吗?关于其既定必需作用的质疑。
Yale J Biol Med. 1986 Mar-Apr;59(2):159-68.
8
Prostaglandin E as the neural mediator of the febrile response.前列腺素E作为发热反应的神经介质。
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Prostaglandin E2 and fever: a continuing debate.前列腺素E2与发热:持续的争论
Yale J Biol Med. 1986 Mar-Apr;59(2):169-74.
10
Is prostaglandin E2 involved in the pathogenesis of fever? Effects of interleukin-1 on the release of prostaglandins.前列腺素E2是否参与发热的发病机制?白细胞介素-1对前列腺素释放的影响。
Yale J Biol Med. 1986 Mar-Apr;59(2):151-8.