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全身性缺氧可促进麻醉大鼠的躯体-心脏交感A反射和C反射。

Systemic hypoxia facilitates somato-cardiac sympathetic A- and C-reflexes in anesthetized rats.

作者信息

Li W M, Sato A, Suzuki A, Trzebski A

机构信息

Department of the Autonomic Nervous System, Tokyo Metropolitan Institute of Gerontology, Japan.

出版信息

Neurosci Lett. 1996 Oct 4;216(3):175-8. doi: 10.1016/0304-3940(96)13024-x.

DOI:10.1016/0304-3940(96)13024-x
PMID:8897486
Abstract

In rats anesthetized with urethane, electrical stimuli applied to tibial nerve afferents produced a somato-sympathetic A-reflex of 41 +/- 2 (mean +/- SEM)ms latency and C-reflex of 210 +/- 13 ms latency recorded in the left inferior cardiac sympathetic nerve. Hypoxia was induced by switching room air to nitrogen/oxygen gas mixture in the inspiratory line reducing end-tidal oxygen from about 18% FETO2 to 10% FETO2 and 6% FETO2 for 60s, respectively. During 6% FETO2 hypoxia, the amplitude of the somato-cardiac sympathetic A-reflex increased significantly to 138 +/- 13% of the control, and that of the C-reflex increased to 186 +/- 18% of the control. During 10% FETO2 hypoxia, the A-reflex increased insignificantly to 117 +/- 8%; the amplitude of the C-reflex was augmented significantly to 149 +/- 11% of the control. Peripheral carotid chemoreceptor denervation abolished the facilitatory effects of systemic hypoxia. It is concluded that carotid chemoreceptor stimulation enhances the responsiveness of somato-cardiac sympathetic excitatory reflexes originating in the hind limb receptors.

摘要

在使用氨基甲酸乙酯麻醉的大鼠中,对胫神经传入纤维施加电刺激,在左下心交感神经中记录到潜伏期为41±2(平均值±标准误)毫秒的躯体-交感A反射和潜伏期为210±13毫秒的C反射。通过将吸气管道中的室内空气切换为氮气/氧气混合气体来诱导缺氧,分别将呼气末氧分压从约18%(FETO2)降至10% FETO2和6% FETO2,持续60秒。在6% FETO2缺氧期间,躯体-心交感A反射的幅度显著增加至对照的138±13%,C反射的幅度增加至对照的186±18%。在10% FETO2缺氧期间,A反射无明显增加,增至117±8%;C反射的幅度显著增大至对照的149±11%。外周颈动脉化学感受器去神经支配消除了全身性缺氧的促进作用。结论是,颈动脉化学感受器刺激增强了起源于后肢感受器的躯体-心交感兴奋性反射的反应性。

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1
Systemic hypoxia facilitates somato-cardiac sympathetic A- and C-reflexes in anesthetized rats.全身性缺氧可促进麻醉大鼠的躯体-心脏交感A反射和C反射。
Neurosci Lett. 1996 Oct 4;216(3):175-8. doi: 10.1016/0304-3940(96)13024-x.
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