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呼吸负荷补偿。III. 脊髓传入神经的作用。

Respiratory load compensation. III. Role of spinal cord afferents.

作者信息

Frazier D T, Xu F, Lee L Y, Taylor R F

机构信息

Department of Physiology and Biophysics, University of Kentucky, Lexington 40536.

出版信息

J Appl Physiol (1985). 1993 Aug;75(2):682-7. doi: 10.1152/jappl.1993.75.2.682.

DOI:10.1152/jappl.1993.75.2.682
PMID:8226469
Abstract

In a previous study, we reported that inspiratory tracheal occlusion (TO) significantly inhibited the motor drive to the diaphragm in a decerebellated bilaterally vagotomized preparation (J. Appl. Physiol. 75:675-681, 1993). The hypothesis to be tested in the present study was that respiratory muscle afferents activated by inspiratory TO provided the inputs responsible for the observed inhibition. Adult cats were anesthetized, tracheotomized, and instrumented with diaphragm electromyographic (EMGdi) recording electrodes. The cerebellum, vagi, and dorsal spinal cord (C2-T2) were surgically exposed. Inspiratory TO was applied before and after cold blockade of the dorsal cord (C6) or dorsal root (C3-6) transection in the intact and decerebellated vagotomized cat. Respiratory timing (inspiratory and expiratory duration) was determined from the EMGdi record, and the peak integrated EMGdi (integral of EMGdi) response was used as an index of respiratory motor drive. Our results showed that 1) cold blockade at the dorsal C6 level in an intact preparation significantly increased the peak of the integral of EMGdi response to TO and was reversible upon rewarming; 2) as previously reported, decerebellation coupled with bilateral vagotomy significantly decreased the peak integral of EMGdi response to TO with no effect on timing; 3) cold blockade (-1 degree C) of the dorsal cord at C6 significantly attenuated this inhibition, and subsequent dorsal rhizotomy at C3-6 completely abolished this inhibition; and 4) decerebellation, cold blockade of the dorsal cord (C6), and dorsal rhizotomy (C3-6) did not significantly affect baseline values in bilaterally vagotomized cats.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在之前的一项研究中,我们报告称,在去小脑双侧迷走神经切断的实验准备中,吸气性气管阻塞(TO)显著抑制了膈肌的运动驱动(《应用生理学杂志》75:675 - 681, 1993)。本研究中要检验的假设是,吸气性TO激活的呼吸肌传入神经提供了导致观察到的抑制作用的输入信号。成年猫被麻醉、气管切开,并植入膈肌肌电图(EMGdi)记录电极。通过手术暴露小脑、迷走神经和脊髓背侧(C2 - T2)。在完整和去小脑迷走神经切断的猫中,分别在脊髓背侧(C6)冷阻断或背根(C3 - 6)横断前后施加吸气性TO。根据EMGdi记录确定呼吸时间(吸气和呼气持续时间),并将EMGdi峰值积分反应(EMGdi积分)用作呼吸运动驱动的指标。我们的结果表明:1)在完整准备中,C6水平的脊髓背侧冷阻断显著增加了EMGdi对TO反应的积分峰值,且复温后可逆;2)如先前报道,去小脑联合双侧迷走神经切断显著降低了EMGdi对TO反应的积分峰值,对呼吸时间无影响;3)C6水平的脊髓背侧冷阻断(-1℃)显著减弱了这种抑制作用,随后C3 - 6背根切断完全消除了这种抑制作用;4)去小脑、脊髓背侧(C6)冷阻断和背根切断(C3 - 6)对双侧迷走神经切断猫的基线值无显著影响。(摘要截断于250字)

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