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下胸段脊髓刺激期间呼气肌激活的机制

Mechanism of expiratory muscle activation during lower thoracic spinal cord stimulation.

作者信息

DiMarco A F, Kowalski K E, Supinski G, Romaniuk J R

机构信息

Department of Physiology and Biophysics, Case Western Reserve University and MetroHealth Medical Center, Cleveland, Ohio 44109, USA.

出版信息

J Appl Physiol (1985). 2002 Jun;92(6):2341-6. doi: 10.1152/japplphysiol.01231.2001.

Abstract

Lower thoracic spinal cord stimulation (SCS) may be a useful method to restore an effective cough mechanism. In dogs, two groups of studies were performed to evaluate the mechanism of the expiratory muscle activation during stimulation at the T(9)-T(10) level, which results in the greatest changes in airway pressure. In one group, expiratory muscle activation was monitored by evoked muscle compound action potentials (CAPs) from the internal intercostal muscles in the 10th, 11th, and 12th interspaces and from portions of the external oblique innervated by the L(1) and L(2) motor roots. SCS, applied with single shocks, resulted in short-latency CAPs at T(10) but not at more caudal levels. SCS resulted in long-latency CAPs at each of the more caudal caudal recording sites. Bilateral dorsal column sectioning, just below the T(11) spinal cord level, did not affect the short-latency CAPs but abolished the long-latency CAPs and also resulted in a fall in airway pressure generation. In the second group, sequential spinal root sectioning was performed to assess their individual mechanical contribution to pressure generation. Section of the ventral roots from T(8) through T(10) resulted in negligible changes, whereas section of more caudal roots resulted in a progressive reduction in pressure generation. We conclude that 1) SCS at the T(9)-T(10) level results in direct activation of spinal cord roots within two to three segments of the stimulating electrode and activation of more distal roots via spinal cord pathways, and 2) pathway activation of motor roots makes a substantial contribution to pressure generation.

摘要

下胸段脊髓刺激(SCS)可能是恢复有效咳嗽机制的一种有用方法。在犬类中,进行了两组研究以评估在T(9)-T(10)水平刺激期间呼气肌激活的机制,该水平刺激导致气道压力变化最大。在一组研究中,通过从第10、11和12肋间间隙的肋间内肌以及由L(1)和L(2)运动神经根支配的部分腹外斜肌诱发的肌肉复合动作电位(CAPs)来监测呼气肌激活。单次电击施加SCS,在T(10)水平产生短潜伏期CAPs,但在更靠尾侧的水平则未产生。SCS在每个更靠尾侧的记录部位均产生长潜伏期CAPs。在T(11)脊髓水平下方进行双侧背柱切断术,并不影响短潜伏期CAPs,但消除了长潜伏期CAPs,并且还导致气道压力产生下降。在第二组研究中,进行了连续的脊髓神经根切断术,以评估它们对压力产生的个体机械贡献。从T(8)到T(10)的腹侧神经根切断导致可忽略不计的变化,而更靠尾侧的神经根切断则导致压力产生逐渐降低。我们得出结论:1)T(9)-T()水平的SCS导致刺激电极两到三个节段内的脊髓神经根直接激活,并通过脊髓通路激活更远端的神经根;2)运动神经根的通路激活对压力产生有重大贡献。

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