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胸骨三角肌和膈神经对渐进性脑缺氧的反应。

Triangularis sterni and phrenic nerve responses to progressive brain hypoxia.

作者信息

Chae L O, Melton J E, Neubauer J A, Edelman N H

机构信息

Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019.

出版信息

J Appl Physiol (1985). 1992 Apr;72(4):1522-8. doi: 10.1152/jappl.1992.72.4.1522.

DOI:10.1152/jappl.1992.72.4.1522
PMID:1592745
Abstract

Activity of the respiratory muscles that are not normally active during eupnea (genioglossal and abdominal) has been shown to be more vulnerable to hypoxic depression than inspiratory diaphragmatic activity. We hypothesized that respiratory muscles that are active at eupnea would be equally vulnerable to isocapnic progressive brain hypoxia (PBH). Phrenic (PHR) and triangularis sterni nerve (TSN) activity were recorded in anesthetized peripherally chemodenervated vagotomized ventilated cats. Hypercapnia [arterial PCO2 (PaCO2) = 57 +/- 3 (SE) Torr] produced parallel increases in peak PHR and TSN activity. PBH [0.5% CO-40% O2-59.5% N2, arterial O2 content (CaO2) reduced from 13.1 +/- 1.0 to 3.7 +/- 0.3 vol%] resulted in parallel decreases of peak PHR and TSN activity to neural apnea. PBH was continued until PHR gasping ensued (CaO2 = 2.9 +/- 0.2 vol%); TSN activity remained silent during gasping. After 6-12 min of recovery (95% O2-5% CO2; CaO2 = 7.8 +/- 0.8 vol%; PaCO2 = 55 +/- 2 Torr), peak PHR activity was increased to 110 +/- 18% (% of activity at 9% CO2) whereas peak TSN activity was augmented to 269 +/- 89%. The greater augmentation of TSN activity during the recovery period could not be explained solely by hypercapnia. In conclusion, we found that 1) TSN expiratory and PHR inspiratory activities are equally vulnerable to hypoxic depression and 2) recovery from severe hypoxia is characterized by a profound augmentation of TSN expiratory activity.

摘要

在平静呼吸时通常不活跃的呼吸肌(颏舌肌和腹肌)的活动已被证明比吸气性膈肌活动更容易受到低氧抑制。我们假设在平静呼吸时活跃的呼吸肌对等容性进行性脑缺氧(PBH)同样敏感。在麻醉的外周化学去神经支配、迷走神经切断、通气的猫中记录膈神经(PHR)和胸骨三角肌神经(TSN)的活动。高碳酸血症[动脉血二氧化碳分压(PaCO2)=57±3(SE)托]使PHR和TSN的峰值活动平行增加。PBH[0.5%一氧化碳-40%氧气-59.5%氮气,动脉血氧含量(CaO2)从13.1±1.0降至3.7±0.3容积%]导致PHR和TSN的峰值活动平行下降至神经性呼吸暂停。持续进行PBH直至出现PHR喘息(CaO2=2.9±0.2容积%);在喘息期间TSN活动保持沉默。恢复6-12分钟后(95%氧气-5%二氧化碳;CaO2=7.8±0.8容积%;PaCO2=55±2托),PHR的峰值活动增加至110±18%(9%二氧化碳时活动的百分比),而TSN的峰值活动增加至269±89%。恢复期间TSN活动的更大增强不能仅用高碳酸血症来解释。总之,我们发现:1)TSN呼气和PHR吸气活动对等容性低氧抑制同样敏感;2)从严重低氧恢复的特征是TSN呼气活动显著增强。

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