呼吸可塑性:连续性和偶发性缺氧和高碳酸血症的不同作用

T.L Baker , D.D Fuller , A.G Zabka , G.S Mitchell
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引用次数: 102

摘要

本文的目的是:(1)回顾了我们对短至中时间域(min至h)间歇性缺氧与连续性缺氧引起的呼吸可塑性机制的理解进展;(2)提出新的数据表明,不同的高碳酸血症模式也会引起不同形式的呼吸可塑性。间歇性而非持续性缺氧引起呼吸运动输出的长期促进(LTF)。膈肌LTF是一种依赖血清素的中枢神经机制,需要:(a)脊髓血清素受体的激活;(b)脊髓蛋白合成。持续性和偶发性高碳酸血症也引起不同的可塑性机制。在麻醉大鼠中,持续的、严重的高碳酸血症(吸入CO2 25分钟~ 10%)引起膈肌运动输出的长期抑制(LTD)(高碳酸血症后60分钟- 33±8%)。相比之下,3,5分钟高碳酸血症发作不会引起LTD(60分钟时为9±17%)。我们假设呼吸运动神经元对血清素能和去甲肾上腺素能调节的反应可能有助于对缺氧和高碳酸血症的模式敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Respiratory plasticity: differential actions of continuous and episodic hypoxia and hypercapnia

The objectives of this paper are: (1) to review advances in our understanding of the mechanisms of respiratory plasticity elicited by episodic versus continuous hypoxia in short to intermediate time domains (min to h); and (2) to present new data suggesting that different patterns of hypercapnia also elicit distinct forms of respiratory plasticity. Episodic, but not continuous hypoxia elicits long-term facilitation (LTF) of respiratory motor output. Phrenic LTF is a serotonin-dependent central neural mechanism that requires: (a) activation of spinal serotonin receptors; and (b) spinal protein synthesis. Continuous and episodic hypercapnia also elicit different mechanisms of plasticity. Continuous, severe hypercapnia (25 min of ∼10% inspired CO2) elicits long-term depression (LTD) of phrenic motor output (−33±8% at 60 min post-hypercapnia) in anesthetized rats. In contrast, 3, 5 min hypercapnic episodes do not elicit LTD (9±17% at 60 min). We hypothesize that the response of respiratory motoneurons to serotonergic and noradrenergic modulation may contribute to pattern sensitivity to hypoxia and hypercapnia.

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