Metabolic and ventilatory responses to CO hypoxia at different levels of oxygenation in the rat

Respiration physiology Pub Date : 2002-01-01 DOI:10.1016/S0034-5687(01)00315-2

Henry Gautier, Cristina Murariu

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引用次数: 2

Abstract

Adult, conscious rats have been exposed to CO-induced hypoxia for 30 min in normoxia, ambient hypoxia (FI_O₂=14%), or hyperoxia (FI_O₂=40%). From arterial blood gas analyses, FICO was adjusted in all experimental conditions to obtain final arterial oxygen saturations (Sa_O₂) of ∼60%. Oxygen uptake ( $V ̇_{O_{2}}$ ), ventilation ( $V ̇$ ) and colonic temperature (Tc) were measured in experiments carried out at an ambient temperature of either 25 or 15 °C. It was found that CO hypoxia induced marked reductions in the hemoglobin O₂ half saturation pressure (P₅₀). Furthermore, isolated reductions in Sa_O₂ (with Pa_O₂ constant) induced decreases in $V ̇_{O_{2}}$ and Tc and increases in ventilation which, as compared with normoxia, were enhanced in ambient hypoxia and reduced but still significant in hyperoxia. As suggested by previous studies, the interactions between Sa_O₂ and Pa_O₂ which operate on the control of metabolism and ventilation originate probably in the central nervous system.

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不同氧合水平下大鼠一氧化碳缺氧的代谢和通气反应

成年有意识大鼠在常氧、环境缺氧(FIO2=14%)或高氧(FIO2=40%)条件下暴露于co诱导的缺氧30分钟。根据动脉血气分析，在所有实验条件下调整FICO以获得最终动脉血氧饱和度(SaO2)为~ 60%。在25°C或15°C的环境温度下进行实验，测量吸氧(V O2)、通气量(V O2)和结肠温度(Tc)。结果发现，CO缺氧诱导血红蛋白O2半饱和压明显降低(P50)。此外，SaO2的单独降低(PaO2不变)导致V (O2)和Tc的降低以及通气量的增加，与常氧相比，在环境缺氧时增强，在高氧时减弱但仍然显著。根据以往的研究，SaO2和PaO2之间的相互作用可能起源于中枢神经系统，并对代谢和通气的控制起作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Respiration physiology

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