Gautier Henry, Murariu Cristina
Atelier de Physiologie Respiratoire, Faculté de Médecine Saint-Antoine, 27, rue Chaligny, 75012 Paris, France.
Respir Physiol. 2002 Jan;129(3):307-15. doi: 10.1016/s0034-5687(01)00315-2.
Adult, conscious rats have been exposed to CO-induced hypoxia for 30 min in normoxia, ambient hypoxia (FI(O(2))=14%), or hyperoxia (FI(O(2))=40%). From arterial blood gas analyses, FICO was adjusted in all experimental conditions to obtain final arterial oxygen saturations (Sa(O(2))) of approximately 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 degrees C. It was found that CO hypoxia induced marked reductions in the hemoglobin O(2) half saturation pressure (P(50)). Furthermore, isolated reductions in Sa(O(2)) (with Pa(O(2)) 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(O(2)) and Pa(O(2)) which operate on the control of metabolism and ventilation originate probably in the central nervous system.
成年清醒大鼠在常氧、环境性低氧(吸入氧分数[FI(O₂)] = 14%)或高氧(FI(O₂) = 40%)条件下,暴露于一氧化碳诱导的低氧环境30分钟。通过动脉血气分析,在所有实验条件下调节一氧化碳浓度,以使最终动脉血氧饱和度(Sa(O₂))达到约60%。在环境温度为25℃或15℃的实验中,测量了氧摄取量(V(O₂))、通气量(V)和结肠温度(Tc)。结果发现,一氧化碳低氧显著降低了血红蛋白氧半饱和压力(P₅₀)。此外,单独降低Sa(O₂)(动脉血氧分压[Pa(O₂)]保持恒定)会导致V(O₂)和Tc降低,通气量增加,与常氧相比,在环境性低氧中增强,在高氧中降低但仍显著。如先前研究所表明的,作用于代谢和通气控制的Sa(O₂)和Pa(O₂)之间的相互作用可能起源于中枢神经系统。