Bakehe M, Miramand J L, Chambille B, Gaultier C, Escourrou P
Physiology Laboratory, School of Medicine, Paris-Sud University, Kremlin-Bicêtre, France.
Eur Respir J. 1995 Oct;8(10):1675-80. doi: 10.1183/09031936.95.08101675.
It has been shown that chronic repetitive ambient hypoxia, simulating pulmonary gas disturbances observed in apnoea, leads to systemic hypertension in rats. However, the relative roles of hypoxia (HO), hypercapnia (HC), gas stress and vigilance on the cardiovascular changes have not yet been demonstrated. The aim of this study was to investigate the acute haemodynamic changes observed during the repetitive inhalation of various gas mixtures in rats for HO alone and HO+HC, and to analyse the effects of vigilance and of the stress of gas administration. We studied 6 unanaesthetized Wistar rats chronically instrumented with an aortic catheter. Nitrogen, nitrogen+CO2 mixtures and compressed air were randomly administered in a Plexiglass chamber for 10 s and then flushed by compressed air for 20 s. Two cycles were repeated every min for 10 to 12 min. The inhaled gas fractions (FI,O2,FI,CO2) were monitored by O2 and CO2 analysers. Blood pressure (BP) was measured by a P23XL transducer. The blood gases were analysed by a 1306 IL meter. In control experiments, with compressed air alone, there were no significant acute changes in heart rate (HR) and BP. During HO there were no changes in HR or BP at FI,O2 values from 0.05-0.14, whilst at FI,O2 values from 0-0.05 systolic blood pressure (SBP) rose significantly (+25.3 +/- 25.7 (SD) mmHg) and HR decreased (-93.8 +/- 124.1 bpm). During HOHC, SBP rose (+35.1 +/- 26.4 mmHg) and HR decreased (-139.3 +/- 75.7 bpm), significantly more than in HO alone. SBP was linearly correlated with Pa,O2 during HO (r = 0.53) and also during HOHC (r = 0.44) and was not directly related to Pa,CO2 which has, nevertheless, an additive effect to HO. SBP rose with each challenge significantly more when the rats were awake than when asleep (behavioural sleep). We conclude that in this acute repetitive inhalation model, the rise in SBP is not related to gas stress or to Pa,CO2 but to a decrease in Pa,O2 and is enhanced by wakefulness.
研究表明，模拟呼吸暂停时出现的肺部气体紊乱的慢性重复性环境低氧会导致大鼠系统性高血压。然而，低氧（HO）、高碳酸血症（HC）、气体应激和警觉性对心血管变化的相对作用尚未得到证实。本研究的目的是调查大鼠在重复性吸入各种气体混合物过程中，单独低氧和低氧+高碳酸血症时观察到的急性血流动力学变化，并分析警觉性和气体给药应激的影响。我们研究了6只长期植入主动脉导管的未麻醉Wistar大鼠。在有机玻璃舱中随机给予氮气、氮气+二氧化碳混合物和压缩空气10秒，然后用压缩空气冲洗20秒。每分钟重复两个周期，持续10至12分钟。吸入气体分数（FI，O2，FI，CO2）由氧气和二氧化碳分析仪监测。血压（BP）由P23XL传感器测量。血气由1306型IL仪分析。在对照实验中，仅使用压缩空气时，心率（HR）和血压没有明显的急性变化。在低氧期间，当FI，O2值在0.05 - 0.14时，心率或血压没有变化，而当FI，O2值在0 - 0.05时，收缩压（SBP）显著升高（+25.3±25.7（标准差）mmHg），心率降低（-93.8±124.1次/分钟）。在低氧+高碳酸血症期间，收缩压升高（+35.1±26.4 mmHg），心率降低（-139.3±75.7次/分钟），显著高于单独低氧时。在低氧期间（r = 0.53）以及低氧+高碳酸血症期间（r = 0.44），收缩压与动脉血氧分压（Pa，O2）呈线性相关，且与动脉血二氧化碳分压（Pa，CO2）无直接关系，不过，高碳酸血症对低氧有叠加作用。当大鼠清醒时，每次刺激后收缩压升高明显大于睡眠时（行为性睡眠）。我们得出结论，在这个急性重复性吸入模型中，收缩压升高与气体应激或动脉血二氧化碳分压无关，而是与动脉血氧分压降低有关，并且清醒状态会增强这种升高。
