Folkhälsan Institute of Genetics, Folkhälsan Research Center, University of Helsinki, Helsinki, Finland.
Diabetologia. 2011 Aug;54(8):2164-73. doi: 10.1007/s00125-011-2195-4. Epub 2011 Jun 7.
AIMS/HYPOTHESIS: We hypothesised that the blunted baroreflex sensitivity (BRS) typical of type 1 diabetes is caused by a higher degree of tissue hypoxia in diabetes, and tested whether oxygen increased BRS and ventilation less, equally or more than in healthy control participants (the latter suggesting higher tissue hypoxia). In addition, we also considered the possible interference between oxygen and breathing pattern.
In 96 participants with type 1 diabetes and 40 age-matched healthy controls, we measured BRS (average of six different standard methods), oxygen saturation, end-tidal carbon dioxide and ventilation changes during spontaneous and controlled breathing at 15 and six breaths/min, in normoxia and during 5 l/min oxygen administration.
BRS was blunted and blood pressure higher in diabetic participants during spontaneous breathing (p < 0.05). BRS increased with oxygen during spontaneous breathing in diabetic (p < 0.001) but not in control participants, and with oxygen the difference in BRS was no longer significant. Slow breathing in normoxia restored BRS to a similar extent to giving oxygen. Oxygen increased systolic and diastolic blood pressure, RR interval, heart rate variability, minute ventilation and tidal volume to a greater extent in diabetic patients than in controls, and decreased carbon dioxide similarly to controls.
CONCLUSIONS/INTERPRETATION: The increased response to hyperoxia suggests a pre-existing condition of tissue hypoxia that functionally restrains parasympathetic activity in patients with type 1 diabetes. Autonomic abnormalities can be partially and temporarily reversed by functional manoeuvres such as slow breathing or oxygen administration through enhancement of parasympathetic activity and/or correction of tissue hypoxia.
目的/假设：我们假设 1 型糖尿病患者典型的血压反射敏感性（BRS）降低是由糖尿病中更高程度的组织缺氧引起的，并测试了氧气是否会增加 BRS 和通气，其效果是否不如健康对照组（后者表明更高的组织缺氧），或者比健康对照组更显著。此外，我们还考虑了氧气和呼吸模式之间可能存在的相互干扰。
在 96 名 1 型糖尿病患者和 40 名年龄匹配的健康对照者中，我们测量了 BRS（六种不同标准方法的平均值）、氧饱和度、呼气末二氧化碳和通气在自主和控制呼吸下的变化，呼吸频率为 15 次/分和 6 次/分，在常氧和 5L/min 吸氧时。
与对照组相比，1 型糖尿病患者在自主呼吸时 BRS 降低，血压升高（p<0.05）。在自主呼吸期间，糖尿病患者的 BRS 在吸氧时增加（p<0.001），但在对照组中没有增加，并且在吸氧时，BRS 的差异不再显著。在常氧下进行缓慢呼吸可以将 BRS 恢复到与给氧相似的程度。与对照组相比，糖尿病患者的收缩压和舒张压、RR 间期、心率变异性、分钟通气量和潮气量增加得更多，而二氧化碳的下降与对照组相似。
结论/解释：对高氧的反应增加表明存在组织缺氧的预先存在的情况，这种情况在 1 型糖尿病患者中功能性地限制了副交感神经活动。自主神经异常可以通过功能操作（如缓慢呼吸或通过增强副交感神经活动和/或纠正组织缺氧来供氧）部分和暂时逆转。
