Hjalmarsen A, Aasebø U, Aleksandersen G, Jorde R
Department of Pulmonary Medicine, University Hospital of Tromsø, Norway.
J Auton Nerv Syst. 1996 Sep 12;60(3):169-74. doi: 10.1016/0165-1838(96)00053-7.
The aim of this study was to investigate autonomic neuropathy, with and without oxygen therapy, in patients with chronic obstructive pulmonary disease (COPD). Four cardiovascular tests for autonomic function were used, and in addition, basal pancreatic polypeptide (PP) was measured. The following COPD patients were studied: 10 normoxemic (mean PaO2 10.9 +/- SD 1.1 kPa), 10 hypoxemic (PaO2 7.6 +/- 0.7 kPa before, and 10.6 +/- 1.4 kPa after 24 h oxygen therapy), and 6 hypoxemic on long-term oxygen therapy (LTOT) (PaO2 10.3 +/- 1.3 kPa before, and 7.0 +/- 0.8 kPa after 4 h of low dose or oxygen free interval). Twenty healthy age-matched subjects served as controls. In the individual tests the hypoxemic and the LTOT groups had a significantly decreased heart rate response to the Valsalva manoeuvre (ratio 1.23 +/- 0.17 and 1.12 +/- 0.07 versus control's 1.45 +/- 0.26 (p < 0.01 and 0.005, respectively) and versus the normoxemic group 1.46 +/- 0.30 (p < 0.05)) and the hypoxemic as well as the LTOT group had a significantly decreased heart rate response to standing up (ratio 0.97 +/- 0.04 and 0.97 +/- 0.07, respectively, versus the controls 1.06 +/- 0.09 (p < 0.005 and 0.05)). The blood pressure response to standing up and to sustained handgrip did not differ significantly between the groups. In spite of apparent autonomic dysfunction, PP levels in the LTOT group were significantly higher than in the controls (p < 0.01-0.001) and the normoxemic group (p < 0.05-0.01). Twenty-four hours of oxygen treatment in the hypoxemic group or four hours of oxygen withdrawal in the LTOT group did not change the results significantly. In conclusion, our findings are consistent with the previous notion of neurological dysfunction from hypoxemia, but this may not be corrected by the use of short term oxygen treatment. This contrasts to previous findings in which longer term oxygen did correct some of these problems.
本研究旨在调查慢性阻塞性肺疾病（COPD）患者在接受和未接受氧疗情况下的自主神经病变情况。采用了四项自主神经功能的心血管测试，此外，还测量了基础胰多肽（PP）。研究了以下COPD患者：10名血氧正常者（平均动脉血氧分压[PaO₂]为10.9±标准差1.1kPa），10名低氧血症患者（治疗前PaO₂为7.6±0.7kPa，24小时氧疗后为10.6±1.4kPa），以及6名长期氧疗（LTOT）的低氧血症患者（治疗前PaO₂为10.3±1.3kPa，低剂量或无吸氧间隔4小时后为7.0±0.8kPa）。20名年龄匹配的健康受试者作为对照。在各项测试中，低氧血症组和LTOT组对瓦尔萨尔瓦动作的心率反应显著降低（比值分别为1.23±0.17和1.12±0.07，而对照组为1.45±0.26（分别为p<0.01和0.005），与血氧正常组1.46±0.30相比（p<0.05）），低氧血症组和LTOT组对站立的心率反应也显著降低（比值分别为0.97±0.04和0.97±0.07，而对照组为1.06±0.09（分别为p<0.005和0.05））。各组对站立和持续握力的血压反应无显著差异。尽管存在明显的自主神经功能障碍，但LTOT组的PP水平显著高于对照组（p<0.01至0.001）和血氧正常组（p<0.05至0.01）。低氧血症组进行24小时氧疗或LTOT组进行4小时停止吸氧治疗，结果均无显著变化。总之，我们的研究结果与先前关于低氧血症导致神经功能障碍的观点一致，但短期氧疗可能无法纠正这一问题。这与先前的研究结果形成对比，先前的研究表明长期氧疗确实可以纠正其中一些问题。
