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慢性阻塞性肺疾病患者及放血后继发性红细胞增多症患者的呼吸控制

Control of breathing in patients with chronic obstructive lung diseases and secondary polycythemia after venesection.

作者信息

Patakas D A, Christaki P I, Louridas G E, Sproule B J

出版信息

Respiration. 1986;49(4):257-62. doi: 10.1159/000194888.

Abstract

Using the mouth occlusion pressure technique, we have studied the control of breathing in 10 hypercapnic patients with chronic obstructive pulmonary diseases and polycythemia before and after venesection. The mean hematocrit value was 59.9 +/- 5.5% which, following venesection (approximately 1,200-1,600 cm3 of blood was removed from each patient over three consecutive days), fell to 44.4 +/- 2.2%. Respiratory drive, expressed as P0.1 (mouth occlusion pressure 0.1 s after the onset of occluded inspiration at functional residual capacity) and as mean inspired flow (VT/TI), was diminished after venesection (p less than 0.001 and p less than 0.05); in contrast to that, we found no changes in respiratory timing (TI and TI/Ttot). The arterial PCO2 was decreased (p less than 0.001) and arterial PO2 was increased after venesection, these improvements are mainly attributed to decreased dead space ventilation (p less than 0.05). It seems that the improvements of blood gases after venesection is probably responsible for the decrease in respiratory drive.

摘要

我们采用口腔阻断压力技术,研究了10例患有慢性阻塞性肺疾病且伴有红细胞增多症的高碳酸血症患者在放血前后的呼吸控制情况。平均血细胞比容值为59.9±5.5%,在放血后(连续三天从每位患者身上抽取约1200 - 1600立方厘米的血液),降至44.4±2.2%。以P0.1(功能残气量时阻断吸气开始后0.1秒的口腔阻断压力)和平均吸气流量(VT/TI)表示的呼吸驱动力在放血后降低(p<0.001和p<0.05);与此相反,我们发现呼吸时间(TI和TI/Ttot)没有变化。放血后动脉PCO2降低(p<0.001),动脉PO2升高,这些改善主要归因于死腔通气减少(p<0.05)。放血后血气的改善似乎是呼吸驱动力降低的原因。

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