Javaheri S, Lucey E C, Snider G L
Am Rev Respir Dis. 1985 Nov;132(5):1055-9. doi: 10.1164/arrd.1985.132.5.1055.
Marked variability in resting steady-state arterial PCO2 (PaCO2) values are observed among patients with chronic obstructive pulmonary disease (COPD), independent of severity of their obstructive airways defect. The reasons for the development of hypercapnia in some but not in the others remain unclear. One hypothesis states that the level of morbid resting PaCO2 may be related to the premorbid hypercapnic ventilatory response (HCVR); accordingly, subjects who were relatively insensitive to CO2 breathing (low responders) develop CO2 retention in the face of lung disease. The present study investigated this hypothesis in the hamster model of elastase-induced emphysema. After obtaining steady-state HCVR in 19 unanesthetized unrestrained hamsters, emphysema was induced by intratracheal instillation of pancreatic elastase. Forty-five days later, minute ventilation and PaCO2 measurements were done, and lung function tests were obtained. The slopes of HCVR and morbid PaCO2 values varied from -0.09 to 2.36 ml/min/mmHg inspired PCO2 and 48.7 to 63.1 mmHg, respectively. There were no significant correlations between morbid PaCO2 values and premorbid HCVR or lung function test abnormalities caused by emphysema. These animal model studies do not support the hypothesis that the level of PaCO2 in patients with COPD is related to their premorbid HCVR.
在慢性阻塞性肺疾病（COPD）患者中，静息稳态动脉血二氧化碳分压（PaCO2）值存在显著差异，且与气道阻塞缺陷的严重程度无关。部分患者出现高碳酸血症而其他患者未出现的原因尚不清楚。一种假说认为，病态静息PaCO2水平可能与病前高碳酸通气反应（HCVR）有关；因此，对二氧化碳呼吸相对不敏感的受试者（低反应者）在患有肺部疾病时会出现二氧化碳潴留。本研究在弹性蛋白酶诱导的肺气肿仓鼠模型中对这一假说进行了探究。在19只未麻醉、未束缚的仓鼠中获得稳态HCVR后，通过气管内注入胰弹性蛋白酶诱导肺气肿。45天后，测量分钟通气量和PaCO2，并进行肺功能测试。HCVR斜率和病态PaCO2值分别在-0.09至2.36 ml/min/mmHg吸入PCO2和48.7至63.1 mmHg之间变化。病态PaCO2值与病前HCVR或肺气肿引起的肺功能测试异常之间无显著相关性。这些动物模型研究不支持COPD患者的PaCO2水平与其病前HCVR相关的假说。
