Redline S, Leitner J, Arnold J, Tishler P V, Altose M D
Department of Medicine, Cleveland Veterans Affairs Medical Center, OH 44106, USA.
Am J Respir Crit Care Med. 1997 Jul;156(1):155-60. doi: 10.1164/ajrccm.156.1.9610016.
The role of ventilatory-control abnormalities in predisposing to familial sleep-disordered breathing (SDB) was assessed in 31 subjects 28 +/- 10 yr of age (mean +/- SD). Subjects with (n = 10) and without SDB (n = 12) were recruited from 13 families having two or more members with SDB. Nine age- and gender-matched controls were recruited from families having no member with SDB. Respiratory responses to eucapnic hypoxia, and ventilatory and occlusion pressure responses to hyperoxic hypercapnia with and without added resistive loads (6.5 cm H2O/L/s), were assessed through rebreathing. Age, FEV1, and FVC did not differ among the groups. Hypoxic responses (delta VE/delta SaO2) were significantly lower among the first-degree relatives of SDB families than among controls (-0.76 +/- 0.47 L/min/% SaO2, and -1.32 +/- 0.92 L/min/% SaO2, respectively, p < 0.05). Respiratory responses to hypercapnia during unloaded conditions were similar among the groups. With resistive loading, inspiratory impedance, as measured through the relationship of mouth occlusion pressure (P100) to inspiratory flow (VT/TI), increased with increasing hypercapnia to a greater extent in members of SDB families than in controls (0.169 +/- 0.054 cm H2O/L/min versus 0.122 +/- 0.051, respectively, p < 0.05). These data suggest that familial SDB may be based partly on a familial abnormality in ventilatory control associated with blunting of the hypoxic ventilatory response. The greater increase in impedance during inspiratory loading in members of affected families also suggests a propensity for dynamic airway narrowing.
在31名年龄为28±10岁（均值±标准差）的受试者中，评估了通气控制异常在家族性睡眠呼吸障碍（SDB）易感性中的作用。从13个有两名或更多成员患有SDB的家庭中招募了患有SDB的受试者（n = 10）和未患有SDB的受试者（n = 12）。从没有成员患有SDB的家庭中招募了9名年龄和性别匹配的对照者。通过重复呼吸评估对等碳酸性低氧的呼吸反应，以及在有和没有附加阻力负荷（6.5 cm H₂O/L/s）情况下对高氧性高碳酸血症的通气和闭塞压反应。各组之间的年龄、第一秒用力呼气容积（FEV₁）和用力肺活量（FVC）没有差异。SDB家族的一级亲属的低氧反应（△VE/△SaO₂）显著低于对照组（分别为-0.76±0.47 L/min/% SaO₂和-1.32±0.92 L/min/% SaO₂，p<0.05）。在无负荷条件下，各组对高碳酸血症的呼吸反应相似。在有阻力负荷时，通过口闭塞压（P₁₀₀）与吸气流量（VT/TI）的关系测量的吸气阻抗，随着高碳酸血症的增加，SDB家族成员比对照组增加的幅度更大（分别为0.169±0.054 cm H₂O/L/min和0.122±0.051，p<0.05）。这些数据表明，家族性SDB可能部分基于与低氧通气反应减弱相关的通气控制家族性异常。受影响家族成员在吸气负荷期间阻抗的更大增加也表明存在动态气道狭窄的倾向。
