A SPECIFIC AND POTENT PRESSOR EFFECT OF HYPOXIA IN PATIENTS WITH SLEEP-APNEA
A SPECIFIC AND POTENT PRESSOR EFFECT OF HYPOXIA IN PATIENTS WITH SLEEP-APNEA
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DOI：
10.1164/ajrccm/146.5_pt_1.1240
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发表时间：
1992-11-01
期刊：
影响因子：
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通讯作者：
SULLIVAN, CE
中科院分区：
文献类型：
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作者：
HEDNER, JA;WILCOX, I;SULLIVAN, CE
对17例阻塞性睡眠呼吸暂停（OSA）患者进行了清醒状态下低氧斜坡试验（至75%动脉血氧饱和度）。血压监测与留置动脉线（桡动脉），并确定对二氧化碳缺氧的缓解反应。8例患者血压正常。其余9名高血压患者进行了为期3周的降压药物洗脱后的研究。与低氧血症不影响血压的血压正常、无打鼾的对照组相比，所有OSA患者在低氧时均表现出不同程度的升压反应。血压正常和高血压合并OSA患者的升压反应相似。在正常血压和高血压患者中，对缺氧的舒张反应和升压反应之间存在显著关系（p = 0.03）。虽然疾病的严重程度表示为呼吸暂停指数（每小时睡眠呼吸暂停的数量）或最低动脉血氧饱和度在夜间记录与升压反应的幅度相关（p = 0.03和0.045，分别），缺氧的缓解反应与疾病的严重程度无关。低氧血症引起对照组和血压正常患者心率相似的增加，但高血压受试者在血氧饱和度最低点时心率反应减弱（p < 0.05）。这些数据表明阻塞性睡眠呼吸暂停患者对缺氧有升压反应。这种反应可能与OSA患者呼吸暂停时的血压波动有关。虽然升压反应的幅度与静息血压无关，但这种机制可能有助于OSA患者心血管疾病的发展。
A hypoxic ramp test (to 75% arterial oxygen saturation) during the awake state was performed in 17 patients with obstructive sleep apnea (OSA). Blood pressure was monitored with an indwelling arterial line (radial artery), and the ventilatory response to eucapnic hypoxia was determined. Eight of the patients were normotensive. The remaining nine hypertensive patients were studied after a 3-wk washout of antihypertensive medication. Compared with a nonmatched group of normotensive nonsnoring control subjects in whom hypoxemia did not affect blood pressure, all OSA patients showed various degrees of pressor responses during hypoxia. The pressor response was of similar magnitude in normotensive and hypertensive patients with OSA. There was a significant relationship between the ventilatory and the pressor responses to hypoxia (p = 0.03) that was similar in both normotensive and hypertensive patients. Although disease severity expressed as apnea index (number of apneas per hour of sleep) or minimum arterial oxygen saturation reached during the overnight recording correlated with the magnitude of the pressor response (p = 0.03 and 0.045, respectively), the ventilatory response to hypoxia was unrelated to disease severity. Hypoxemia induced a similar increase in heart rate in controls and in normotensive patients, but an attenuated heart rate response was seen at the nadir of oxygen saturation in hypertensive subjects (p < 0.05). These data demonstrate that patients with obstructive sleep apneas have a pressor response to hypoxia. This response is likely to be involved in the blood pressure swings seen during apnea in patients with OSA. Although the magnitude of the pressor response was unrelated to resting blood pressure, this mechanism may contribute to the development of cardiovascular disease in patients with OSA.