HYPOXEMIA ALONE DOES NOT EXPLAIN BLOOD-PRESSURE ELEVATIONS AFTER OBSTRUCTIVE APNEAS
HYPOXEMIA ALONE DOES NOT EXPLAIN BLOOD-PRESSURE ELEVATIONS AFTER OBSTRUCTIVE APNEAS
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DOI：
10.1152/jappl.1990.69.6.2143
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发表时间：
1990-12-01
影响因子：
3.3
通讯作者：
WEISS, JW
中科院分区：
文献类型：
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作者：
RINGLER, J;BASNER, RC;WEISS, JW
在阻塞性睡眠呼吸暂停 (OSA) 患者中，伴随呼吸暂停终止，全身血压 (BP) 大幅升高，氧合血红蛋白饱和度 (Sa(o)2) 降低。 血压升高是 OSA 夜间高血压的重要原因，但其原因尚未明确。 为了评估动脉低氧血症的相对影响，我们观察了 11 名 OSA 患者在非快速眼动 (NREM) 睡眠期间发生阻塞性呼吸暂停后的平均动脉压 (MAP) 变化，然后在三种实验条件下进行：1) 呼吸暂停补充 O2； 2）低氧血症（Sa(o)2 80%），无呼吸暂停； 3）从睡眠中醒来，既没有低氧血症也没有呼吸暂停。 我们发现，与未补充氧气的呼吸暂停（Sa(o)2 最低点 79-82%）相比，六名受试者在补充 O2 期间记录的呼吸暂停（Sa(o)2 最低点 93.6% +/- 2.4；平均值 +/- SD）与同等的呼吸暂停后 MAP 升高相关：18.8 +/- 7.1 vs 21.3 +/- 9.2 mmHg（MAP 平均变化 +/-标准差）；在 8 名受试者中，在没有呼吸和睡眠中断的情况下，低氧血症与呼吸暂停后观察到的血压升高无关：-5.4 +/- 19 与 19.1 +/- 7.8 mmHg (P < 0.01)：在 5 名受试者中，单独的听觉唤醒与 MAP 升高相关，类似于呼吸暂停后观察到的情况：24.0 +/- 8.1 与 22.0 +/- 6.9毫米汞柱。 我们得出的结论是，在 NREM 睡眠中，呼吸暂停后血压升高并不是主要归因于动脉低氧血症。 与呼吸暂停终止相关的其他因素，包括从睡眠中唤醒、肺部再充气以及胸腔内压力的变化，可能是造成这些升高的原因。
In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (Sa(o)2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (Sa(o)2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (Sa(o)2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (Sa(o)2 nadir 79-82%): 18.8 +/- 7.1 vs 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P < 0.01): and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.