Acute and chronic blood pressure response to recurrent acoustic arousal in rats
Acute and chronic blood pressure response to recurrent acoustic arousal in rats
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DOI：
10.1016/s0895-7061(99)00032-1
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发表时间：
1999-05-01
影响因子：
3.2
通讯作者：
Fletcher, EC
中科院分区：
文献类型：
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作者：
Bao, G;Metreveli, N;Fletcher, EC
先前的研究表明，每 30 秒对 Sprague-Dawley (SD) 大鼠进行慢性反复间歇性缺氧会导致白天血压 (BP) 持续升高。人类在清醒或睡眠期间的声学唤醒会导致血压急剧升高。接下来的问题是，以与间歇性缺氧相同的频率和持续时间施加的慢性间歇性声唤醒是否会引起血压升高。我们将单独笼子中的 14 周龄（N = 10）SD 大鼠暴露在重复的蜂鸣器噪声（500 Hz，100 db）中，每 30 秒 6 次，每天 7 小时，持续 35 天。每天将另外 10 只大鼠放入类似的笼子中，但不暴露在噪音中，以提供假条件。带有探测器的红外光束位于每个笼子的末端。这使我们能够通过记录大鼠每 7 小时打破横梁的次数来量化运动。在基线和 35 天结束时测量无约束意识动物的平均动脉内血压。急性间歇性声刺激引起血压和心率的立即反应。习惯发生的原因是，第一天对每小时 120 次噪音的运动反应在第一小时为 75%，在第二小时至第七小时为 20%。到第 35 天，运动反应进一步降低，但仍显着高于未受噪音刺激的动物。心血管对噪音的反应也显示出习惯的迹象。接触慢性噪音刺激 35 天后，血压并未持续升高。
Repetitive episodic hypoxia every 30 sec administered chronically to Sprague-Dawley (SD) rats has been shown by previous studies to cause a sustained increase in daytime blood pressure (BP). Acoustic arousal in humans during wake or sleep produces an acute BP rise. The question then arises as to whether chronic episodic acoustic arousal applied with the same frequency and duration as episodic hypoxia induces elevated BP. We exposed 14-week-old (N = 10) SD rats in individual cages to recurrent buzzer noise (500 Hz, 100 db) 6 out of every 30 sec, 7 h/day for 35 days. Ten other rats were placed in similar cages daily but not exposed to noise, to provide a sham condition. An infrared beam with a detector was positioned at the end of each cage. This allowed us to quantify motion by registering the number of times the rat broke the beam per 7 h period. Mean intraarterial BP was measured in unrestrained conscious animals at baseline and at the end of 35 days of their respective conditions. Acute episodic acoustic stimulation caused an immediate response in BP and heart rate. Habituation occurred in that the movement response to 120 noises per hour was 75% in hour one and 20% in hours two through seven on day one. The movement response was further reduced by day 35 but remained significantly higher than in animals not stimulated by noise. The cardiovascular response to noise also showed signs of habituation. Chronic noise stimulation produced no sustained increases in BP after 35 days of exposure.