Acute and chronic blood pressure response to recurrent acoustic arousal in rats

被引:50
作者
Bao, G
Metreveli, N
Fletcher, EC
机构
[1] Univ Louisville, Sch Med, Div Resp Crit Care & Environm Med, Louisville, KY 40292 USA
[2] Louisville Vet Affairs Med Ctr, Dept Med, Div Resp Crit Care & Environm Med, Louisville, KY USA
关键词
stress; blood pressure; sympathetic nervous system; sleep disorders; sleep apnea; hemodynamics; arousal; noise; Sprague-Dawley rat;
D O I
10.1016/S0895-7061(99)00032-1
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
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.
引用
收藏
页码:504 / 510
页数:7
相关论文
共 23 条
  • [11] THE RELATIONSHIP BETWEEN SYSTEMIC HYPERTENSION AND OBSTRUCTIVE SLEEP-APNEA - FACTS AND THEORY
    FLETCHER, EC
    [J]. AMERICAN JOURNAL OF MEDICINE, 1995, 98 (02) : 118 - 128
  • [12] PHYSIOLOGICAL-ASPECTS OF PRIMARY HYPERTENSION
    FOLKOW, B
    [J]. PHYSIOLOGICAL REVIEWS, 1982, 62 (02) : 347 - 504
  • [13] FOLKOW B, 1987, CIRCULATION, V76, P10
  • [14] STRESS-INDUCED ACTIVATION OF THE SYMPATHETIC NERVOUS-SYSTEM
    GOLDSTEIN, DS
    [J]. BAILLIERES CLINICAL ENDOCRINOLOGY AND METABOLISM, 1987, 1 (02): : 253 - 278
  • [15] GOODNIGHTWHITE S, 1995, J APPL PHYSIOL, V79, P324
  • [16] A SPECIFIC AND POTENT PRESSOR EFFECT OF HYPOXIA IN PATIENTS WITH SLEEP-APNEA
    HEDNER, JA
    WILCOX, I
    LAKS, L
    GRUNSTEIN, RR
    SULLIVAN, CE
    [J]. AMERICAN REVIEW OF RESPIRATORY DISEASE, 1992, 146 (05): : 1240 - 1245
  • [17] CARDIOVASCULAR-RESPONSE TO STRESS
    HERD, JA
    [J]. PHYSIOLOGICAL REVIEWS, 1991, 71 (01) : 305 - 330
  • [18] Airway obstruction during sleep increases blood pressure without arousal
    ODonnell, CP
    Ayuse, T
    King, ED
    Schwartz, AR
    Smith, PL
    Robotham, JL
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1996, 80 (03) : 773 - 781
  • [19] SYSTEMIC BLOOD-PRESSURE ELEVATION AFTER AIRWAY OCCLUSION DURING NREM SLEEP
    RINGLER, J
    GARPESTAD, E
    BASNER, RC
    WEISS, JW
    [J]. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (04) : 1062 - 1066
  • [20] HYPOXEMIA ALONE DOES NOT EXPLAIN BLOOD-PRESSURE ELEVATIONS AFTER OBSTRUCTIVE APNEAS
    RINGLER, J
    BASNER, RC
    SHANNON, R
    SCHWARTZSTEIN, R
    MANNING, H
    WEINBERGER, SE
    WEISS, JW
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1990, 69 (06) : 2143 - 2148