Daytime blood pressure elevation after nocturnal hypoxia

被引:43
作者
Arabi, Y
Morgan, BJ
Goodman, B
Puleo, DS
Xie, AL
Skatrud, JB
机构
[1] William S Middleton Mem Vet Hosp, Madison, WI 53705 USA
[2] Univ Wisconsin, Dept Med, Madison, WI 53792 USA
[3] Univ Wisconsin, Dept Surg, Madison, WI 53792 USA
关键词
high altitude; hypobaric chamber;
D O I
10.1152/jappl.1999.87.2.689
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The purpose of this study was to investigate whether nocturnal hypoxia causes daytime blood pressure (BP) elevation. We hypothesized that overnight exposure to hypoxia leads the next morning to elevation in BP that outlasts the hypoxia stimulus. We studied the effect on BP of two consecutive night exposures to hypobaric hypoxia in 10 healthy normotensive subjects. During the hypoxia nights, subjects slept for 8 h in a hypobaric chamber at a simulated altitude of 4,000 m (barometric pressure = 462 mmHg). Arterial O-2 saturation and electrocardiogram were monitored throughout the night. For 30 min before the nocturnal simulated ascent and for 4 h after return to baseline altitude the next morning, BP was measured every 5 min while the subject was awake. The same measurements were made before and after 2 normoxic nights of sleep in the hypobaric chamber at ambient barometric pressure (745 mmHg). Principal components analysis was applied to evaluate patterns of BP response after the second night of hypoxia and normoxia. A distinct pattern of diastolic BP (DBP) elevation was observed after the hypoxia night in 9 of the 10 subjects but in none after the normoxia night. This pattern showed a mean increase of 4 mmHg in DBP compared with the presleep-awake baseline in the first 60 min and a return to baseline by 90 min. We conclude that nocturnal hypoxia leads to a carryover elevation of daytime DBP.
引用
收藏
页码:689 / 698
页数:10
相关论文
共 36 条
[1]  
[Anonymous], 1999, APPL MULTIVARIATE AN
[2]   Obstructive sleep apnea as a cause of systemic hypertension - Evidence from a canine model [J].
Brooks, D ;
Horner, RL ;
Kozar, LF ;
RenderTeixeira, CL ;
Phillipson, EA .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (01) :106-109
[3]  
BROWN MJ, 1985, Q J MED, V57, P637
[4]   HIGH PREVALENCE OF HYPERTENSION IN SLEEP-APNEA PATIENTS INDEPENDENT OF OBESITY [J].
CARLSON, JT ;
HEDNER, JA ;
EJNELL, H ;
PETERSON, LE .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (01) :72-77
[5]   AUGMENTED RESTING SYMPATHETIC ACTIVITY IN AWAKE PATIENTS WITH OBSTRUCTIVE SLEEP-APNEA [J].
CARLSON, JT ;
HEDNER, J ;
ELAM, M ;
EJNELL, H ;
SELLGREN, J ;
WALLIN, BG .
CHEST, 1993, 103 (06) :1763-1768
[6]   PULSATILE VERSUS STEADY COMPONENT OF BLOOD-PRESSURE - A CROSS-SECTIONAL ANALYSIS AND A PROSPECTIVE ANALYSIS ON CARDIOVASCULAR MORTALITY [J].
DARNE, B ;
GIRERD, X ;
SAFAR, M ;
CAMBIEN, F ;
GUIZE, L .
HYPERTENSION, 1989, 13 (04) :392-400
[7]  
DAULTREY S, 1976, GEO ABSTR, V8, P1
[8]  
DeAmbroggi L, 1997, CIRCULATION, V96, P4314
[9]   RELATION OF BLOOD-VISCOSITY TO DEMOGRAPHIC AND PHYSIOLOGIC VARIABLES AND TO CARDIOVASCULAR RISK-FACTORS IN APPARENTLY NORMAL ADULTS [J].
DESIMONE, G ;
DEVEREUX, RB ;
CHIEN, S ;
ALDERMAN, MH ;
ATLAS, SA ;
LARAGH, JH .
CIRCULATION, 1990, 81 (01) :107-117
[10]   EFFECT OF NOCTURNAL ATRIAL DEMAND CARDIAC PACING ON DIURNAL HEMODYNAMIC PATTERNS [J].
ENGEL, BT ;
TALAN, MI ;
CHEW, PH .
JOURNAL OF APPLIED PHYSIOLOGY, 1992, 72 (05) :1798-1802