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Department of Medicine, Division of Respiratory and Environmental Medicine, Louisville Veterans Affairs Medical Center and University of Louisville School of Medicine, Louisville, Kentucky 40292
Received 12 September 1996; accepted in final form 19 November 1996.
Bao, Gang, Preet M. Randhawa, and Eugene C. Fletcher.
Acute blood pressure elevation during repetitive hypocapnic and eucapnic hypoxia in rats. J. Appl.
Physiol. 82(4): 1071-1078, 1997.
Using a rat
model, we investigated whether episodic eucapnic hypoxia was a more
potent stimulus to acute blood pressure (BP) elevation and bradycardia
than episodic hypocapnic hypoxia. We also investigated the
role of sympathetic and parasympathetic nervous system in this
cardiovascular response. Sprague-Dawley (SD) and Wistar Kyoto (WKY)
rats were exposed to repetitive 30-s cycles of hypocapnic or eucapnic
hypoxia before and after intravenous injection of the
1-adrenergic blocker prazosin,
2-adrenergic blocker yohimbine,
or atropine. Eucapnic hypoxia caused a threefold elevation in systolic
BP from baseline (83.5 ± 3.5 mmHg in WKY, 70.6 ± 4.6 mmHg in
SD) and greater bradycardia (
178 ± 20 beats/min in WKY,
178 ± 21 beats/min in SD) compared with hypocapnic hypoxia (29.8 ± 3.6 mmHg and 43 ± 15 beats/min in WKY,
19.0 ± 4.1 mmHg and 45 ± 12 beats/min in SD). After
prazosin, the BP increase from eucapnic hypoxia was blunted, yohimbine
showed no effect, and atropine blocked the bradycardia. Direct
measurement of sympathetic nerve activity confirmed that adding
CO2 to the hypoxic gas mixture caused a 61% increase in sympathetic nerve activity. WKY rats seem
more vulnerable than SD rats to both hypoxia exposures in terms of the
elevation in BP. We conclude that, in the rat, eucapnic hypoxia is a
more potent stimulus to acute BP elevation and bradycardia than is
hypocapnic hypoxia. An increased sympathetic tone appears to be
involved in the BP response to acute episodic hypoxia.
apnea; sleep apnea syndromes; hypoxemia; sympathetic nervous system; bradycardia
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