Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice
Autor: | Mark W. Chapleau, David Gozal, William B. Wead, Rugao Liu, Robert D. Wurster, Min Lin, Zixi Jack Cheng |
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Rok vydání: | 2007 |
Předmět: |
Nitroprusside
medicine.medical_specialty Physiology Vasodilator Agents Efferent Central nervous system Blood Pressure Stimulation Anesthesia General Baroreflex Efferent Pathways Mice Phenylephrine Heart Rate Tachycardia Physiology (medical) Internal medicine Heart rate medicine Animals Hypoxia Anesthetics Nucleus ambiguus Afferent Pathways Dose-Response Relationship Drug Ethanol business.industry Heart Vagus Nerve Hypoxia (medical) Electric Stimulation Mice Inbred C57BL Disease Models Animal Endocrinology medicine.anatomical_structure Chronic Disease Hypertension Circulatory system medicine.symptom Cardiology and Cardiovascular Medicine business Adrenergic alpha-Agonists |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 293:H997-H1006 |
ISSN: | 1522-1539 0363-6135 |
Popis: | Chronic intermittent hypoxia (CIH) leads to increased sympathetic nerve activity and arterial hypertension. In this study, we tested the hypothesis that CIH impairs baroreflex (BR) control of heart rate (HR) in mice, and that decreased cardiac chronotropic responsiveness to vagal efferent activity contributes to such impairment. C57BL/6J mice were exposed to either room air (RA) or CIH (6-min alternations of 21% O2and 5.7% O2, 12 h/day) for 90 days. After the treatment period, mice were anesthetized (Avertin) and arterial blood pressure (ABP) was measured from the femoral artery. Mean ABP (MABP) was significantly increased in mice exposed to CIH (98.7 ± 2.5 vs. RA: 78.9 ± 1.4 mmHg, P < 0.001). CIH increased HR significantly (584.7 ± 8.9 beats/min; RA: 518.2 ± 17.9 beats/min, P < 0.05). Sustained infusion of phenylephrine (PE) at different doses (0.1–0.4 μg/min) significantly increased MABP in both CIH and RA mice, but the ABP-mediated decreases in HR were significantly attenuated in mice exposed to CIH ( P < 0.001). In contrast, decreases in HR in response to electrical stimulation of the left vagus nerve (30 μA, 2-ms pulses) were significantly enhanced in mice exposed to CIH compared with RA mice at low frequencies. We conclude that CIH elicits a sustained impairment of baroreflex control of HR in mice. The blunted BR-mediated bradycardia occurs despite enhanced cardiac chronotropic responsiveness to vagal efferent stimulation. This suggests that an afferent and/or a central defect is responsible for the baroreflex impairment following CIH. |
Databáze: | OpenAIRE |
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