New insights into differential baroreflex control of heart rate in humans

1  Department of Integrative Physiology and Cardiovascular Research Institute, University of North Texas Health Science Center, Fort Worth, Texas 76107; and 2  Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2200 Copenhagen, Denmark Recent d...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2003-02, Vol.284 (2), p.H735-H743
Hauptverfasser: Fadel, P. J, Stromstad, M, Wray, D. W, Smith, S. A, Raven, P. B, Secher, N. H
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Sprache:eng
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Zusammenfassung:1  Department of Integrative Physiology and Cardiovascular Research Institute, University of North Texas Health Science Center, Fort Worth, Texas 76107; and 2  Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2200 Copenhagen, Denmark Recent data indicate that bilateral carotid sinus denervation in patients results in a chronic impairment in the rapid reflex control of blood pressure during orthostasis. These findings are inconsistent with previous human experimental investigations indicating a minimal role for the carotid baroreceptor-cardiac reflex in blood pressure control. Therefore, we reexamined arterial baroreflex [carotid (CBR) and aortic baroreflex (ABR)] control of heart rate (HR) using newly developed methodologies. In 10 healthy men, 27   ± 1 yr old, an abrupt decrease in mean arterial pressure (MAP) was induced nonpharmacologically by releasing a unilateral arterial thigh cuff (300 Torr) after 9 min of resting leg ischemia under two conditions: 1 ) ABR and CBR deactivation (control) and 2 ) ABR deactivation. Under control conditions, cuff release decreased MAP by 13 ± 1 mmHg, whereas HR increased 11 ± 2 beats/min. During ABR deactivation, neck suction was gradually applied to maintain carotid sinus transmural pressure during the initial 20 s after cuff release (suction). This attenuated the increase in HR (6   ± 1 beats/min) and caused a greater decrease in MAP (18 ± 2 mmHg, P  
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00246.2002