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  • American Physiological Society  (1)
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  • American Physiological Society  (1)
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    In: Journal of Applied Physiology, American Physiological Society, Vol. 118, No. 7 ( 2015-04-01), p. 839-848
    Abstract: Peripheral chemoreceptor activity/sensitivity is enhanced in chronic heart failure (HF), and sensitivity is linked to greater mortality. This study aimed to determine the role of the peripheral chemoreceptor in cardiovascular control at rest and during exercise in HF patients and controls. Clinically stable HF patients ( n = 11; ejection fraction: 39 ± 5%) and risk-matched controls ( n = 10; ejection fraction: 65 ± 2%) performed randomized trials with or without dopamine infusion (2 μg·min −1 ·kg −1 ) at rest and during 40% maximal voluntary contraction handgrip (HG) exercise, and a resting trial of 2 min of inspired 100% oxygen. Both dopamine and hyperoxia were used to inhibit the peripheral chemoreceptor. At rest in HF patients, dopamine decreased ventilation ( P = 0.02), decreased total peripheral resistance index ( P = 0.003), and increased cardiac and stroke indexes ( P ≤ 0.01), yet there was no effect of dopamine on these variables in controls ( P ≥ 0.7). Hyperoxia lowered ventilation in HF ( P = 0.01), but not in controls ( P = 0.9), indicating suppression of the peripheral chemoreceptors in HF. However, no decrease of total peripheral resistance index was observed in HF. As expected, HG increased heart rate, ventilation, and brachial conductance of the nonexercising arm in controls and HF patients. During dopamine infusion, there were no changes in mean arterial pressure, heart rate, or ventilation responses to HG in either group ( P ≥ 0.26); however, brachial conductance increased with dopamine in the control group ( P = 0.004), but decreased in HF ( P = 0.02). Our findings indicate that the peripheral chemoreceptor contributes to cardiovascular control at rest in HF patients and during exercise in risk-matched controls.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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