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Cardiac diastolic and autonomic dysfunction are aggravated by central chemoreflex activation in heart failure with preserved ejection fraction rats

dc.contributor.authorToledo C.
dc.contributor.authorAndrade D.C.
dc.contributor.authorLucero C.
dc.contributor.authorArce-Alvarez A.
dc.contributor.authorDíaz H.S.
dc.contributor.authorAliaga V.
dc.contributor.authorSchultz H.D.
dc.contributor.authorMarcus N.J.
dc.contributor.authorManríquez M.
dc.contributor.authorFaúndez M.
dc.contributor.authorDel Rio R.
dc.date.accessioned2020-09-02T22:29:16Z
dc.date.available2020-09-02T22:29:16Z
dc.date.issued2017
dc.identifier10.1113/JP273558
dc.identifier.citation595, 8, 2479-2495
dc.identifier.issn00223751
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6391
dc.descriptionKey points: Heart failure with preserved ejection fraction (HFpEF) is associated with disordered breathing patterns, and sympatho-vagal imbalance. Although it is well accepted that altered peripheral chemoreflex control plays a role in the progression of heart failure with reduced ejection fraction (HFrEF), the pathophysiological mechanisms underlying deterioration of cardiac function in HFpEF are poorly understood. We found that central chemoreflex is enhanced in HFpEF and neuronal activation is increased in pre-sympathetic regions of the brainstem. Our data showed that activation of the central chemoreflex pathway in HFpEF exacerbates diastolic dysfunction, worsens sympatho-vagal imbalance and markedly increases the incidence of cardiac arrhythmias in rats with HFpEF. Abstract: Heart failure (HF) patients with preserved ejection fraction (HFpEF) display irregular breathing, sympatho-vagal imbalance, arrhythmias and diastolic dysfunction. It has been shown that tonic activation of the central and peripheral chemoreflex pathway plays a pivotal role in the pathophysiology of HF with reduced ejection fraction. In contrast, no studies to date have addressed chemoreflex function or its effect on cardiac function in HFpEF. Therefore, we tested whether peripheral and central chemoreflexes are hyperactive in HFpEF and if chemoreflex activation exacerbates cardiac dysfunction and autonomic imbalance. Sprague-Dawley rats (n = 32) were subjected to sham or volume overload to induce HFpEF. Resting breathing variability, chemoreflex gain, cardiac function and sympatho-vagal balance, and arrhythmia incidence were studied. HFpEF rats displayed [mean ± SD; chronic heart failure (CHF) vs. Sham, respectively] a marked increase in the incidence of apnoeas/hypopnoeas (20.2 ± 4.0 vs. 9.7 ± 2.6 events h−1), autonomic imbalance [0.6 ± 0.2 vs. 0.2 ± 0.1 low/high frequency heart rate variability (LF/HFHRV)] and cardiac arrhythmias (196.0 ± 239.9 vs. 19.8 ± 21.7 events h−1). Furthermore, HFpEF rats showed increase central chemoreflex sensitivity but not peripheral chemosensitivity. Accordingly, hypercapnic stimulation in HFpEF rats exacerbated increases in sympathetic outflow to the heart (229.6 ± 43.2% vs. 296.0 ± 43.9% LF/HFHRV, normoxia vs. hypercapnia, respectively), incidence of cardiac arrhythmias (196.0 ± 239.9 vs. 576.7 ± 472.9 events h−1) and diastolic dysfunction (0.008 ± 0.004 vs. 0.027 ± 0.027 mmHg μl−1). Importantly, the cardiovascular consequences of central chemoreflex activation were related to sympathoexcitation since these effects were abolished by propranolol. The present results show that the central chemoreflex is enhanced in HFpEF and that acute activation of central chemoreceptors leads to increases of cardiac sympathetic outflow, cardiac arrhythmogenesis and impairment in cardiac function in rats with HFpEF. © 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society
dc.language.isoen
dc.publisherBlackwell Publishing Ltd
dc.subjectautonomic imbalance
dc.subjectcardiac function
dc.subjectcentral chemoreflex
dc.subjectheart failure preserved ejection fraction
dc.subjectrespiratory disorders
dc.subjectpropranolol
dc.subjectadult
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectapnea hypopnea index
dc.subjectarrhythmogenesis
dc.subjectArticle
dc.subjectautonomic dysfunction
dc.subjectbrain stem
dc.subjectbreathing
dc.subjectcell activation
dc.subjectchemoreceptor reflex
dc.subjectcontrolled study
dc.subjectdiastolic dysfunction
dc.subjectdisease exacerbation
dc.subjectheart arrhythmia
dc.subjectheart failure with preserved ejection fraction
dc.subjectheart rate variability
dc.subjecthypercapnia
dc.subjectincidence
dc.subjectmale
dc.subjectnerve cell
dc.subjectnonhuman
dc.subjectrat
dc.subjectrest
dc.subjectSprague Dawley rat
dc.subjectsympathetic innervation
dc.subjectsympathetic tone
dc.subjectvagus tone
dc.subjectanimal
dc.subjectchemoreceptor cell
dc.subjectdiastole
dc.subjectheart arrhythmia
dc.subjectheart failure
dc.subjectheart rate
dc.subjectheart stroke volume
dc.subjectmetabolism
dc.subjectoxidative stress
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectAnimals
dc.subjectArrhythmias, Cardiac
dc.subjectChemoreceptor Cells
dc.subjectDiastole
dc.subjectHeart Failure
dc.subjectHeart Rate
dc.subjectHypercapnia
dc.subjectMale
dc.subjectOxidative Stress
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectStroke Volume
dc.titleCardiac diastolic and autonomic dysfunction are aggravated by central chemoreflex activation in heart failure with preserved ejection fraction rats
dc.typeArticle


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