Attenuated Pre‐ejection Period Response to Tyramine in Patients with Cardiac Sympathetic Denervation
Identifieur interne : 001A52 ( Main/Curation ); précédent : 001A51; suivant : 001A53Attenuated Pre‐ejection Period Response to Tyramine in Patients with Cardiac Sympathetic Denervation
Auteurs : Richard Imrich [États-Unis] ; Basil A. Eldadah [États-Unis] ; Oladi Bentho [États-Unis] ; Sandra Pechnik [États-Unis] ; Yehonatan Sharabi [États-Unis] ; Courtney Holmes [États-Unis] ; David S. Goldstein [États-Unis]Source :
- Annals of the New York Academy of SciencesStress, Neurotransmitters, and Hormones Neuroendocrine and Genetic Mechanisms [ 0077-8923 ] ; 2008-12.
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Abstract
Stress is a well‐known factor affecting cardiac contractility through the cardiac sympathetic nerves. A positive inotropic effect of the cardiac sympathetic nerves on the myocardium is reflected by pre‐ejection period (PEP) shortening. Patients with Parkinson disease (PD) and neurogenic orthostatic hypotension (NOH) (PD + NOH) or with pure autonomic failure (PAF) have markedly decreased myocardial 6‐[18F]Fluorodopamine‐derived radioactivity, reflecting cardiac sympathetic denervation. The functional effects of the cardiac sympathetic denervation have been unknown. We measured PEP and heart rate–corrected PEP (PEPI) responses to i.v. tyramine (1 mg/min) in 13 patients (9 PD + NOH and 4 PAF) with low 6‐[18F]Fluorodopamine‐derived radioactivity and in subjects with normal radioactivity (15 multiple system atrophy with NOS patients (MSA + NOS). Baseline PEP and PEPI did not differ between the groups. By 10 min after initiation of tyramine infusion, PEP and PEPI were significantly lower (P < 0.01) in MSA + NOS, compared to base line, whereas PEP and PEPI remained unchanged in the PD + NOH/PAF group. The PEP and PEPI decrease was larger in the MSA + NOS group than in the PD + NOH/PAF group (P < 0.05). One of the functional consequences of cardiac sympathetic denervation is failure to increase contractility in response to stimuli that depend on endogenous norepinephrine release.
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DOI: 10.1196/annals.1410.066
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Eldadah</name><affiliation wicri:level="1"><mods:affiliation>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Bentho, Oladi" sort="Bentho, Oladi" uniqKey="Bentho O" first="Oladi" last="Bentho">Oladi Bentho</name><affiliation wicri:level="1"><mods:affiliation>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Pechnik, Sandra" sort="Pechnik, Sandra" uniqKey="Pechnik S" first="Sandra" last="Pechnik">Sandra Pechnik</name><affiliation wicri:level="1"><mods:affiliation>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Sharabi, Yehonatan" sort="Sharabi, Yehonatan" uniqKey="Sharabi Y" first="Yehonatan" last="Sharabi">Yehonatan Sharabi</name><affiliation wicri:level="1"><mods:affiliation>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Holmes, Courtney" sort="Holmes, Courtney" uniqKey="Holmes C" first="Courtney" last="Holmes">Courtney Holmes</name><affiliation wicri:level="1"><mods:affiliation>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Goldstein, David S" sort="Goldstein, David S" uniqKey="Goldstein D" first="David S." last="Goldstein">David S. 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A positive inotropic effect of the cardiac sympathetic nerves on the myocardium is reflected by pre‐ejection period (PEP) shortening. Patients with Parkinson disease (PD) and neurogenic orthostatic hypotension (NOH) (PD + NOH) or with pure autonomic failure (PAF) have markedly decreased myocardial 6‐[18F]Fluorodopamine‐derived radioactivity, reflecting cardiac sympathetic denervation. The functional effects of the cardiac sympathetic denervation have been unknown. We measured PEP and heart rate–corrected PEP (PEPI) responses to i.v. tyramine (1 mg/min) in 13 patients (9 PD + NOH and 4 PAF) with low 6‐[18F]Fluorodopamine‐derived radioactivity and in subjects with normal radioactivity (15 multiple system atrophy with NOS patients (MSA + NOS). Baseline PEP and PEPI did not differ between the groups. By 10 min after initiation of tyramine infusion, PEP and PEPI were significantly lower (P < 0.01) in MSA + NOS, compared to base line, whereas PEP and PEPI remained unchanged in the PD + NOH/PAF group. The PEP and PEPI decrease was larger in the MSA + NOS group than in the PD + NOH/PAF group (P < 0.05). One of the functional consequences of cardiac sympathetic denervation is failure to increase contractility in response to stimuli that depend on endogenous norepinephrine release.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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