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Acute vagal stimulation attenuates cardiac metabolic response to β‐adrenergic stress
Author(s) -
Vimercati Claudio,
Qanud Khaled,
Ilsar Itamar,
Mitacchione Gianfranco,
Sarnari Roberto,
Mania Daniella,
Faulk Ryan,
Stanley William C.,
Sabbah Hani N.,
Recchia Fabio A.
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2012.241943
Subject(s) - medicine , stimulation , endocrinology , adrenergic , efferent , heart rate , catecholamine , vagal tone , vagus nerve , fatty acid , chemistry , autonomic nervous system , receptor , biochemistry , blood pressure , afferent
Key points• Whereas the effects of catecholamines on myocardial metabolism are well characterized, the potential role of the parasympathetic system is generally considered minor or absent. • We tested the hypothesis that acute stimulation of the right vagus nerve alters the balance between cardiac free fatty acid and carbohydrate oxidation and opposes the metabolic effects of beta‐adrenergic stimulation. • Using a clinical‐type selective stimulator of the vagal efferent fibers in dogs, we found that vagal stimulation did not significantly affect baseline cardiac performance, haemodynamics and myocardial metabolism. • During dobutamine stress, vagal stimulation attenuated the increase in left ventricular mechanical performance, cardiac oxygen consumption and myocardial glucose oxidation, while free fatty acid oxidation was affected only at low catecholamine dose. • Our results elucidate a previously unexplored parasympathetic function, indicating that selective vagal efferent stimulation antagonizes the effects of beta‐adrenergic activation on myocardial metabolism.Abstract The effects of vagal stimulation (VS) on cardiac energy substrate metabolism are unknown. We tested the hypothesis that acute VS alters the balance between free fatty acid (FFA) and carbohydrate oxidation and opposes the metabolic effects of β‐adrenergic stimulation. A clinical‐type selective stimulator of the vagal efferent fibres was connected to the intact right vagus in chronically instrumented dogs. VS was set to reduce heart rate by 30 beats min −1 , and the confounding effects of bradycardia were then eliminated by pacing the heart at 165 beats min −1 . [ 3 H]Oleate and [ 14 C]glucose were infused to measure FFA and glucose oxidation. The heart was subjected to β‐adrenergic stress by infusing dobutamine at 5, 10 and 15 μg kg −1 min −1 before and during VS. VS did not significantly affect baseline cardiac performance, haemodynamics or myocardial metabolism. However, at peak dobutamine stress, VS attenuated the increase in left ventricular pressure–diameter area from 235.9 ± 72.8 to 167.3 ± 55.8%, and in cardiac oxygen consumption from 173.9 ± 23.3 to 127.89 ± 6.2% (both P < 0.05), and thus mechanical efficiency was not enhanced. The increase in glucose oxidation fell from 289.3 ± 55.5 to 131.1 ± 20.9%( P < 0.05), while FFA oxidation was not increased by β‐adrenergic stress and fell below baseline during VS only at the lowest dose of dobutamine. The functional and in part the metabolic changes were reversed by 0.1 mg kg −1 atropine i.v. Our data show that acute right VS does not affect baseline cardiac metabolism, but attenuates myocardial oxygen consumption and glucose oxidation in response to adrenergic stress, thus functioning as a cardio‐selective antagonist to β‐adrenergic activation.