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Acute vagal stimulation attenuates cardiac metabolic response to β-adrenergic stress
Claudio Vimercati1, Khaled Qanud, Itamar Ilsar
1Department of Physiology, New York Medical College, Valhalla, NY, USA.
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.
Insights
Vagal stimulation (VS) does not change resting heart metabolism but reduces oxygen consumption and glucose use during adrenergic stress. This suggests VS acts as a cardio-selective antagonist to beta-adrenergic activation.
Area of Science:
- Cardiovascular Physiology
- Metabolic Regulation
- Autonomic Nervous System
Background:
- The impact of vagal stimulation (VS) on cardiac energy substrate metabolism remains largely unexplored.
- Understanding how VS influences the balance between fatty acid and carbohydrate oxidation is crucial.
- Investigating whether VS can counteract the metabolic effects of beta-adrenergic stimulation is of clinical interest.
Purpose of the Study:
- To determine the effects of acute vagal stimulation on cardiac energy substrate metabolism.
- To test the hypothesis that VS alters the balance between free fatty acid (FFA) and carbohydrate oxidation.
- To evaluate if VS opposes the metabolic consequences of beta-adrenergic stimulation.
Main Methods:
- Utilized chronically instrumented dogs with a selective stimulator for vagal efferent fibers.
- Controlled for bradycardia by pacing the heart at a constant rate (165 beats min(-1)).
- Measured FFA and glucose oxidation using isotope tracers during dobutamine-induced beta-adrenergic stress, with and without VS.
Main Results:
- Acute right vagal stimulation did not significantly alter baseline cardiac performance, hemodynamics, or myocardial metabolism.
- During peak dobutamine stress, VS attenuated increases in left ventricular pressure-diameter area and cardiac oxygen consumption.
- VS reduced the rise in glucose oxidation and, at the lowest dobutamine dose, decreased FFA oxidation, with effects partially reversed by atropine.
Conclusions:
- Acute right vagal stimulation does not affect baseline cardiac metabolism.
- VS attenuates myocardial oxygen consumption and glucose oxidation in response to adrenergic stress.
- Vagal stimulation functions as a cardio-selective antagonist to beta-adrenergic activation.
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