Effect of autonomic blocking agents on the respiratory-related oscillations of ventricular action potential duration in humans
| Autor: | Stefan, van Duijvenboden, Ben, Hanson, Nick, Child, Michele, Orini, Christopher A, Rinaldi, Jaswinder S, Gill, Peter, Taggart |
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| Rok vydání: | 2015 |
| Předmět: |
Atropine
Male Heart Ventricles Adrenergic beta-Antagonists Action Potentials Blood Pressure Muscarinic Antagonists Ventricular Function Left Electrocardiography Heart Rate Tachycardia Supraventricular Humans Aged parasympathetic blockade Cardiac Excitation and Contraction β-adrenergic blockade Parasympatholytics Middle Aged Respiratory Mechanics Ventricular Function Right Female Anti-Arrhythmia Agents cardiac electrophysiology respiration Autonomic Nerve Block Metoprolol |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology |
| ISSN: | 1522-1539 |
| Popis: | Ventricular action potential repolarization is critical to electrical stability and arrhythmogenesis. Oscillations at the respiratory frequency were investigated in humans by combining endocardial electrophysiological recordings, controlled respiration with adrenergic blocking agents. Results are consistent with a partial role of the sympathetic nervous system combined with additional mechanisms, possibly involving mechano-electric feedback. Ventricular action potential duration (APD) is an important component of many physiological functions including arrhythmogenesis. APD oscillations have recently been reported in humans at the respiratory frequency. This study investigates the contribution of the autonomic nervous system to these oscillations. In 10 patients undergoing treatment for supraventricular arrhythmias, activation recovery intervals (ARI; a conventional surrogate for APD) were measured from multiple left and right ventricular (RV) endocardial sites, together with femoral artery pressure. Respiration was voluntarily regulated and heart rate clamped by RV pacing. Sympathetic and parasympathetic blockade was achieved using intravenous metoprolol and atropine, respectively. Metroprolol reduced the rate of pressure development (maximal change in pressure over time): 1,271 (± 646) vs. 930 (± 433) mmHg/s; P < 0.01. Systolic blood pressure (SBP) showed a trend to decrease after metoprolol, 133 (± 21) vs. 128 (± 25) mmHg; P = 0.06, and atropine infusion, 122 (± 26) mmHg; P < 0.05. ARI and SBP exhibited significant cyclical variations (P < 0.05) with respiration in all subjects with peak-to-peak amplitudes ranging between 0.7 and 17.0 mmHg and 1 and 16 ms, respectively. Infusion of metoprolol reduced the mean peak-to-peak amplitude [ARI, 6.2 (± 1.4) vs. 4.4 (± 1.0) ms, P = 0.008; SBP, 8.4 (± 1.6) vs. 6.2 (± 2.0) mmHg, P = 0.002]. The addition of atropine had no significant effect. ARI, SBP, and respiration showed significant coupling (P < 0.05) at the breathing frequency in all subjects. Directed coherence from respiration to ARI was high and reduced after metoprolol infusion [0.70 (± 0.17) vs. 0.50 (± 0.23); P < 0.05]. These results suggest a role of respiration in modulating the electrophysiology of ventricular myocardium in humans, which is partly, but not totally, mediated by β-adrenergic mechanisms. |
| Databáze: | OpenAIRE |
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