Key result
Norepinephrine and acetylcholine significantly increased the excitable gap from a baseline of 27 ms to 34 ms and 50 ms, respectively (P<0.001), in a canine model of atrial flutter.
Why the study?
Do autonomic neurotransmitters (norepinephrine and acetylcholine) alter the excitable gap composition in a canine model of atrial flutter?
Do autonomic neurotransmitters (norepinephrine and acetylcholine) alter the excitable gap composition in a canine model of atrial flutter?
Both sympathetic and parasympathetic activation increase the safety margin of full excitability ahead of the wavefront in atrial flutter, facilitating the persistence of the arrhythmia.
Answers are grounded in this paper and cite their sources.
Does not support clinical use of autonomic modulation in atrial flutter; leaves open translation of excitable gap effects to human mechanisms.
Atrial arrhythmias are believed to be influenced by autonomic nervous system tone. We evaluated the effects of sympathetic and parasympathetic activation on atrial flutter (AF1) by determining the effects of norepinephrine (NE) and acetylcholine (ACh) on the composition of the excitable gap. A model of reentry around the tricuspid valve was produced in 17 chloralose anesthetized dogs using a Y-shaped lesion in the intercaval area that extended to the right atrial appendage. Excitable gap characteristics were determined during AF1 by scanning diastole with a single premature extrastimulus at progressively shorter coupling intervals to define the reset-response curve. Measurements were made during a constant infusion of NE (15 microg/min) into the right coronary artery and repeated during ACh infusion (2 microg/min) following a 15 min recovery period. The excitable gap (27 +/- 1 ms) was significantly (P < 0.001) increased by NE (34 +/- 1 ms) and ACh (50 +/- 2 ms). The fully excitable portion (7 +/- 1 ms) was also significantly (P < 0.001) increased by NE (17 +/- 1 ms) and ACh (43 +/- 2 ms). We conclude that both neurotransmitters increase the safety margin of full excitability ahead of the wavefront, demonstrating that parasympathetic and sympathetic activation can facilitate the persistence of this refractory atrial arrhythmia.
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Rahme et al. (2001) studied Atrial flutter (n=17). Norepinephrine and Acetylcholine vs. Baseline was evaluated on Excitable gap duration (p=< 0.001). Norepinephrine and acetylcholine significantly increased the excitable gap from a baseline of 27 ms to 34 ms and 50 ms, respectively (P<0.001), in a canine model of atrial flutter.
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