Abstract| Volume 177, ISSUE 1, P34, August 2013

Subpopulations and latency variations in multi-unit action potentials from human sympathetic nerve recording: Impact of age and disease

      Mironeurographic recordings of sympathetic nerve activity in humans present a poor signal-to-noise neurogram from bundles containing postganglionic C-fibres of uncertain number and size. Thus, the traditional method of analysis includes band-pass filtering and integration the raw neurogram producing a neurogram of bursts that vary in frequency and size. This approach loses the information regarding the independent action potentials (APs) that make up the integrated neurogram. The symposia will highlight the new observations made by studying the multi-unit AP discharge patterns in the human MSNA neurogram. A modified wavelet denoising approach was developed that exposes the timing and shape of each AP in the filtered MSNA signal. This approach has enabled testing of hypotheses regarding the existence of latent, fast-conducting postganglionic sympathetic APs and/or synaptic delays that affect burst-by-burst variations in AP content. During severe chemoreflex and baroreflex stress a new population of fast-conducting, large amplitude, APs are exposed. In contrast, Valsalva’s manoeuvre elicits more bursts but no new AP families are detected; rather, each AP family has a shorter conduction velocity suggesting reflex-specific modulation of synaptic delays. Based on burst frequency of integrated MSNA data, advanced age and cardiovascular disease are characterized by heightened sympathetic drive to skeletal muscle. Congestive heart failure increased APs per burst and number of active AP families per burst and decreased (but did not abolish) the overall ability to recruit more APs during post-PVC sympathetic bursts. Overall, AP families of various sizes exist within the MSNA neurogram, and options appear to exist for modulating MSNA outflow through increased frequency of APs recruited at baseline, recruitment of latent axons, or modulating synaptic delays of already-recruited axons.
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