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Quantitative analysis of cardiovascular modulation in respiratory neural activity
Author(s) -
Dick Thomas E.,
Morris Kendall F.
Publication year - 2004
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.2003.060418
Subject(s) - respiratory system , respiration , expiration , cardiorespiratory fitness , stimulation , cardiac cycle , control of respiration , medicine , cardiology , chemistry , anatomy
We propose the ‘δ 2 ‐statistic’ for assessing the magnitude and statistical significance of arterial pulse‐modulated activity of single neurones and present the results of applying this tool to medullary respiratory‐modulated units. This analytical tool is a modification of the η 2 ‐statistic and, consequently, based on the analysis of variance. The η 2 ‐statistic reflects the consistency of respiratory‐modulated activity on a cycle‐by‐cycle basis. However, directly applying this test to activity during the cardiac cycle proved ineffective because subjects‐by‐treatments matrices did not contain enough ‘information’. We increased information by dividing the cardiac cycle into fewer bins, excluding cycles without activity and summing activity over multiple cycles. The analysed neuronal activity was an existing data set examining the neural control of respiration and cough. Neurones were recorded in the nuclei of the solitary tracts, and in the rostral and caudal ventral respiratory groups of decerebrate, neuromuscularly blocked, ventilated cats ( n = 19). Two hundred of 246 spike trains were respiratory modulated; of these 53% were inspiratory (I), 36.5% expiratory (E), 6% IE phase spanning and 4.5% EI phase spanning and responsive to airway stimulation. Nearly half ( n = 96/200) of the respiratory‐modulated units were significantly pulse modulated and 13 were highly modulated with δ 2 values exceeding 0.3. In 10 of these highly modulated units, η 2 values were greater than 0.3 and all 13 had, at least, a portion of their activity during expiration. We conclude that cardiorespiratory interaction is reciprocal; in addition to respiratory‐modulated activity in a subset of neuronal activity patterns controlling the cardiovascular system, pulse‐modulated activity exists in a subset of neuronal activity patterns controlling the respiratory system. Thus, cardio‐ventilatory coupling apparent in respiratory motor output is evident and, perhaps, derived from the neural substrate driving that output.