The Influence of Chemical and Mechanical Feedback on Ventilatory Pattern in a Model of the Central Respiratory Pattern Generator

Author(s):  
K. A. E. Geitz ◽  
D. W. Richter ◽  
A. Gottschalk
2009 ◽  
Vol 10 (Suppl 1) ◽  
pp. P248
Author(s):  
David M Baekey ◽  
Thomas E Dick ◽  
Roberto F Galán

1993 ◽  
Vol 75 (2) ◽  
pp. 675-681 ◽  
Author(s):  
F. Xu ◽  
R. F. Taylor ◽  
L. Y. Lee ◽  
D. T. Frazier

Effects of inspiratory tracheal occlusion (TO) on respiratory duration (inspiratory and expiratory duration), ventilation, and the peak integrated diaphragm electromyographic (integral of EMGdi) response were tested in 16 anesthetized cats before and after decerebellation with and without vagal input. The same protocols were repeated in the decerebrate preparation. Decerebellation did not significantly affect the baseline or the loaded values [tracheal occlusion (TO)] for respiratory duration, tidal volume, or magnitude of the integral of EMGdi response. Vagal blockade eliminated the load-compensating responses in the intact and the decerebrate preparation. However, vagal blockade in concert with decerebellation resulted in a significant (P < 0.05) reversible inhibition of the peak integral of EMGdi response during inspiratory TO. This suggests that removal of vagal and cerebellar influences during loaded breathing unmasked inhibitory inputs to the respiratory pattern generator. With vagus intact, decerebellation before or after decerebration abolished the attenuation of the peak integral of EMGdi response to TO observed with decerebration alone. We conclude that the cerebellum does play a role in determining the pattern of the respiratory response to TO. This influence may be direct and/or indirect via interaction with information emanating from suprapontine, vagal, and nonvagal sources.


1994 ◽  
Vol 6 (1) ◽  
pp. 56-68 ◽  
Author(s):  
Allan Gottschalk ◽  
Malcolm D. Ogilvie ◽  
Diethelm W. Richter ◽  
Allan I. Pack

To help evaluate the hypothesis that the central respiratory rhythm is generated by a network of interacting neurons, a network model of respiratory rhythmogenesis is formulated and examined computationally. The neural elements of the network are driven by tonic inputs and generate a continuous variable representing firing rate. Each neural element in the model can be described by an activation time constant, an adaptation time constant, and a step nonlinearity. Initial network connectivity was based on an earlier proposed model of the central respiratory pattern generator. These connections were adjusted interactively until the model trajectories resembled those observed electrophysiologically. The properties of the resulting network were examined computationally by simulation, determination of the phase resetting behavior of the network oscillator, and examination of the localized eigenstructure of the network. These results demonstrate that the network model can account for a number of diverse physiological observations, and, thus, support the network hypothesis of respiratory rhymogenesis.


2005 ◽  
Vol 100 (1) ◽  
pp. 175-182 ◽  
Author(s):  
Shin Onizuka ◽  
Toshiharu Kasaba ◽  
Toshiro Hamakawa ◽  
Mayumi Takasaki

1995 ◽  
Vol 79 (3) ◽  
pp. 1048-1054 ◽  
Author(s):  
A. R. Patwardhan ◽  
S. Vallurupalli ◽  
J. M. Evans ◽  
E. N. Bruce ◽  
C. F. Knapp

We investigated the effects of voluntary control of breathing on autonomic function in cardiovascular regulation. Variability in heart rate was compared between 5 min of spontaneous and controlled breathing. During controlled breathing, for 5 min, subjects voluntarily reproduced their own spontaneous breathing pattern (both rate and volume on a breath-by-breath basis). With the use of this experimental design, we could unmask the effects of voluntary override of the spontaneous respiratory pattern generator on autonomic function in cardiovascular regulation without the confounding effects of altered respiratory pattern. Results from 10 subjects showed that during voluntary control of breathing, mean values of heart rate and blood pressure increased, whereas fractal and spectral powers in heart rate in the respiratory frequency region decreased. End-tidal PCO2 was similar during spontaneous and controlled breathing. These results indicate that the act of voluntary control of breathing decreases the influence of the vagal component, which is the principal parasympathetic influence in cardiovascular regulation.


1984 ◽  
Vol 56 (4) ◽  
pp. 1027-1031 ◽  
Author(s):  
N. K. Burki

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.


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