Effects of changes in peripheral and central on ventilation during recovery from submergence in ducks

1983 ◽  
Vol 61 (11) ◽  
pp. 2388-2393 ◽  
Author(s):  
William K. Milsom ◽  
David R. Jones ◽  
Geoffrey R. J. Gabbott

The effects of increases in arterial CO2 tension at peripheral and central chemoreceptors on ventilation during recovery from submergence were studied using cross-perfusion techniques on unanaesthetized, White Pekin ducks. Immediately upon surfacing, under normal conditions, minute ventilation [Formula: see text] was elevated four to five times due to roughly equal increases in tidal volume (VT) and breathing frequency (f). Tidal volume returned to resting levels far more rapidly than breathing frequency. If only a peripheral hypercapnia was allowed to develop during diving, it produced the same maximum ventilatory reponse upon surfacing but recovery was much quicker. Central hypercapnia interacted with the peripheral hypercapnia in an additive fashion. There is evidence to suggest that hypercapnia has a greater effect in increasing VT, and hypoxia in increasing f, during the postdive recovery period. The prolonged tachypnea which normally persists after blood gas levels have returned to normal only occurs when hypoxia is allowed to develop during the dive.

1992 ◽  
Vol 72 (3) ◽  
pp. 842-850 ◽  
Author(s):  
F. Cerny ◽  
L. Armitage ◽  
J. A. Hirsch ◽  
B. Bishop

We hypothesized that the hyperinflation and pulmonary dysfunction of cystic fibrosis (CF) would distort feedback and therefore alter the abdominal muscle response to graded expiratory threshold loads (ETLs). We compared the respiratory and abdominal muscle responses with graded ETLs of seven CF patients with severe lung dysfunction with those of matched healthy control subjects in the supine and 60 degrees head-up positions. Breathing frequency, tidal volume, and ventilatory timing were determined from inspiratory flow recordings. Abdominal electromyograms (EMGs) were detected with surface electrodes placed unilaterally over the external and internal oblique and the rectus abdominis muscles. Thresholds, times of onset, and durations of phasic abdominal activity were determined from raw EMGs; peak amplitudes were determined from integrated EMGs. Graded ETLs were imposed by submerging a tube from the expiratory port of the breathing valve into a column of water at depths of 0–25 cmH2O. We found that breathing frequency, tidal volume, and expired minute ventilation were higher in CF patients than in control subjects during low ETLs; a change in body position did not alter these ventilatory responses in the CF patients but did in the control subjects. All CF patients, but none of the control subjects, had tonic abdominal activity while supine. CF patients recruited abdominal muscles at lower loads, earlier in the respiratory cycle, and to a higher recruitment level in both positions than the control subjects, but burst duration of phasic activity was not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 152 (1) ◽  
pp. 93-100 ◽  
Author(s):  
JOHN BRACKENBURY ◽  
JANE AMAKU

Ventilation and respiratory and blood gas tensions were monitored at rest and during running exercise, following bilateral occlusion of the cranial and caudal thoracic and the abdominal air sacs. This represents a removal of approximately 70% of the total air-sac capacity. At rest, the birds were strongly hypoxaemic/hypercapnaemic. Ventilation was maintained at its control value but respiratory frequency was significantly increased and tidal volume diminished. The birds were capable of sustained running at approximately three times the pre-exercise metabolic rate. Minute ventilation during exercise was the same as that of the controls, but breathing was faster and shallower. Exercise had no effect on blood gas tensions in either the control or the experimental birds. There was no evidence of a detrimental effect of air-sac occlusion on the effectiveness of inspiratory airflow valving in the lung: hypoxaemia appeared to be due to the altered respiratory pattern, which resulted in increased dead-space inhalation.


Author(s):  
William J.M. Kinnear ◽  
James H. Hull

This chapter describes how the amount of air going in and out of the lungs increases on exercise. The predicted value for minute ventilation (VE) is calculated for each subject from their own forced expiratory volume in one second (FEV1), rather than taken from published tables. Normally, ventilation does not limit exercise and VE does not reach 80% of the predicted value. If VE at peak exercise is more than 80% of predicted, it is likely there is something wrong with the lungs. VE increases by a combination of a larger tidal volume and an increase in breathing frequency. The pattern of increase is normally gradual. An erratic pattern suggests dysfunctional breathing.


1987 ◽  
Vol 63 (5) ◽  
pp. 1822-1828 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
N. S. Cherniack ◽  
M. D. Altose

The study evaluated the interrelationships between the extent of thoracic movements and respiratory chemical drive in shaping the intensity of the sensation of dyspnea. Normal subjects rated their sensations of dyspnea as PCO2 increased during free rebreathing and during rebreathing while ventilation was voluntarily maintained at a constant base-line level. Another trial evaluated the effects on the intensity of dyspnea, of voluntary reduction in the level of ventilation while PCO2 was held constant. During rebreathing, there was a power function relationship between changes in PCO2 and the intensity of dyspnea. At a given PCO2, constraining tidal volume and breathing frequency to the prerebreathing base-line level resulted in an increase in dyspnea. The fractional differences in the intensity of dyspnea between free and constrained rebreathing were independent of PCO2. However, the absolute difference in the intensity of dyspnea between free and constrained rebreathing enlarged with increasing hypercapnia. At PCO2 of 50 Torr, this difference correlated significantly with the increase in both minute ventilation (r = 0.675) and tidal volume (r = 0.757) above the base line during free rebreathing. Similarly, during steady-state hypercapnia at 50 Torr PCO2, the intensity of dyspnea increased progressively as ventilation was voluntarily reduced from the spontaneously adopted free-breathing level. These results indicate that dyspnea increases with the level of respiratory chemical drive but that the intensity of the sensation is further accentuated when ventilation is constrained below that demanded by the level of chemical drive. This may be explained by a loss of inhibitory feedback from lung or chest wall mechanoreceptors acting on brain stem and/or cortical centers.


1988 ◽  
Vol 65 (2) ◽  
pp. 934-939 ◽  
Author(s):  
D. W. Ray ◽  
C. Hernandez ◽  
N. Munoz ◽  
A. R. Leff ◽  
J. Solway

We demonstrated spontaneous self-limited bronchoconstriction after eucapnic dry gas hyperpnea in 22 anesthetized, mechanically ventilated guinea pigs pretreated with propranolol (1 mg/kg iv). Eucapnic hyperpnea "challenges" of room temperature dry or humidified gas (5% CO2-95% O2) were performed by mechanically ventilating animals (150 breaths/min, 3-6 ml tidal volume) for 5 min. During a "recovery" period after hyperpnea, animals were returned to standard ventilation conditions (6 ml/kg, 60 breaths/min, 50% O2 in air, fully saturated at room temperature). After dry gas hyperpnea (5 ml, 150 breaths/min), respiratory system resistance (Rrs) increased in the recovery period by 7.7-fold and dynamic compliance (Cdyn) decreased by 79.7%; changes were maximal at approximately 3 min posthyperpnea and spontaneously returned to base line in 10-40 min. This response was markedly attenuated by humidification of inspired air. Four consecutive identical dry air challenges resulted in similar posthyperpnea responses in four animals. Increasing the minute ventilation during hyperpnea (by varying tidal volume from 3 to 6 ml) caused increased bronchoconstriction in a dose-dependent fashion in six animals. Neither vagotomy nor atropine altered the airway response to dry gas hyperpnea. We conclude that dry gas hyperpnea in anesthetized guinea pigs results in a bronchoconstrictor response that shares five similar features with hyperpnea-induced bronchoconstriction in human asthma: 1) time course of onset and spontaneous resolution, 2) diminution with humidification of inspired gas, 3) reproducibility on consecutive identical challenges, 4) stimulus-response relationship with minute ventilation during hyperpnea, and 5) independence of parasympathetic neurotransmission.


1996 ◽  
Vol 80 (5) ◽  
pp. 1772-1784 ◽  
Author(s):  
J. A. Spahija ◽  
A. Grassino

To examine the effect of pursed-lips breathing (PLB) on breathing pattern and respiratory mechanics, we studied 11 healthy subjects breathing with and without PLB at rest and during steady-state bicycle exercise. Six of these subjects took part in a second study, which compared the effects of PLB to expiratory resistive loading (ERL). PLB was found to prolong expiratory and total breath durations and to promote a slower and deeper breathing pattern. During exercise, the compensatory increase that occurred in tidal volume was not sufficient to counter the reduction in breathing frequency, causing minute ventilation to be reduced. Although ERL similarly caused minute ventilation and breathing frequency to be decreased, unlike PLB, it produced no change in tidal volume and prolonged expiratory and total breath durations to a lesser extent. PLB and ERL increased the expiratory resistance to a comparable degree, also increasing the expiratory resistive work of breathing and promoting greater expiratory rib cage and abdominal muscle recruitment in response to the expiratory loads. End-expiratory lung volume, which was determined from inspiratory capacity maneuvers, was not altered by PLB; however, with ERL it was increased by 0.20 and 0.24 liter during rest and exercise, respectively. Inspiratory muscle recruitment patterns were not altered by PLB at rest, although small increases in the relative contribution of the rib cage/accessory muscles in conjunction with abdominal muscle relaxation occurred during exercise. Similar trends were observed with ERL. We conclude that, although ERL and PLB induce comparable respiratory muscle recruitment responses, they are not equivalent with respect to breathing pattern changes and effect on end-expiratory lung volume.


1984 ◽  
Vol 56 (6) ◽  
pp. 1541-1549 ◽  
Author(s):  
C. A. Smith ◽  
L. C. Jameson ◽  
G. S. Mitchell ◽  
T. I. Musch ◽  
J. A. Dempsey

We assessed the ventilatory interaction between central [central nervous system (CNS)] and peripheral chemoreceptor stimuli in five awake goats. CNS extracellular fluid (ECF) [H+] was altered with cisterna magna perfusion of mock CSF. Peripheral chemoreceptors were stimulated with three doses of NaCN given intravenously. The resulting dose-response curves were used to assess interaction of the central and peripheral stimuli. The observed interaction was hypoadditive; i.e., the average slope of the NaCN-inspired minute ventilation dose-response line was significantly greater during alkaline perfusion than during acidic perfusion. This correlation can be described by slope = -0.24 (CSF [H+]) + 30.7; r = 0.67 (P less than 0.01). Increased ventilatory responses were accompanied by increases in mean inspiratory flow, tidal volume, and breathing frequency and decreases in expiratory time in response to peripheral chemoreceptor stimulation. Unlike previous reports in anesthetized and denervated animals, in our awake intact goats the ventilatory and tidal volume responses showed no significant dependence on the level of control (pre-NaCN stimulus) inspired minute ventilation. We conclude that the level of [H+] in cerebral ECF exerts a significant reflex-mediated hypoadditive effect on the ventilatory responses to peripheral chemoreceptor stimulation.


2003 ◽  
Vol 19 (2) ◽  
pp. 109-119 ◽  
Author(s):  
Merrill Landers ◽  
Greg Barker ◽  
Scott Wallentine ◽  
J. Wesley McWhorter ◽  
Claire Peel

1979 ◽  
Vol 47 (1) ◽  
pp. 192-196 ◽  
Author(s):  
J. Askanazi ◽  
J. Milic-Emili ◽  
J. R. Broell ◽  
A. I. Hyman ◽  
J. M. Kinney

Ventilatory patterns during rest, CO2 inhalation (2, 3, and 4%) and three levels of exercise were analyzed in supine men using a canopy system for noninvasive measurements. Changes in tidal volume (VT) and breathing frequency (f) with equal increases in minute ventilation (VE) differed significantly during exercise and CO2 inhalation. Increases in VE during exercise was accompanied by increases in VT and f. During CO2 inhalation, the change in frequency was less than during exercise. However, when analyzed in terms of inspiratory flow (VT/TI) and inspiratory duty cycle (TI/Ttot), the response to both stimuli was similar. With increases to twice control VE both TI/Ttot and VT/VI increased. Thereafter only VTTI increased with increasing VE. At rest, inspiratory time on a breath by breath basis increased minimally with VT, while changes in inspiratory flow accounted for the variability in VT. These two respiratory stimulants appear to increase ventilation through different mechanisms when analyzed in terms of VT and f. However, changes in inspiratory flow and duty cycle are similar in both.


1996 ◽  
Vol 81 (2) ◽  
pp. 716-723 ◽  
Author(s):  
C. Tankersley ◽  
S. Kleeberger ◽  
B. Russ ◽  
A. Schwartz ◽  
P. Smith

Attenuated hypercapnic chemosensitivity and hypoventilation are characteristics periodically associated with human obesity. We tested the hypothesis that ventilatory control is altered by genetic determinants and age-dependent factors that influence the obese phenotype. To this end, the magnitude and pattern of breathing were examined before and associated with the development of obesity in C57BL/6J mice homozygous and heterozygous at the ob gene locus. Breathing frequency and tidal volume were measured using whole body plethysmography, and minute ventilation was assessed during acute hypoxic and hypercapnic challenges with intermittent room air exposures. In age- and weight-matched mice before pronounced obesity, significant (P < 0.05) reductions in hypercapnic ventilatory sensitivity occurred in mutant (ob/ob) mice relative to wild-type (+/+) homozygotes primarily because of an attenuated tidal volume. Longitudinal studies indicated that mutant ob mice developed rapid baseline breathing relative to the wild type, accompanying a twofold greater increase in body mass. Early differences between homozygotes in hypercapnic ventilatory sensitivity were maintained through 230 days. These data demonstrate that genetic determinants at or closely linked to the ob locus influence hypercapnic ventilation before the emergence of pronounced obesity, whereas changes in baseline breathing appear due to age-dependent increases in body weight.


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