Vagal control of respiratory pattern during hyperpnea in domestic fowl

1984 ◽  
Vol 56 (6) ◽  
pp. 1650-1654 ◽  
Author(s):  
M. Gleeson ◽  
J. H. Brackenbury

Minute volume, tidal volume, and respiratory frequency were measured during hyperpnea induced by exercise, increased body temperature, and CO2 inhalation. Ventilatory characteristics were compared before and after the vagus nerve had been blocked. In normal birds exercise produced increases in both tidal volume and respiratory frequency; hyperthermia produced a typical thermal polypnea consisting of greatly increased respiratory frequency and reduced tidal volume; CO2 inhalation produced increases in tidal volume and respiratory frequency when the birds were euthermic but a slowing of respiratory rate when the birds were hyperthermic. After vagal block these pronounced differences in the pattern of ventilatory response to the various respiratory stimuli were abolished. Instead there was a uniform ventilatory response to all three stimuli consisting mainly of increases in tidal volume combined with small increases in respiratory frequency. It is concluded that in the normal animal control of the varied pattern of ventilatory response to different respiratory stimuli is dependent on vagal fiber activity.

1982 ◽  
Vol 53 (6) ◽  
pp. 1397-1404 ◽  
Author(s):  
J. H. Brackenbury ◽  
M. Gleeson ◽  
P. Avery

Minute volume (V), tidal volume (VT), respiratory frequency (f), venous lactate, and clavicular air sac gas composition were measured in domestic fowl at rest and during exercise, breathing hypoxic, hyperoxic, or hypercapnic gas. Hyperoxia produced no significant change in ventilation, CO2 inhalation produced increases in V and VT, but the changes in f appeared to be related to the stage of exercise at which CO2 was administered. The sensitivity of the hypercapnic response was similar in resting and exercising birds. Compared with the effects of CO2, hypoxia elicited only a weak ventilatory response in rest and exercise conditions despite severe tissue anaerobiosis.


1960 ◽  
Vol 15 (5) ◽  
pp. 907-910 ◽  
Author(s):  
Fred W. Zechman ◽  
Neil S. Cherniack ◽  
Alvin S. Hyde

Two series of experiments dealing with the effect of forward acceleration on respiration in man were performed. In both series of studies the trunk was inclined 12 degrees in the direction of acceleration and a rate of onset of 1 g/sec. was used. In the first series, the effect of 5, 8 and 12 g on respiratory frequency, tidal volume, minute volume and nitrogen elimination was determined. Frequency increased, reaching an average of 39.2 cpm and tidal volumes decreased to an average of 318 cc at 12 g. The volume of nitrogen eliminated during a 30-second period, breathing O2 at 12 g, was essentially unchanged, suggesting that alveolar ventilation did not decrease. In the second series, O2 consumptions were measured before, during and after accelerations of 5, 8, 10, and 12 g. O2 consumptions increased with acceleration and it is presumed that the extra work of breathing may be an important contributing factor. Submitted on March 2, 1960


1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.


2020 ◽  
Vol 57 (1) ◽  
pp. 64-68
Author(s):  
Verônica Lourenço WITTMER ◽  
Rozy Tozetti LIMA ◽  
Michele Coutinho MAIA ◽  
Halina DUARTE ◽  
Flávia Marini PARO

ABSTRACT BACKGROUND: Liver cirrhosis is a highly prevalent disease that, at an advanced stage, usually causes ascites and associated respiratory changes. However, there are few studies evaluating and quantifying the impact of ascites and its relief through paracentesis on lung function and symptoms such as fatigue and dyspnea in cirrhotic patients. OBJECTIVE: To assess and quantify the impact of acute reduction of ascitic volume on respiratory parameters, fatigue and dyspnea symptoms in patients with hepatic cirrhosis, as well as to investigate possible correlations between these parameters. METHODS: Thirty patients with hepatic cirrhosis and ascites who underwent the following pre and post paracentesis evaluations: vital signs, respiratory pattern, thoracoabdominal mobility (cirtometry), pulmonary function (ventilometry), degree of dyspnea (numerical scale) and fatigue level (visual analog scale). RESULTS: There was a higher prevalence of patients classified as CHILD B and the mean MELD score was 14.73±5.75. The comparison of pre and post paracentesis parameters evidenced after paracentesis: increase of predominantly abdominal breathing pattern, improvement of ventilatory variables, increase of the differences obtained in axillary and abdominal cirtometry, reduction of dyspnea and fatigue level, blood pressure reduction and increased peripheral oxygen saturation. Positive correlations found: xiphoid with axillary cirtometry, degree of dyspnea with fatigue level, tidal volume with minute volume, Child “C” with higher MELD score, volume drained in paracentesis with higher MELD score and with Child “C”. We also observed a negative correlation between tidal volume and respiratory rate. CONCLUSION: Since ascites drainage in patients with liver cirrhosis improves pulmonary volumes and thoracic expansion as well as reduces symptoms such as fatigue and dyspnea, we can conclude that ascites have a negative respiratory and symptomatological impact in these patients.


1980 ◽  
Vol 87 (1) ◽  
pp. 229-236
Author(s):  
G. Benchetrit ◽  
P. Dejours

1. Ventilation was recorded by pneumotachography, before and after bilateral vagotomy, in conscious tortoises (Testudo horsfieldi) (breathing 0, 2, 3 or 4% CO2 in air or oxygen). 2. Each breath consists of expiratory and inspiratory phases and an apneic plateau (absence of air flow). Inhalation of hypercapnic mixtures led to increased ventilatory flow, augmentation of tidal volume, and an increase in respiratory frequency through the shortening of the apneic plateau. 3. Intact tortoises breathing hypercapnic-hyperoxic mixtures hyperventilated less than with hypercapnic-normoxic mixtures. 4. In bivagotomized animals, the respiratory frequency decreased, the expiratory and inspiratory durations lengthened, and the apneic plateau was prolonged. The tidal volume was increased, but ventilation, nevertheless, decreased slightly. 5. Bivagotomized animals breathing hypercapnic-normoxic or hypercapnic-hyperoxic mixtures hyperventilated, but less than intact animals under the same conditions. 6. It is concluded that in tortoises there are: (1) peripheral chemoreceptors which are innervated by branches of the vagus nerves, and are sensitive to CO2; and (2) an extrathoracic, probably central, ventilatory CO2 drive.


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.


1976 ◽  
Vol 41 (5) ◽  
pp. 612-622 ◽  
Author(s):  
W. M. St John ◽  
S. C. Wang

Ventilatory regulation by pontile pneumotaxic and apneustic centers and by rostral medullary sites was evaluated in intercollicular decerebrate cats. Following pneumotaxic center ablation, PAco2 was significantly elevated.Moreover, in response to hypercapina or hypoxia, frequency responses were significantly diminished whereas tidal volume responses were unchanged or elevated. Interruption of apneustic center function by caudal pontile transection or radiofrequency lesions in the caudal pons and/or rostral medulla resulted in significant decreases of tidal volume responses and significant elevations of frequency responses to both hypercapnia and hypoxia. Neither minute volume responses nor the PAco2 level was altered. It is concluded that the apneustic center exercises a primary role in the brainstem definitionof tidal volume responses for both peripheral and central chemoreceptor afferent stimuli. The apneustic center is also considered to exert an impoetant function in the definition of respiratory frequency. A medially placed pathway in the rostral medulla is proposed to interconnect the apneustic center with the medullary respiratory nuclei.


1991 ◽  
Vol 71 (4) ◽  
pp. 1254-1260 ◽  
Author(s):  
L. Daristotle ◽  
M. J. Engwall ◽  
W. Z. Niu ◽  
G. E. Bisgard

We utilized selective carotid body (CB) perfusion while changing inspired O2 fraction in arterial isocapnia to characterize the non-CB chemoreceptor ventilatory response to changes in arterial PO2 (PaO2) in awake goats and to define the effect of varying levels of CB PO2 on this response. Systemic hyperoxia (PaO2 greater than 400 Torr) significantly increased inspired ventilation (VI) and tidal volume (VT) in goats during CB normoxia, and systemic hypoxia (PaO2 = 29 Torr) significantly increased VI and respiratory frequency in these goats. CB hypoxia (CB PO2 = 34 Torr) in systemic normoxia significantly increased VI, VT, and VT/TI; the ventilatory effects of CB hypoxia were not significantly altered by varying systemic PaO2. We conclude that ventilation is stimulated by systemic hypoxia and hyperoxia in CB normoxia and that this ventilatory response to changes in systemic O2 affects the CB O2 response in an additive manner.


1980 ◽  
Vol 48 (5) ◽  
pp. 794-798 ◽  
Author(s):  
T. C. Lloyd ◽  
J. A. Cooper

Using anesthetized spontaneously breathing dogs, we compared the respiratory effects of tracheal distension with the effects of changes in lung volume before and after vagotomy. We used an endotracheal tube with a long cuff to distend the trachea to pressures of 10, 20, and 40 cmH2O. Lung volume increases were imposed by expiratory threshold loading, and volume was decreased by abdominal compression, both of which caused outward rib cage displacement. During expiratory loading, the tidal volume was unchanged but respiratory frequency and minute volume fell and an active expiratory effort appeared; whereas frequency and minute volume rose, but tidal volume fell during abdominal compression. Tracheal distension evoked no discernible change in breathing. Following vagotomy, tidal volume and minute volume fell, and frequency rose slightly, during expiratory loading but abdominal compression was without effect. After vagotomy, 40 cmH2O tracheal distension caused a slight frequency increase. We concluded that the potential role of tracheal deformation in the reflex control of breathing is insignificant in comparison with the other airways.


1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.


Sign in / Sign up

Export Citation Format

Share Document