Control of ventilation in running birds: effects of hypoxia, hyperoxia, and CO2

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.

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.


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.


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.


1991 ◽  
Vol 70 (3) ◽  
pp. 1271-1276 ◽  
Author(s):  
T. D. Sweeney ◽  
D. E. Leith ◽  
J. D. Brain

Does the restraint required for head or nose-only exposure of rodents to inhaled aerosols or gases alter their breathing pattern? And does prior exercise training, which may increase muscle strength, affect this response to restraint? To answer those questions, we measured breathing pattern in 11 adult male hamsters while they were either 1) free to move in small cages or 2) closely restrained in head-out cones. The measurements were repeated after hamsters spent 6 wk either sedentary in standard cages or in cages with exercise wheels. Hamsters were placed in a plethysmograph to measure respiratory frequency (f) and tidal volume (VT). Their product is minute volume (V). When restrained, f and V were 1.9 and 1.7 times, respectively, greater than when hamsters were free, but VT did not change. After 6 wk, the sedentary group responded differently to restraint; f increased 3-fold, VT decreased by one-half, and V increased 1.6-fold. Exercised hamsters increased f 2.3-fold and decreased VT by one-third; V increased by 1.5-fold. In inhalation studies, changes in breathing pattern would significantly influence the amount of material inhaled, the fraction retained, and thus the amount and distribution of material deposited in the lungs.


PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P < .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P > .1), but the intercept was shifted to the right (P < .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P < .05). In addition, transcutaneous Po2 increased during administration of CPAP (P < .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.


1975 ◽  
Vol 38 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
L. J. Folinsbee ◽  
F. Silverman ◽  
R. J. Shephard

We have tested the response of 28 subjects to a three-stage ergometer test, with loads adjusted to 45, 60, and 75% of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W. sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure VE, respiratory frequency (fR), mixed expired PO2 and PCO2, and electrocardiogram were monitored continuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (r = 0.98) and was accompanied by a decrease in tidal volume (r = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.


1975 ◽  
Vol 39 (3) ◽  
pp. 417-422 ◽  
Author(s):  
S. M. Lewis

Steady-state ventilatory responses to CO2 in trained awake baboons were studied to determine the response to a venous CO2 load. CO2 was loaded either directly into the venous blood through an arteriovenous shunt or by addition to the inhaled air. The two modes of loading were adjusted to produce the same increase in minute volume. Minute volume, tidal volume respiratory frequency, end-tidal PCO2, PaCO2, and pHa were measured. PaCO2 and PETCO2 increased the same amount during the two modes of CO2 loading; thus, the response to changes in arterial PCO2, deltaVE/deltaPaCO2, was the same. I conclude that the ventilatory response to venous CO2 loading occurs only through the change in mean arterial PCO2 and thus it is unlikely that there are any important venous CO2 receptors.


1996 ◽  
Vol 91 (3) ◽  
pp. 337-345 ◽  
Author(s):  
Ken D. O'halloran ◽  
Aidan K. Curran ◽  
Aidan Bradford

1. Ventilation was measured during normoxia, hypoxia and hypercapnia before and after administration of almitrine in conscious, unrestrained, tracheostomized rats with the superior laryngeal nerves intact or cut. In superior laryngeal nerve-intact animals breathing air, almitrine increased minute ventilation due to an increase in respiratory frequency with no change in tidal volume. In superior laryngeal nerve-sectioned animals, the minute ventilatory response to almitrine was reduced due to a reduced tidal volume component of the response. Almitrine increased the ventilatory response to hypercapnia in superior laryngeal nerve-intact but not in sectioned animals. 2. In anaesthetized, vagotomized rats breathing spontaneously through a low-cervical tracheostomy, diaphragm and geniohyoid electromyographic activities were recorded. Arterial blood pressure and rectal temperature were continuously monitored. A single dose of almitrine was administered intravenously. In all animals, the geniohyoid muscle had phasic inspiratory activity which slightly preceded diaphragm activity. Almitrine had no effect on respiratory frequency or inspiratory and expiratory duration but increased mean peak integrated diaphragm (+29.3 ±13.6%) and geniohyoid (+ 132.0 ±21.3%) muscle activity. 3. These results show that almitrine exerts part of its ventilatory effects through superior laryngeal nerve afferents. Almitrine preferentially excites upper airway compared with diaphragm muscle activity, suggesting a potential role in the alleviation of obstructive apnoea.


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