Brain hypoxia and control of breathing: neuromechanical control

1980 ◽  
Vol 49 (3) ◽  
pp. 497-505 ◽  
Author(s):  
R. W. Chapman ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Neural Function ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Lung Inflation ◽  
Brain Hypoxia ◽  
Load Compensation ◽  
Airway Occlusion ◽  
Airway Occlusion Pressure ◽  
Unanesthetized Animals ◽  
And Control

The effects of graded brain hypoxia on respiratory cycle timing, the lung inflation reflex, and respiratory compensation for an inspiratory flow-resistive load were studied in unanesthetized goats. Two models, inhalation and CO and acute reduction of brain blood flow (BBF) were used to produce comparable levels of brain hypoxia. The lung inflation reflex was assessed as the ratio of inspiratory time of an occluded breath to that of the preceding spontaneous breath (TIoccl/TIspont). Compensation for flow-resistive loading was assessed as the effect of the load upon the airway occlusion pressure response to rebreathing CO2 (delta P 0.1/delta PCO2). Major findings were 1) severe brain hypoxia (HbCO of 60% or BBF of 42%) caused tachypnea due to a 50% or more reduction of expiratory time but only a 20% or less reduction of inspiratory time; 2) moderate carboxyhemoglobinemia (HbCO of 25-30%) enhanced TIoccl/TIspont from 1.5 +/- 0.1 at control to 2.1 +/- 0.1, while severe brain hypoxia (HbCO of 60% and BBF of 42%) reduced the ratio to 1.0 +/- 0.2; and 3) compensation for a flow-resistive load, manifested by increases of delta P 0.1/delta PCO2 of 75-300% in the control state, was abolished at HbCO of 45-50% and BBF of 60%. The data suggest that in unanesthetized animals brain hypoxia elicits tachypnea largely by an effect on the expiratory phase of the bulbopontine timing mechanism. The observed enhancement of the lung inflation reflex and abolition of flow-resistive load compensation are best explained by hypoxic depression of higher than brain stem neural function.

Brain hypoxia and control of breathing: role of the vagi

1982 ◽  
Vol 53 (1) ◽  
pp. 212-217 ◽  
Author(s):  
R. W. Chapman ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Ventilatory Response ◽  
Control Of Breathing ◽  
Inspiratory Time ◽  
Small Magnitude ◽  
Lung Inflation ◽  
Brain Hypoxia ◽  
And Control ◽  
Respiratory Responses ◽  
Spontaneous Breath

Vagally mediated reflexes play an important role in the generation of respiratory responses to various stimuli. This study examined the role of vagally mediated mechanisms in the generation of the respiratory responses to progressive brain hypoxia secondary to carboxyhemoglobinemia (HbCO 013;55%) in six unanesthetized goats. Ventilation, respiratory cycle timing, and the lung inflation reflex were measured before and during CO inhalation in intact and bilaterally vagotomized animals. Our results indicate that vagal reflexes contribute a small magnitude of the hyperpnea caused by carboxyhemoglobinemia. Furthermore, in contrast to that reported for CO2 inhalation, the tachypneic nature of the ventilatory response to CO is not a vagally mediated phenomenon. CO inhalation had a biphasic influence on the strength of the lung inflation reflex measured as the ratio of inspiratory time during occlusion (TIoccl) to inspiratory time of the preceding spontaneous breath (TIspont). At HbCO levels of 35%, TIoccl/TIspont was enhanced, whereas at HbCO levels of 55% of ratio fell to unity, indicating abolition of the reflex. After vagotomy, this ratio was unity at all levels of carboxyhemoglobinemia.

Expiratory load compensation is associated with electroencephalographic premotor potentials in humans

2015 ◽  
Vol 118 (8) ◽  
pp. 1023-1030 ◽  
Author(s):  
Elise Morawiec ◽  
Mathieu Raux ◽  
Felix Kindler ◽  
Louis Laviolette ◽  
Thomas Similowski
Keyword(s):  
Physiological Response ◽  
Supplementary Motor Area ◽  
Resistive Load ◽  
Elastic Recoil ◽  
Ensemble Averaging ◽  
Quiet Breathing ◽  
Load Compensation ◽  
Normal Humans ◽  
Respiratory Discomfort ◽  
And Control

In normal humans during quiet breathing, expiration is mostly driven by elastic recoil of the lungs. Expiration becomes active when ventilation must be increased to meet augmented metabolic demands, or in response to expiratory loading, be it experimental or disease-related. The response to expiratory loading is considered to be mediated by both reflex and cortical mechanisms, but the latter phenomenon have not been neurophysiologically characterized. We recorded the EEG in 20 healthy volunteers (9 men, 11 women, age: 22 to 50 yr) during unloaded breathing, voluntary expirations, and in response to 50 cmH2O·l−1·s expiratory resistive load (ERL), 20 cmH2O expiratory threshold load (high ETL), and 10 cmH2O expiratory threshold load (low ETL). EEGs were processed by ensemble averaging expiratory time-locked segments and examined for pre-expiratory potentials, defined as a slow negative shift from the baseline signal preceding expiration, and suggestive of cortical preparation of expiration involving the supplementary motor area. Four subjects were excluded because of technical EEG problems. Pre-expiratory potentials were present in one subject at baseline and in all subjects during voluntary expirations. They were present in eight subjects during low ETL, in 15 subjects during high ETL, and in 13 subjets during ERL (control vs. low ETL, P = 0.008; control vs. high ETL, P < 0.001; and control vs. ERL, P < 0.001). Respiratory discomfort was more intense in the presence of pre-expiratory potentials ( P < 0.001). These results provide a neurophysiological substrate to a cortical component of the physiological response to experimental expiratory loads in humans.

Attenuated Hering-Breuer inflation reflex 4 years after pulmonary vagal denervation in ponies

1990 ◽  
Vol 69 (6) ◽  
pp. 2163-2167 ◽  
Author(s):  
H. V. Forster ◽  
L. G. Pan ◽  
C. Flynn ◽  
G. E. Bisgard
Keyword(s):  
Control System ◽  
Surgical Procedure ◽  
Treadmill Exercise ◽  
Inspiratory Effort ◽  
Cycle Duration ◽  
Breathing Frequency ◽  
Inspiratory Time ◽  
Ventilatory Control ◽  
Lung Inflation ◽  
Airway Occlusion

The purpose of this study was to determine whether there was any recovery of the Hering-Breuer inflation reflex in ponies between 2-4 wk and 3-4 yr after hilar nerve denervation (HND). Under anesthesia and before HND, airway occlusion after a 3-liter lung inflation lengthened the subsequent occluded breath by nearly 10 times the control breath duration. Between 2 wk and 3-4 yr after HND, this maneuver increased the duration of the occluded breath by only 2.5 times the control breath duration. Also under anesthesia, the airway was occluded at end expiration. This maneuver increased the duration of the subsequent inspiratory effort by 71% in hilar nerve intact ponies but by only 20-25% 2-4 wk and 3-4 yr after HND. For both tests, the pre- and post-HND differences were statistically significant (P less than 0.05), but there were no significant differences (P greater than 0.10) between 2-4 wk and 3-4 yr post-HND. In awake ponies, at rest and during mild and moderate treadmill exercise, breathing frequency was generally lower and inspiratory time was greater after relative to before HND. The inspiratory time-to-total cycle duration ratio was consistently increased by 0.10-0.15 after HND (P less than 0.05). There was no significant change in this ratio between 2-4 wk and 3-4 yr post-HND (P greater than 0.10). We conclude that the surgical procedure for HND used in this study does not permit any significant reinnervation, and there are no significant changes within the ventilatory control system to compensate for loss of hilar nerve afferents.

Effect of pentobarbital sodium on respiratory control in newborn rabbits

1977 ◽  
Vol 42 (6) ◽  
pp. 845-851 ◽  
Author(s):  
M. S. Goldberg ◽  
J. Milic-Emili
Keyword(s):  
Respiratory Mechanics ◽  
Respiratory Control ◽  
Reflex Modulation ◽  
Gas Mixture ◽  
Occlusion Pressure ◽  
Inspiratory Time ◽  
Airway Occlusion ◽  
Inspiratory Muscles ◽  
Airway Occlusion Pressure ◽  
Vagal Reflex

Using the airway occlusion pressure technique, control of breathing was studied in unanesthetized and anesthetized newborn rabbits breathing various gas mixtures under steady-state conditions. Independent of the gas mixture breathed, barbiturate anesthesia resulted in a reduction of ventilation. This was not due to a change in inspiratory drive since for each gas mixture breathed the pressure generated by the inspiratory muscles 0.3 s after the onset of the occluded inspiration (P0.3) remained virtually unchanged, nor could this be attributed to changes in respiratory mechanics as indicated by the fact that the relation between P0.3 and V0.3 (the volume generated 0.3 s after onset of the immediately preceding unoccluded inspiration) did not change. On the other hand, during anesthesia inspiratory time was slightly shortened as a result of a change in both central (bulbopontine) and peripheral (volume-related vagal reflex) modulation, while expiratory duration was markedly prolonged. This disproportionate increase in expiratory duration with respect to inspiratory duration was responsible for most of the depression of ventilation found in the newborn rabbits during barbiturate anesthesia.

Preterm infants: ventilation and P100 changes with CO2 and inspiratory resistive loading

1985 ◽  
Vol 58 (6) ◽  
pp. 1982-1987 ◽  
Author(s):  
S. Duara ◽  
S. Abbasi ◽  
T. H. Shaffer ◽  
W. W. Fox
Keyword(s):  
Minute Ventilation ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Co2 Response ◽  
Airway Occlusion ◽  
Time Ratio ◽  
Mouth Pressure ◽  
Resistive Loading ◽  
Ventilatory Effects ◽  
The Right

The ventilatory effects of inspiratory flow-resistive loading and increased chemical drive were measured in ten neonates during progressive hypercapnia in control and loaded states. Hypercapnia (mean increase PCO2 = 15–20) resulted from inspiring 8% CO2 in room air and inspiratory loading by a flow-resistive load = 100 cmH2O X l-1) X s. Hypercapnia produced an increase in group minute ventilation secondary to increasing tidal volumes and breathing frequencies. Loading shifted the minute ventilation-CO2 response to the right, and slopes decreased significantly (P less than 0.05) consequent to a significant decrease in the frequency-CO2 slopes (P less than 0.05), which became negative in four of the ten subjects. Mouth pressure measured at 100 ms after onset of inspiratory effort (P100) occlusion pressure-CO2 slopes measured in five subjects showed no significant increase with load application. Resistive loading produced significant increases in inspiratory time (P less than 0.02) and the inspiratory time/total breath time ratio (P less than 0.01). Airway occlusion elicited the Hering-Breuer reflex, with a significant increase in inspiratory time-to-total breath time ratio (P less than 0.01). The results show that the inspiratory resistive load produced ventilatory compromise in newborns and insufficient compensatory augmentation of central drive.

Influence of prior ventilatory experience on the estimation of breathlessness during exercise

1990 ◽  
Vol 78 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones
Keyword(s):  
Exercise Test ◽  
Prior Experience ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Borg Scale ◽  
Exercise Tests ◽  
Loaded Breathing ◽  
Inspiratory Load

1. The intensity of breathlessness was measured during exercise in nine normal subjects using a modified Borg scale to examine the effect of prior experience of breathlessness on subsequent estimates of breathlessness. 2. Each subject performed four exercise tests, each of which consisted of two identical runs of workload incrementation (run 1 and run 2). An inspiratory resistive load of 3.8 cmH2O s−1 l−1 was applied during the appropriate run of the exercise test to examine the effect of (a) prior experience of ‘loaded’ breathing on breathlessness estimation during ‘unloaded’ breathing, and (b) prior experience of ‘unloaded’ breathing on breathlessness estimation during ‘loaded’ breathing. Run 1 was the conditioning run; run 2 was the run in which the effect of conditioning was measured. 3. There was a good correlation between breathlessness and minute ventilation during both unloaded’ breathing (median r = 0.93) and ‘loaded’ breathing (median r = 0.95). 4. The slope of the Borg score/minute ventilation relationship was greater during ‘loaded’ breathing than during ‘unloaded’ breathing (P < 0.01). There was no difference in mean Borg score between ‘unloaded’ and ‘loaded’ breathing. 5. After a period of ‘loaded’ breathing during run 1, estimated breathlessness was significantly reduced during ensuing ‘unloaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which ‘unloaded’ breathing was experienced throughout both run 1 and run 2. 6. After a period of ‘unloaded’ breathing in run 1, estimated breathlessness was significantly increased during ensuing ‘loaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which the inspiratory load had already been experienced in run 1. 7. Changes in the pattern of breathing (inspiratory time, expiratory time, total breath duration, inspiration time/total breath duration ratio and tidal volume) were not consistent with the changes in breathlessness. 8. We suggest that perception of breathlessness may be influenced by a subject's immediate prior experience of an altered relationship between breathlessness and ventilation.

Role of N-methyl-D-aspartate receptors in the pontine pneumotaxic mechanism in the cat

1994 ◽  
Vol 76 (3) ◽  
pp. 1138-1143 ◽  
Author(s):  
L. Ling ◽  
D. R. Karius ◽  
D. F. Speck
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Partial Recovery ◽  
Inspiratory Time ◽  
Systemic Injection ◽  
Lung Inflation ◽  
Mk 801 ◽  
Efferent Limb ◽  
Adult Cats

Systemic injection of MK-801, an N-methyl-D-aspartate (NMDA) receptor-associated channel blocker, induces an apneusis in vagotomized cats similar to that produced by pontine respiratory group (PRG) lesions, suggesting the possible involvement of NMDA receptors in the pontine pneumotaxic mechanism. Previous results from our laboratory indicate that the efferent limb of the pontine pneumotaxic mechanism is unlikely to require NMDA receptor-mediated neurotransmission. Therefore, the present study examined the potential involvement of PRG NMDA receptors in the pontine pneumotaxic mechanism. Experiments were conducted in decerebrate, paralyzed, and ventilated adult cats. The effects on inspiratory time (TI) of MK-801 microinjection into PRG were tested in 12 cats. Pressure microinjection of MK-801 (15 mM, 80–3,000 nl) significantly prolonged TI in all animals when lung inflation was withheld. TI progressively increased in most animals for > or = 30 min. After this period, partial recovery of the effect occurred in eight cats as TI shortened toward predrug levels. In three animals, microinjection of MK-801 induced a complete apneusis in the absence of lung inflation from which there was no detectable recovery. Microinjections into regions approximately 2 mm distant from PRG produced little or no effect. These results provide evidence that NMDA receptors located in the region of PRG play an important functional role in the control of the breathing cycle.

Apnea of Prematurity: II. Respiratory Reflexes

PEDIATRICS ◽  
1984 ◽  
Vol 74 (1) ◽  
pp. 63-66
Author(s):  
Tilo Gerhardt ◽  
Eduardo Bancalari
Keyword(s):  
Preterm Infants ◽  
Inspiratory Effort ◽  
Control Group ◽  
Load Compensation ◽  
Airway Occlusion ◽  
Functional Immaturity ◽  
Occlusion Technique ◽  
Apnea Of Prematurity ◽  
Respiratory Reflexes

Airway obstruction is a cause of apnea in preterm infants. The activity of protective respiratory reflexes was determined in 18 preterm infants with apnea (mean of 32 episodes of more than 20 seconds duration per day) and in 18 neonates without apnea used as control subjects. This was done in order to elucidate the role of respiratory reflexes in apnea of prematurity. The infants were matched for birth weight (1,068 g v 1,065 g), gestational age (30.2 weeks v 30.2 weeks), and postnatal age (8.6 days v 8.3 days). The airway occlusion technique was used to determine the inspiratory prolongation of the occluded breath and the effective elastance of the respiratory system. Inspiratory prolongation is a measure for the reflex influence on inspiratory duration, and effective elastance reflects load compensating ability. Inspiratory prolongation was 7.3% ± 33.5% in infants with apnea and 30.6% ± 22.7% in the control group (P &lt; .025). Effective elastance was 1.1 ± 0.5 cm H2O/mL in the apneic group and 1.5 ± 0.5 cm H2O/mL in the infants without apnea (P &lt; .025). The results indicate that during exposure to respiratory loads, the infants with apnea maintained inspiratory effort poorly and had a decreased ability for load compensation. Their respiratory reflexes were significantly more immature than the reflex activity of the infants without apnea. This functional immaturity of respiratory reflexes may be a contributing factor in the etiology of apnea of prematurity.

scholarly journals Airway Occlusion Pressure Revisited

2020 ◽  
Vol 201 (9) ◽  
pp. 1027-1028
Author(s):  
Catherine S. Sassoon ◽  
Magdy Younes
Keyword(s):  
Occlusion Pressure ◽  
Airway Occlusion ◽  
Airway Occlusion Pressure
Sign in / Sign up

Export Citation Format

Share Document