Effect of sleep on nocturnal bronchoconstriction and ventilatory patterns in asthmatics

1989 ◽  
Vol 67 (1) ◽  
pp. 243-249 ◽  
Author(s):  
R. D. Ballard ◽  
M. C. Saathoff ◽  
D. K. Patel ◽  
P. L. Kelly ◽  
R. J. Martin
Keyword(s):  
Airway Resistance ◽  
Minute Ventilation ◽  
The Other ◽  
Lower Airway ◽  
Sleep Laboratory ◽  
Sleep State ◽  
Asthmatic Patients ◽  
Ventilatory Responses ◽  
Rate Of Increase ◽  
Normal Controls

To assess the effect of sleep on airflow resistance and patterns of ventilation in asthmatic patients with nocturnal worsening, 10 adult subjects (6 asthmatic patients with nocturnal worsening, 4 normal controls) were monitored overnight in the sleep laboratory on two separate occasions. During 1 night, subjects were allowed to sleep normally, whereas during the other night all sleep was prevented. The six asthmatic patients demonstrated progressive increases in lower airway resistance (Rla) on both nights, but the rate of increase was twofold greater (P less than 0.0001) during the sleep night compared with the sleep prevention night. However, overnight decrements in forced expired volume in 1 s (FEV1) were similar over the 2 nights. The asthmatic patients maintained their minute ventilation as Rla increased during sleep, demonstrating a stable tidal volume with a mild increase in respiratory frequency. We conclude that in asthmatic patients with nocturnal worsening 1) Rla increases and FEV1 falls overnight regardless of sleep state, 2) sleep enhances the observed overnight increases in Rla, and 3) sleep does not abolish compensatory ventilatory responses to spontaneously occurring bronchoconstriction.

Effect of sleep and sleep deprivation on ventilatory response to bronchoconstriction

1990 ◽  
Vol 69 (2) ◽  
pp. 490-497 ◽  
Author(s):  
R. D. Ballard ◽  
W. C. Tan ◽  
P. L. Kelly ◽  
J. Pak ◽  
R. Pandey ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Airway Resistance ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Lower Airway ◽  
Occlusion Pressure ◽  
Arousal Threshold ◽  
Asthmatic Patients ◽  
Ventilatory Responses ◽  
Normal Sleep

To characterize ventilatory responses to bronchoconstriction during sleep and to assess the effect of prior sleep deprivation on ventilatory and arousal responses to bronchoconstriction, bronchoconstriction was induced in eight asthmatic subjects while they were awake, during normal sleep, and during sleep after a 36-h period of sleep deprivation. Each subject was bronchoconstricted with increasing concentrations of aerosolized methacholine while ventilatory patterns and lower airway resistance (Rla) were continually monitored. The asthmatic patients maintained their minute ventilation as Rla increased under all conditions, demonstrating a stable tidal volume with a mild increase in respiratory frequency. Inspiratory drive, as measured by occlusion pressure (P0.1), increased progressively and significantly as Rla increased under all conditions (slopes of P0.1 vs. Rla = 0.249, 0.112, and 0.154 for awake, normal sleep, and sleep after sleep deprivation, respectively, P less than 0.0006). Chemostimuli did not appear to contribute significantly to the observed increases in P0.1. Prior sleep deprivation had no effect on ventilatory and P0.1 responses to bronchoconstriction but did significantly raise the arousal threshold to induced bronchoconstriction. We conclude that ventilatory responses to bronchoconstriction, unlike extrinsic loading, are not imparied by the presence of sleep, nor are they chemically mediated. However, prior sleep deprivation does increase the subsequent arousal threshold.

Ventilatory behavior after hypoxia in C57BL/6J and A/J mice

2001 ◽  
Vol 91 (5) ◽  
pp. 1962-1970 ◽  
Author(s):  
Fang Han ◽  
Shyam Subramanian ◽  
Thomas E. Dick ◽  
Ismail A. Dreshaj ◽  
Kingman P. Strohl
Keyword(s):  
Airway Resistance ◽  
Minute Ventilation ◽  
Genetic Effect ◽  
Strain Differences ◽  
Whole Body ◽  
Environmental Forcing ◽  
Ventilatory Responses ◽  
Term Potentiation ◽  
Genetic Mechanisms ◽  
Whole Body Plethysmography

Given the environmental forcing by extremes in hypoxia-reoxygenation, there might be no genetic effect on posthypoxic short-term potentiation of ventilation. Minute ventilation (V˙e), respiratory frequency (f), tidal volume (Vt), and the airway resistance during chemical loading were assessed in unanesthetized unrestrained C57BL/6J (B6) and A/J mice using whole body plethysmography. Static pressure-volume curves were also performed. In 12 males for each strain, after 5 min of 8% O2 exposure, B6 mice had a prominent decrease inV˙e on reoxygenation with either air (−11%) or 100% O2 (−20%), due to the decline of f. In contrast, A/J animals had no ventilatory undershoot or f decline. After 5 min of 3% CO2-10% O2 exposure, B6 exhibited significant decrease in V˙e (−28.4 vs. −38.7%, air vs. 100% O2) and f (−13.8 vs. −22.3%, air vs. 100% O2) during reoxygenation with both air and 100% O2; however, A/J mice showed significant increase inV˙e (+116%) and f (+62.2%) during air reoxygenation and significant increase in V˙e (+68.2%) during 100% O2 reoxygenation. There were no strain differences in dynamic airway resistance during gas challenges or in steady-state total respiratory compliance measured postmortem. Strain differences in ventilatory responses to reoxygenation indicate that genetic mechanisms strongly influence posthypoxic ventilatory behavior.

Chemoreceptor Function and Sleep State in Apnea

PEDIATRICS ◽  
1976 ◽  
Vol 58 (1) ◽  
pp. 31-36
Author(s):  
S. Allen Fagenholz ◽  
Kathleen O'Connell ◽  
Daniel C. Shannon
Keyword(s):  
Carbon Dioxide ◽  
Rem Sleep ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Sleep State ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Responses ◽  
Prolonged Apnea ◽  
Normal Controls ◽  
Neonatal Infants

Resting ventilation and ventilatory responses to 100% oxygen and to 5% carbon dioxide in air were measured in REM and non-REM sleep in post-neonatal infants. Normal controls were compared to infants with prolonged apnea and to siblings of sudden infant death victims. No significant differences in ventilatory responses were found between the groups. We conclude that apnea may occur in infants whose central and peripheral chemoreceptor activity is normal while they are breathing.

Acute inhalation of cigarette smoke augments hypoxic chemosensitivity in humans

1985 ◽  
Vol 58 (3) ◽  
pp. 717-723 ◽  
Author(s):  
H. Yamamoto ◽  
S. Inaba ◽  
Y. Nishiura ◽  
F. Kishi ◽  
Y. Kawakami
Keyword(s):  
Cigarette Smoke ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
The Other ◽  
Minimum Level ◽  
Absolute Level ◽  
Ventilatory Responses ◽  
Normal Men ◽  
Airway Conductance ◽  
Ventilatory Response To Hypoxia

Hypoxic and hypercapnic ventilatory responses were measured after two levels of acute inhalation of cigarette smoke, minimum-level nicotine smoke (smoke 1) and nicotine-containing smoke (smoke 2), in 10 normal men. Chemosensitivity to hypoxia and hypercapnia was assessed both in terms of slope factors for ventilation-alveolar PO2 curve (A) and ventilation-alveolar PCO2 line (S) and of absolute levels of minute ventilation (VE) at hypoxia or hypercapnia. Ventilatory response to hypoxia and absolute level of VE at hypoxia significantly increased from 23.5 +/- 22.6 (SD) to 38.6 +/- 31.3 l . min-1 . Torr and from 10.6 +/- 2.5 to 12.6 +/- 3.5 l . min-1, respectively, during inhalation of cigarette smoke 2 (P less than 0.05). Inhalation of cigarette smoke 2 tended to increase the ventilatory response to hypercapnia, and the absolute level of VE at hypercapnia rose from 1.42 +/- 0.75 to 1.65 +/- 0.58 l . min-1 . Torr-1 and from 23.7 +/- 4.9 to 25.5 +/- 5.9 l . min-1, respectively, but these changes did not attain significant levels. Cigarette smoke 2 inhalation induced an increase in heart rate from 64.7 +/- 5.7 to 66.4 +/- 6.3 beats . min-1 (P less than 0.05) during room air breathing, whereas resting ventilation and specific airway conductance did not change significantly. On the other hand, acute inhalation of cigarette smoke 1 changed none of these variables. These results indicate that hypoxic chemosensitivity is augmented after cigarette smoke and that nicotine is presumed to act on peripheral chemoreceptors.

Rib cage and abdominal contributions to ventilatory response to CO2 in infants

1984 ◽  
Vol 56 (5) ◽  
pp. 1211-1216 ◽  
Author(s):  
Y. Honma ◽  
D. Wilkes ◽  
M. H. Bryan ◽  
A. C. Bryan
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Newborn Infants ◽  
Nrem Sleep ◽  
Sleep State ◽  
Co2 Response ◽  
Rib Cage ◽  
Ventilatory Responses ◽  
Significant Linear Correlation ◽  
Co2 Response Curve

We have measured the ventilatory response to inhaled CO2 of six newborn infants in rapid-eye-movement (REM) and non-REM (NREM) sleep. Ventilatory responses were measured using the Read rebreathing technique. The response was further partitioned into the volume contributions of the rib cage and abdominal compartment using the respiratory inductance plethysmograph. Sleep state was defined by electroencephalogram, electrooculogram, and behavioral criteria. In NREM sleep, there was a highly significant linear correlation between both tidal volume (VT) and instantaneous minute ventilation (VI) with CO2. Among infants, the slope of VT varied from 1.0 to 0.34 ml X Torr-1 X kg-1. However, these differences were largely due to differences in rib cage contribution, which varied from 0.56 to -0.08 ml X Torr-1 X kg-1. The abdominal contribution was similar among infants (0.41–0.56 ml X Torr-1 X kg-1). In REM, the slopes of VI were less steep than in NREM, with greater breath-to-breath variability. Slopes of VT also tended to be lower. The abdominal responses were similar to those in NREM, whereas the rib cage response was low and negative in three studies. We conclude that the slope of the CO2 response curve is primarily determined by the extent of rib cage recruitment.

Sexual influence on the control of breathing

1983 ◽  
Vol 54 (4) ◽  
pp. 874-879 ◽  
Author(s):  
D. P. White ◽  
N. J. Douglas ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Co2 Production ◽  
Menstrual Phase ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Chemical Stimuli ◽  
Low Levels ◽  
Normal Women

Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.

Effects of sleep state on ventilatory acclimatization to hypoxia in humans

1984 ◽  
Vol 57 (4) ◽  
pp. 1089-1096 ◽  
Author(s):  
A. D. Berssenbrugge ◽  
J. A. Dempsey ◽  
J. B. Skatrud
Keyword(s):  
Eye Movement ◽  
Chronic Hypoxia ◽  
Minute Ventilation ◽  
Barometric Pressure ◽  
Nrem Sleep ◽  
Hypoxic Exposure ◽  
Adult Males ◽  
Sleep State ◽  
Co2 Partial Pressure ◽  
Arterial O2 Saturation

We assessed the influence of sleep state on ventilatory acclimatization to hypoxia. Ventilation, arterial O2 saturation (SaO2), and arterial acid-base status were monitored in healthy adult males during wakefulness, nonrapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep in normoxia [barometric pressure (PB) = 740 Torr] and over 4 continuous days of hypobaric hypoxia (PB = 455 Torr). The relative hypoventilation observed during sleep compared with wakefulness in normoxia was also observed during all stages of hypoxic acclimatization. The characteristic time-dependent changes associated with acclimatization to chronic hypoxia were similar during wakefulness and all sleep states: 1) arterial CO2 partial pressure (PaCO2) decreased 27–31% by night 4 with approximately half of this fall occurring acutely (0.3–3 h hypoxia); 2) minute ventilation increased progressively with duration of hypoxic exposure including increased levels of hyperventilation throughout the initial night of sleep in hypoxia; 3) SaO2 was lowest acutely and gradually increased coincident with the progressive hyperventilation; and 4) pHa increased acutely and remained unchanged despite additional hyperventilation due to a compensatory reduction in [HCO3-]a. In addition, in the acclimatized subject hyperventilation persisted following acute restoration of normoxia, and this continued hyperventilation was similar in magnitude during both wakefulness and NREM sleep. These results indicate that suprapontine influences on ventilatory control associated with the state of wakefulness are not required in the process of ventilatory acclimatization to chronic hypoxia.

Peripheral chemoreceptor function in children with the congenital central hypoventilation syndrome

1993 ◽  
Vol 74 (1) ◽  
pp. 379-387 ◽  
Author(s):  
D. Gozal ◽  
C. L. Marcus ◽  
D. Shoseyov ◽  
T. G. Keens
Keyword(s):  
Vital Capacity ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Clinical Manifestations ◽  
Congenital Central Hypoventilation Syndrome ◽  
Tidal Breathing ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Responses ◽  
Central Hypoventilation ◽  
Hypoventilation Syndrome

In children with the congenital central hypoventilation syndrome (CCHS), some patients require mechanical ventilation during sleep, whereas others need respiratory assistance even when awake. The cause of this disparity is unclear. We hypothesized that differences in peripheral chemoreceptor response (PCR) could provide an explanatory mechanism for this disparity in clinical manifestations. PCR was measured in five children with CCHS and five sex- and age-matched controls by measuring the ventilatory responses induced by 100% O2 breathing, five tidal breaths of 100% N2, and vital capacity breaths of 5% and 15% CO2 in O2 and 5% CO2–95% N2. Tidal breathing of 100% O2 resulted in similar ventilatory responses in CCHS patients and controls with various changes dependent on the method of analysis of response used. Acute hypoxia by N2 tidal breathing resulted in a 39.2 +/- 22% increase in respiratory rate in CCHS patients and a 15.1 +/- 11.1% increase in controls (P < 0.05), with similar increases in minute ventilation (VE) of 124 +/- 69% and 85 +/- 11%, respectively. Vital capacity breaths of each of the CO2-containing gas mixtures induced similar increases in VE in CCHS patients and controls. The changes in VE obtained with 15% CO2–85% O2 and with 5% CO2–95% N2 were significantly greater than those with 5% CO2–95% O2, suggesting a dose-dependent response as well as additive effects of hypercapnic and hypoxic stimuli. We conclude that the PCR, when assessed by acute hypoxia, hyperoxia, or hypercapnia, is present and intact in CCHS children who are able to sustain adequate ventilation during wakefulness.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory responses of hamsters and rats to hypoxia and hypercapnia

1985 ◽  
Vol 59 (6) ◽  
pp. 1955-1960 ◽  
Author(s):  
B. R. Walker ◽  
E. M. Adams ◽  
N. F. Voelkel
Keyword(s):  
Duty Cycle ◽  
Minute Ventilation ◽  
Natural Habitat ◽  
Blood Gases ◽  
Atmospheric Conditions ◽  
Arterial Blood Gases ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Rat Experiments ◽  
Fossorial Species

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).

Ventilatory responses to CO2 and lung inflation in tonic versus phasic REM sleep

1979 ◽  
Vol 47 (6) ◽  
pp. 1304-1310 ◽  
Author(s):  
C. E. Sullivan ◽  
E. Murphy ◽  
L. F. Kozar ◽  
E. A. Phillipson
Keyword(s):  
Eye Movements ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Minute Volume ◽  
Sleep State ◽  
Lung Inflation ◽  
Ventilatory Responses ◽  
Sustained Inflation ◽  
Per Se ◽  
Phasic Rem Sleep

Ventilatory responses to CO2 and to lung inflation were compared in four dogs during tonic and phasic segments of rapid-eye-movement (REM) sleep. Phasic REM sleep (P-REM) was identified by the presence of bursts of rapid eye movements, visible muscle twitchings, and frequent phasic discharges in the nuchal electromyogram. These features were absent during tonic REM sleep (T-REM). During P-REM the response of minute volume of ventilation (VI) to progressive hypercapnia (0.58 +/- 0.19 (l/min)/Torr, mean +/- SE) was significantly less than in slow-wave sleep (SWS) (1.40 +/- 0.14; P less than 0.05). In contrast, during T-REM the response (1.48 +/- 0.19) was similar to that in SWS. Similarly, during P-REM the duration of apnea (5.9 +/- 1.5 s) elicited by sustained inflation of the lungs with 1.0 liter of air, was significantly shorter than in SWS (25.8 +/- 0.8); in contrast, during T-REM the duration of apnea (17.8 +/- 3.6) was similar to that in SWS. The results indicate that previously described decreases in VI responses to CO2 and apneic responses to lung inflation during P-REM, compared to SWS, are related to the phasic phenomena of REM sleep, rather than to the REM sleep state per se.

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