Ventilatory response of the cat to hypoxia in sleep and wakefulness

2003 ◽  
Vol 95 (2) ◽  
pp. 545-554 ◽  
Author(s):  
Andrew T. Lovering ◽  
Witali L. Dunin-Barkowski ◽  
Edward H. Vidruk ◽  
John M. Orem
Keyword(s):  
Tidal Volume ◽  
Central Pattern Generator ◽  
Eye Movement ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Pattern Generator ◽  
Rapid Eye Movement Sleep ◽  
Inspiratory Activity ◽  
Adult Cat ◽  
Ventilatory Response To Hypoxia

This study characterized ventilation, the airflow waveform, and diaphragmatic activity in response to hypoxia in the intact adult cat during sleep and wakefulness. Exposure to hypoxia for up to 3 h caused sustained hyperventilation during both wakefulness and sleep. Hyperventilation resulted from significant increases in minute ventilation due to increases in both tidal volume and frequency. Diaphragmatic activity changed significantly from augmenting activity with little postinspiratory-inspiratory activity (PIIA) in normoxia to augmenting activity with increased PIIA in hypoxia. The increase in PIIA was least in rapid eye movement sleep. These changes in diaphragmatic activity were associated with changes in airflow waveforms in inspiration and expiration. We conclude that the ventilatory response to hypoxia involves a change in the output of the central pattern generator and that the change is dependent in part on the state of consciousness.

Ventilatory response to hypoxia in unanesthetized newborn kittens

1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Sleep ◽  
Newborn Kitten ◽  
Peripheral Mechanism ◽  
Flow Through ◽  
Ventilatory Response To Hypoxia

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.

Respiration of conscious kittens in acute hypoxia and effect of almitrine bismesylate

1985 ◽  
Vol 59 (1) ◽  
pp. 18-23 ◽  
Author(s):  
H. B. McCooke ◽  
M. A. Hanson
Keyword(s):  
Ambient Temperature ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Second Phase ◽  
Biphasic Response ◽  
Almitrine Bismesylate ◽  
Peak Increase ◽  
Ventilatory Response To Hypoxia

Respiration was measured noninvasively in conscious kittens at an ambient temperature of 28–32 degrees C. Inspired O2 fraction (FIO2) was reduced abruptly from 0.21 to 0.12, 0.10, or 0.08 for 5 min on the day of birth and then on days 4, 7, 14, and 28. The ventilatory response to hypoxia was biphasic, as reported previously in anesthetized kittens, with minute ventilation (VE) increasing in the first minute and then falling towards control over the next 4 min. The fall in VE was due to a consistent fall in tidal volume, the changes in frequency during the second phase being more variable. The size of the first phase of the response increased up to 14 days, but the time at which the peak increase in VE occurred was not correlated with age. The degree of the secondary fall in VE was similar at each age and at each FIO2 studied. The degree of the biphasic response was significantly reduced after administration of almitrine (2 mg/kg ip) on days 1 and 4, but almitrine did not affect the response in older kittens.

scholarly journals Ventilatory responses to specific CNS hypoxia in sleeping dogs

2000 ◽  
Vol 88 (5) ◽  
pp. 1840-1852 ◽  
Author(s):  
Aidan K. Curran ◽  
Joshua R. Rodman ◽  
Peter R. Eastwood ◽  
Kathleen S. Henderson ◽  
Jerome A. Dempsey ◽  
...  
Keyword(s):  
Eye Movement ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Whole Body ◽  
Hypoxic Exposure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Cardiorespiratory Control ◽  
Ventilatory Responses

Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and extracorporeal perfusion of the carotid body to assess the effects of systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial [Formula: see text] = 52, 45, and 38 Torr) in the presence of a normocapnic, normoxic, and normohydric carotid body during non-rapid eye movement sleep. A lack of ventilatory response to systemic boluses of sodium cyanide during carotid body perfusion demonstrated isolation of the perfused carotid body and lack of other significant peripheral chemosensitivity. Four additional dogs were carotid body denervated and exposed to whole body hypoxia for comparison. In the sleeping dog with an intact and perfused carotid body exposed to specific CNS hypoxia, we found the following. 1) CNS hypoxia for 5–25 min resulted in modest but significant hyperventilation and hypocapnia (minute ventilation increased 29 ± 7% at arterial [Formula: see text] = 38 Torr); carotid body-denervated dogs showed no ventilatory response to hypoxia. 2) The hyperventilation was caused by increased breathing frequency. 3) The hyperventilatory response developed rapidly (<30 s). 4) Most dogs maintained hyperventilation for up to 25 min of hypoxic exposure. 5) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS hypoxia, in the presence of an intact carotid body maintained normoxic and normocapnic, does not depress and usually stimulates breathing during non-rapid eye movement sleep. The rapidity of the response suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.

Development of the ventilatory response to hypoxia in Swiss CD-1 mice

2000 ◽  
Vol 88 (5) ◽  
pp. 1907-1914 ◽  
Author(s):  
Dean M. Robinson ◽  
Henry Kwok ◽  
Brandon M. Adams ◽  
Karen C. Peebles ◽  
Gregory D. Funk
Keyword(s):  
Tidal Volume ◽  
Body Mass ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Developmental Changes ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
Expiratory Time ◽  
Ventilatory Response To Hypoxia

We examined developmental changes in breathing pattern and the ventilatory response to hypoxia (7.4% O2) in unanesthetized Swiss CD-1 mice ranging in age from postnatal day 0 to 42(P0–P42) using head-out plethysmography. The breathing pattern of P0 mice was unstable. Apneas were frequent at P0 (occupying 29 ± 6% of total time) but rare by P3 (5 ± 2% of total time). Tidal volume increased in proportion to body mass (∼10–13 ml/kg), but increases in respiratory frequency (f) (55 ± 7, 130 ± 13, and 207 ± 20 cycles/min for P0, P3, and P42, respectively) were responsible for developmental increases in minute ventilation (690 ± 90, 1,530 ± 250, and 2,170 ± 430 ml ⋅ min− 1 ⋅ kg− 1for P0, P3, and P42, respectively). Between P0 and P3, increases in f were mediated by reductions in apnea and inspiratory and expiratory times; beyond P3, increases were due to reductions in expiratory time. Mice of all ages showed a biphasic hypoxic ventilatory response, which differed in two respects from the response typical of most mammals. First, the initial hyperpnea, which was greatest in mature animals, decreased developmentally from a maximum, relative to control, of 2.58 ± 0.29 in P0 mice to 1.32 ± 0.09 in P42mice. Second, whereas ventilation typically falls to or below control in most neonatal mammals, ventilation remained elevated relative to control throughout the hypoxic exposure in P0 (1.73 ± 0.31), P3 (1.64 ± 0.29), and P9 (1.34 ± 0.17) mice but not in P19 or P42 mice.

Breathing during sleep with mild hypoxia

1989 ◽  
Vol 67 (3) ◽  
pp. 1198-1207 ◽  
Author(s):  
K. Chin ◽  
M. Ohi ◽  
M. Hirai ◽  
T. Kuriyama ◽  
Y. Sagawa ◽  
...  
Keyword(s):  
Eye Movement ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Rapid Eye Movement Sleep ◽  
Considerable Influence ◽  
Hypoxic Ventilatory Response ◽  
Venturi Mask ◽  
Mild Hypoxia

To investigate ventilatory response to mild hypoxia during non-rapid-eye-movement sleep, we administered approximately 16% O2 (which corresponds to concentrations found in commercial high altitude air craft) to 12 normal subjects by using a Venturi mask, which did not alter the breathing pattern during this study. Under mild hypoxia, inspiratory minute ventilation during sleep showed an initial rapid increase (P less than 0.001) but then declined significantly (P less than 0.001) and stabilized. Stable levels differed among individuals and, compared with those measured before hypoxia, were significantly lower in some subjects, higher in one, and essentially unchanged in the others. The initial rapid increase in minute ventilation after mild hypoxia during sleep correlated with the respective values of hypoxic ventilatory response during the awake state (P less than 0.01), but the final lowered levels did not. We conclude that the ventilatory response after mild hypoxia during sleep is biphasic and hypoxic depression exerts considerable influence on ventilation under mild hypoxia during sleep. So we should take hypoxic depression into consideration to evaluate the response to hypoxia during sleep.

Response to Acute Hypercapnia in the Parents of Victims of Sudden Infant Death Syndrome

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 652-655
Author(s):  
Jonathan M. Couriel ◽  
Anthony Olinsky
Keyword(s):  
Tidal Volume ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Cycle Time ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Sudden Infant Death ◽  
Respiratory Cycle ◽  
Sudden Infant ◽  
Inspiratory Time

The ventilatory response to acute hypercapnia was studied in 68 parents of victims of sudden infant death syndrome and 56 control subjects. Tidal volume, inspiratory time, and total respiratory cycle time were measured before and immediately after a vital capacity breath of 13% CO2 in oxygen. Instantaneous minute ventilation, mean inspiratory flow (tidal volume/inspiratory time), and respiratory timing (inspiratory time/total respiratory cycle time) were calculated. Both groups of subjects showed a marked increase in tidal volume (48.4% ± 26.5%), instantaneous minute ventilation (56% ± 35%), and tidal volume/inspiratory time (56.8% ± 33.5%) after inhalation of the test gas, with little change in inspiratory time/total respiratory cycle time. There were no significant differences between the two groups for ventilation before or after inhalation of the test gas. The ventilatory response to acute hypercapnia is mediated by the peripheral chemoreceptors. These results suggest that an inherited abnormality of peripheral chemoreceptor function is unlikely to be a factor leading to sudden infant death syndrome.

Stress-induced attenuation of the hypercapnic ventilatory response in awake rats

2001 ◽  
Vol 90 (5) ◽  
pp. 1729-1735 ◽  
Author(s):  
Richard Kinkead ◽  
Lydie Dupenloup ◽  
Nadine Valois ◽  
Roumiana Gulemetova
Keyword(s):  
Control System ◽  
Immobilization Stress ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Whole Body ◽  
Respiratory Homeostasis ◽  
Whole Body Plethysmography ◽  
Ventilatory Response To Hypoxia ◽  
Awake Rats

To test the hypothesis that stress alters the performance of the respiratory control system, we compared the acute (20 min) responses to moderate hypoxia and hypercapnia of rats previously subjected to immobilization stress (90 min/day) with responses of control animals. Ventilatory measurements were performed on awake rats using whole body plethysmography. Under baseline conditions, there were no differences in minute ventilation between stressed and unstressed groups. Rats previously exposed to immobilization stress had a 45% lower ventilatory response to hypercapnia (inspiratory CO2 fraction = 0.05) than controls. In contrast, stress exposure had no statistically significant effect on the ventilatory response to hypoxia (inspiratory O2 fraction = 0.12). Stress-induced attenuation of the hypercapnic response was associated with reduced tidal volume and inspiratory flow increases; the frequency and timing components of the response were not different between groups. We conclude that previous exposure to a stressful condition that does not constitute a direct challenge to respiratory homeostasis can elicit persistent (≥24 h) functional plasticity in the ventilatory control system.

Respiratory and cardiovascular responses to increased and decreased carotid sinus pressure in sleeping dogs

1995 ◽  
Vol 78 (5) ◽  
pp. 1688-1698 ◽  
Author(s):  
K. W. Saupe ◽  
C. A. Smith ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Eye Movement ◽  
Carotid Sinus ◽  
Minute Ventilation ◽  
Control Level ◽  
Cardiovascular Responses ◽  
Systemic Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

The purpose of this study was to determine the effects of changing blood pressure in the carotid sinus (Pcs) on ventilatory output during wakefulness and non-rapid-eye-movement sleep in unanesthetized dogs. Eight dogs were chronically instrumented so that ventilation, heart rate, and blood pressure could be measured while pressure in the isolated carotid sinus was rapidly changed by means of an extracorporeal perfusion circuit. Raising Pcs 35–75 mmHg consistently reduced ventilation 15–40% in a dose-response fashion, with little or no further diminution in minute ventilation as Pcs was further increased > 75 mmHg above control level. This decrease in minute ventilation was immediate, due primarily to a decrease in tidal volume, and was sustained over the 20-s period of elevated Pcs. Increases in Pcs also caused immediate sustained reductions in systemic blood pressure and heart rate, both of which also fell in a dose-dependent fashion. The ventilatory and systemic cardiovascular responses to increased Pcs were the same during wakefulness and non-rapid-eye-movement sleep. Decreasing Pcs 40–80 mmHg caused a sudden carotid chemoreceptor-mediated hyperpnea that was eliminated by hyperoxia. We conclude that increasing Pcs causes a reflex inhibition of ventilation and that this reflex may play a role in sleep-disordered breathing.

Ventilation during early and late rapid-eye-movement sleep in normal humans

1991 ◽  
Vol 71 (4) ◽  
pp. 1201-1215 ◽  
Author(s):  
J. B. Neilly ◽  
E. A. Gaipa ◽  
G. Maislin ◽  
A. I. Pack
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Respiratory Frequency ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Rib Cage ◽  
Ventilatory Parameters ◽  
Normal Humans

Because successive rapid-eye-movement (REM) sleep periods in the night are longer in duration and have more phasic events, ventilation during late REM sleep might be more affected than in earlier episodes. Despite the increase in eye movement density (EMD) in late REM sleep, average minute ventilation was, however, not reduced compared with that in early REM sleep. Decreases in rib cage motion (mean inspiratory flow of the rib cage) in association with increasing EMD were offset by increments in respiratory frequency. Apart from expiratory time, there were no significant changes in the slopes of the relationships between EMD and specific ventilatory components, from early to late REM sleep periods. However, there was an increase in the number of episodes when ventilation was reduced during late REM sleep. Changes in ventilatory pattern during late REM sleep are due to changes in the underlying nature of REM sleep. The ventilatory response during eye movements is, however, subject specific. Some subjects exhibit large decrements in mean inspiratory flow of the rib cage and increments in respiratory frequency during bursts of eye movement, whereas other individuals demonstrate only small changes in these ventilatory parameters.

Metabolic rate and breathing during sleep

1985 ◽  
Vol 59 (2) ◽  
pp. 384-391 ◽  
Author(s):  
D. P. White ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Metabolic Rate ◽  
Eye Movement ◽  
Sleep Stage ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Normal Subjects ◽  
Co2 Production ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

Recent investigation suggests that both ventilation (VE) and the chemical sensitivity of the respiratory control system correlate closely with measures of metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)]. However, these associations have not been carefully investigated during sleep, and what little information is available suggests a deterioration of the relationships. As a result we measured VE, ventilatory pattern, VO2, and VCO2 during sleep in 21 normal subjects (11 males and 10 females) between the ages of 21 and 77 yr. When compared with values for awake subjects, expired ventilation decreased 8.2 +/- 2.3% (SE) during sleep and was associated with a 8.5 +/- 1.6% decrement in VO2 and a 12.3 +/- 1.7% reduction in VCO2, all P less than 0.01. The decrease in ventilation was a product primarily of a significant decrease in tidal volume with little change in frequency. None of these findings were dependent on sleep stage with results in rapid-eye-movement (REM) and non-rapid-eye-movement sleep being similar. Through all sleep stages ventilation remained tightly correlated with VO2 and VCO2 both within a given individual and between subjects. Although respiratory rhythmicity was somewhat variable during REM sleep, minute ventilation continued to correlate with VO2 and VCO2. None of the parameters described above were influenced by age or gender, with male and female subjects demonstrating similar findings. Ten of the subjects demonstrated at least occasional apneas. These individuals, however, were not found to differ from those without apnea in any other measure of ventilation or metabolic rate.

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