Diphasic ventilatory response to hypoxia in newborn lambs

The ventilatory response of newborn lambs to hypoxemia was evaluated in two groups of seven awake lambs studied at 2 and 7 days of life. Minute ventilation (VE) and airway occlusion pressure (P0.1) were monitored as the animals were exposed in sequence to room air, 12% O2 (15 min), 7% O2 (15 min), and room air. On 12 and 7% O2, 2-day-old lambs experienced a brisk hyperventilation followed by a VE depression, previously described in newborns of other species (diphasic response). The 7-day-old lambs had a clear diphasic VE response only on 7% O2 breathing. In the 2-day-old lambs, at the time of the relative VE depression to 12% O2, the respiratory centers showed a persisting responsiveness to further hypoxia; switching to 7% O2 caused a brisk increase in VE and P0.1 of 70 and 130%, respectively, which was followed again by a VE depression. The magnitude of the immediate VE response to hypoxia, taken as an index of the chemoreceptor strength, was inversely related to the magnitude of the VE depression (R = 0.81, P less than 0.001). It was concluded that 1) lambs as well as other neonates have an age-related diphasic VE response to hypoxia; 2) at the time of the VE depression, the respiratory centers maintain their responsiveness to further acute hypoxia; and 3) the weakness of the chemoreceptors in the newborn is a major determinant of the diphasic response.

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

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.1.18 ◽

1985 ◽

Vol 59 (1) ◽

pp. 18-23 ◽

Cited By ~ 14

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.

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Ventilatory response to hypoxia in unanesthetized newborn kittens

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.6.2544 ◽

1988 ◽

Vol 64 (6) ◽

pp. 2544-2551 ◽

Cited By ~ 15

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.

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Airway Occlusion Pressure and Breathing Pattern as Predictors of Weaning Outcome

American Review of Respiratory Disease ◽

10.1164/ajrccm/148.4_pt_1.860 ◽

1993 ◽

Vol 148 (4_pt_1) ◽

pp. 860-866 ◽

Cited By ~ 94

Author(s):

Catherine S. H. Sassoon ◽

C. Kees Mahutte

Keyword(s):

Breathing Pattern ◽

Occlusion Pressure ◽

Airway Occlusion ◽

Airway Occlusion Pressure ◽

Weaning Outcome

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

Journal of Applied Physiology ◽

10.1152/jappl.2001.90.5.1729 ◽

2001 ◽

Vol 90 (5) ◽

pp. 1729-1735 ◽

Cited By ~ 28

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.

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Airway Occlusion Pressure Revisited

American Journal of Respiratory and Critical Care Medicine ◽

10.1164/rccm.202003-0585ed ◽

2020 ◽

Vol 201 (9) ◽

pp. 1027-1028

Author(s):

Catherine S. Sassoon ◽

Magdy Younes

Keyword(s):

Occlusion Pressure ◽

Airway Occlusion ◽

Airway Occlusion Pressure

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Effect of hypoxia on the pressure developed by inspiratory muscles during airway occlusion

Journal of Applied Physiology ◽

10.1152/jappl.1976.40.3.372 ◽

1976 ◽

Vol 40 (3) ◽

pp. 372-378 ◽

Cited By ~ 16

Author(s):

S. G. Kelsen ◽

M. D. Altose ◽

N. N. Stanley ◽

R. S. Levinson ◽

N. S. Cherniack ◽

...

Keyword(s):

Pressure Response ◽

Occlusion Pressure ◽

Airway Occlusion ◽

Single Breath ◽

Inspiratory Muscles ◽

Resistive Loading ◽

Expired Gas ◽

Motoneuron Activity ◽

Maximal Pressure ◽

Ventilatory Response To Hypoxia

The effect of progressive isocapnic hypoxia on the pressure generated by the inspiratory muscle during airway occlusion was studied in 10 awake subjects during normal and obstructed breathing. Isocapnic hypoxia was produced by rebreathing a gas mixture of 6% CO2 in air while the expired gas was passed through a CO2 scrubber so as to maintain PACO2 constant (42.6 mmHg +/- 2.2 SE). Occlusion of the airway was performed randomly for a single breath at FRC. In all 10 subjects maximal pressure (Ppeak) and the pressures measured 100, 200, 300, and 400 ms after the onset of inspiration increased during hypoxia. Furthermore, good correlation was noted between the occlusion pressure response to hypoxia (delta P/DELTA[1/PO2-32]) and simultaneous changes in ventilatory response to hypoxia (delta VI/DELTA[1/PO2-32]). The occlusion pressure response to hypoxia therefore seems to be a reliable measure of respiratory center output. When rebreathing was repeated during inspiratory resistive loading, the occlusion pressure at any given PO2 and delta P/DELTA(1PO2-32) measured in the first 400 ms of inspiration increased in 9 of 10 subjects. Since PACO2 and PAO2 during both control and loaded experiments were the same, the increase in occlusion pressure in the presence of flow-resistive loading appeared to represent a neurally mediated increase in inspiratory motoneuron activity.

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Prediction of Successful Ventilator Weaning Using Airway Occlusion Pressure and Hypercapnic Challenge

CHEST Journal ◽

10.1378/chest.91.4.496 ◽

1987 ◽

Vol 91 (4) ◽

pp. 496-499 ◽

Cited By ~ 72

Author(s):

A. Bruce Montgomery ◽

Rolf H.O. Holle ◽

Sara R. Neagley ◽

David J. Pierson ◽

Robert B. Schoene

Keyword(s):

Ventilator Weaning ◽

Occlusion Pressure ◽

Airway Occlusion ◽

Airway Occlusion Pressure

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Calcium/calmodulin-dependent kinase II mediates critical components of the hypoxic ventilatory response within the nucleus of the solitary tract in adult rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00249.2005 ◽

2005 ◽

Vol 289 (3) ◽

pp. R871-R876 ◽

Cited By ~ 4

Author(s):

Stephen R. Reeves ◽

Edwin S. Carter ◽

Shang Z. Guo ◽

David Gozal

Keyword(s):

Ventilatory Response ◽

Minute Ventilation ◽

Acute Hypoxia ◽

Respiratory Frequency ◽

Whole Body ◽

Solitary Tract ◽

Hypoxic Ventilatory Response ◽

Adult Rats ◽

Osmotic Pumps ◽

Calcium Calmodulin Dependent

Calcium/calmodulin-dependent kinase II (CaMKII) is an ubiquitous second messenger that is highly expressed in neurons, where it has been implicated in some of the pathways regulating neuronal discharge as well as N-methyl-d-aspartate receptor-mediated synaptic plasticity. The full expression of the mammalian hypoxic ventilatory response (HVR) requires intact central relays within the nucleus of the solitary tract (NTS), and neural transmission of hypoxic afferent input is mediated by glutamatergic receptor activity, primarily through N-methyl-d-aspartate receptors. To examine the functional role of CaMKII in HVR, KN-93, a highly selective antagonist of CaMKII, was microinjected in the NTS via bilaterally placed osmotic pumps in freely behaving adult male Sprague-Dawley rats for 3 days. Vehicle-loaded osmotic pumps were surgically placed in control animals, and adequate placement of cannulas was ascertained for all animals. HVR was measured using whole body plethysmography during exposure to 10% O2-balance N2 for 20 min. Compared with control rats, KN-93 administration elicited marked attenuations of peak HVR (pHVR) but did not modify normoxic minute ventilation. Differences in pHVR were primarily attributable to diminished respiratory frequency recruitments during pHVR without significant differences in tidal volume. These findings indicate that CaMKII activation in the NTS mediates respiratory frequency components of the ventilatory response to acute hypoxia; however, CaMKII activity does not appear to underlie components of normoxic ventilation.

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