Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats

1980 ◽  
Vol 49 (5) ◽  
pp. 769-777 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora
Keyword(s):  
Control Systems ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Monoamine Metabolism ◽  
Moderate Hypoxia ◽  
Significant Depression ◽  
Brain Monoamine ◽  
Conscious Animals ◽  
Ventilatory Response To Hypoxia ◽  
Stimulation Of

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.

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.

Hypoxic ventilatory decline: site of action

1995 ◽  
Vol 79 (2) ◽  
pp. 373-374 ◽  
Author(s):  
P. A. Robbins
Keyword(s):  
Ventilatory Response ◽  
Good Evidence ◽  
Striking Similarity ◽  
Moderate Hypoxia ◽  
Ventilatory Responses ◽  
Site Of Action ◽  
Working Out ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Hypoxia ◽  
Awake Animal

Although superficially similar, HVD appears to arise from different mechanisms in the awake animal as compared with the anesthetized animal. Consequently, the good evidence supporting a central site of action for hypoxia in the genesis of HVD in the anesthetized animal cannot be used as evidence for a central site of action for hypoxia in the awake animal. In their paper on HVD in the awake cat, Long et al. (10) conclude: “The striking similarity between feline and human ventilatory responses to moderate hypoxia illustrated by this and previous experiments leads us to believe that it is likely similar mechanisms apply to both species. Thus it seems probable that working out the mechanisms of the ventilatory response to hypoxia in the awake cat will go a long way toward solving the same problems in humans.” This activity should not neglect a consideration of whether adaptation at the carotid body during sustained hypoxia may be involved in the genesis of HVD in the awake state.

Estimation of response slopes in respiratory control

1984 ◽  
Vol 56 (2) ◽  
pp. 536-539 ◽  
Author(s):  
D. L. Sherrill ◽  
G. D. Swanson
Keyword(s):  
Statistical Approach ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Major Axis ◽  
Bivariate Normal Distribution ◽  
Directional Statistics ◽  
Control Behavior ◽  
Slope Estimate ◽  
Partial Pressure Of Co2 ◽  
Reduced Major Axis

The ventilatory response to changes in alveolar (arterial) CO2 is widely used as an index of respiratory control behavior. Methods for estimating these response slopes should incorporate the possibility that there may be errors in both the independent (partial pressure of CO2) and dependent (ventilation) variables. In a recent paper Daubenspeck and Ogden (J. Appl. Physiol. Respirat. Environ. Exercise Physiol. 45:823–829, 1978) have suggested problems inherent in the traditional technique of reduced major axis and have suggested a more contemporary technique of directional statistics. We have previously analyzed both techniques and developed a method to overcome the problems of reduced major axis and problems inherent in the use of directional statistics. Under the assumption of a bivariate normal distribution, we demonstrate that our slope estimate is similar to the maximum likelihood estimate proposed by Mardia et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 54: 309–313, 1983) for this problem. In addition, we demonstrate a bootstrap statistical approach when the distributions are not normally distributed. These concepts are illustrated using O2-CO2 interaction data.

Effects of pentylenetetrazol and trimethadione on feline brain monoamine metabolism

1978 ◽  
Vol 27 (14) ◽  
pp. 1815-1820 ◽  
Author(s):  
Brian A. McMillen ◽  
Lawrence Isaac
Keyword(s):  
Monoamine Metabolism ◽  
Brain Monoamine

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.

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