Influence of halothane on control of breathing in intact and decerebrated cats

1987 ◽  
Vol 63 (2) ◽  
pp. 546-553 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora ◽  
D. Zaoui
Keyword(s):  
Brain Stem ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Control Of Breathing ◽  
Halothane Anesthesia ◽  
Peripheral Chemoreceptor ◽  
Duration Relationship ◽  
The Brain ◽  
Ventilatory Response To Co2

The effects of halothane anesthesia have been investigated in intact and in decerebrated cats. Pulmonary ventilation and breathing pattern were studied during room-air breathing, hypercapnia, and O2 inhalation. The following results have been demonstrated. First, halothane anesthesia does not modify pulmonary ventilation, but a tachypnea much more intense in intact than in decerebrated cats is observed. This indicates that halothane-induced tachypnea originates mainly in structures rostral to the brain stem. Second, decerebrated animals exhibit a breathing pattern and a ventilatory response to CO2 similar to those of intact conscious cats, suggesting that forebrain facilitatory and inhibitory influences on brain stem are cancelled out by decerebration. However, the tidal volume vs. inspiratory duration relationship observed in decerebrated cats differs from that in conscious cats. Finally, during halothane anesthesia, ventilatory response to CO2 is markedly depressed. Third, during O2 inhalation, except in decerebrated, anesthetized animals, ventilation is only slightly depressed. This suggests that central stimulatory effect of O2 is enhanced and/or that peripheral chemoreceptor drive is reduced.

scholarly journals Tracheal occlusion-evoked respiratory load compensation and inhibitory neurotransmitter expression in rats

2014 ◽  
Vol 116 (8) ◽  
pp. 1006-1016 ◽  
Author(s):  
Hsiu-Wen Tsai ◽  
Paul W. Davenport
Keyword(s):  
Neural Network ◽  
Brain Stem ◽  
Breathing Pattern ◽  
Respiratory Rhythm ◽  
Inhibitory Neurotransmitter ◽  
Load Compensation ◽  
Efferent Projections ◽  
Motor Reflex ◽  
Sensory Pathway ◽  
The Brain

Respiratory load compensation is a sensory-motor reflex generated in the brain stem respiratory neural network. The nucleus of the solitary tract (NTS) is thought to be the primary structure to process the respiratory load-related afferent activity and contribute to the modification of the breathing pattern by sending efferent projections to other structures in the brain stem respiratory neural network. The sensory pathway and motor responses of respiratory load compensation have been studied extensively; however, the mechanism of neurogenesis of load compensation is still unknown. A variety of studies has shown that inhibitory interconnections among the brain stem respiratory groups play critical roles for the genesis of respiratory rhythm and pattern. The purpose of this study was to examine whether inhibitory glycinergic neurons in the NTS were activated by external and transient tracheal occlusions (ETTO) in anesthetized animals. The results showed that ETTO produced load compensation responses with increased inspiratory, expiratory, and total breath time, as well as elevated activation of inhibitory glycinergic neurons in the caudal NTS (cNTS) and intermediate NTS (iNTS). Vagotomized animals receiving transient respiratory loads did not exhibit these load compensation responses. In addition, vagotomy significantly reduced the activation of inhibitory glycinergic neurons in the cNTS and iNTS. The results suggest that these activated inhibitory glycinergic neurons in the NTS might be essential for the neurogenesis of load compensation responses in anesthetized animals.

Effect of temperature on central chemical control of ventilation in the alligator Alligator mississippiensis

1993 ◽  
Vol 179 (1) ◽  
pp. 261-272
Author(s):  
L. G. Branco ◽  
S. C. Wood
Keyword(s):  
Fourth Ventricle ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Gas Mixtures ◽  
Alligator Mississippiensis ◽  
Effect Of Temperature ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Ph Values ◽  
Arterial Ph

Central chemoreceptor function was assessed in unanesthetized alligators, Alligator mississippiensis, at body temperatures of 15, 25 and 35 degrees C. Two experiments were performed. In the first experiment, the fourth ventricle was perfused with mock cerebrospinal fluid (CSF) solutions of different pH values (7.1-7.9). Changes in pulmonary ventilation were evaluated with a pneumotachograph and arterial pH (pHa) was measured. Perfusion with low-pH solutions increased ventilation and arterial pH. Perfusion with high-pH solutions decreased ventilation and arterial pH. Mock CSF pH had a greater effect at higher temperatures. In the second experiment, the relative contributions of central and peripheral chemoreceptor drive to breathing were evaluated using hypercapnic gas mixtures to stimulate both central and peripheral chemoreceptors. Hypercapnia caused an increase in ventilation which was larger at higher temperatures. To stimulate only the peripheral chemoreceptors, the same hypercapnic gas mixtures were applied while the CSF pH of the fourth ventricle was kept constant by perfusion with a mock CSF solution. This reduced significantly the ventilatory response induced by hypercapnia. These data indicate that, regardless of the temperature, central chemoreceptors play a major role in the ventilatory regulation of the alligator. The change in pHa with temperature is compatible with the alphastat hypothesis.

An assessment of nasal functions in control of breathing

1988 ◽  
Vol 65 (4) ◽  
pp. 1520-1524 ◽  
Author(s):  
Y. Tanaka ◽  
T. Morikawa ◽  
Y. Honda
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Airway Resistance ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Control Of Breathing ◽  
Mouth Breathing ◽  
Occlusion Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Breathing pattern and steady-state CO2 ventilatory response during mouth breathing were compared with those during nose breathing in nine healthy adults. In addition, the effect of warming and humidification of the inspired air on the ventilatory response was observed during breathing through a mouthpiece. We found the following. 1) Dead space and airway resistance were significantly greater during nose than during mouth breathing. 2) The slope of CO2 ventilatory responses did not differ appreciably during the two types of breathing, but CO2 occlusion pressure response was significantly enhanced during nose breathing. 3) Inhalation of warm and humid air through a mouthpiece significantly depressed CO2 ventilation and occlusion pressure responses. These results fit our observation that end-tidal PCO2 was significantly higher during nose than during mouth breathing. It is suggested that a loss of nasal functions, such as during nasal obstruction, may result in lowering of CO2, fostering apneic spells during sleep.

Dynamics of ventilatory response to step changes in PCO2 of blood perfusing the brain stem

1989 ◽  
Vol 66 (5) ◽  
pp. 2168-2173 ◽  
Author(s):  
A. Berkenbosch ◽  
D. S. Ward ◽  
C. N. Olievier ◽  
J. DeGoede ◽  
J. VanHartevelt
Keyword(s):  
Brain Stem ◽  
Time Delays ◽  
Ventilatory Response ◽  
Roller Pump ◽  
Mean Values ◽  
Artificial Brain ◽  
Alpha Chloralose ◽  
The Brain ◽  
Single Exponential Function ◽  
Single Exponential

The technique of artificial brain stem perfusion was used to assess the ventilatory response to step changes in PCO2 of the blood perfusing the brain stem of the cat. A two-channel roller pump and a four-way valve allow switching the gas exchanger into and out of the extracorporeal circuit, which controlled the perfusion to the brain stem. Seven alpha-chloralose-urethan-anesthetized cats were studied, and 25 steps of increasing and 23 steps of decreasing PCO2 were analyzed. A model consisting of a single-exponential function with time delay best described the ventilatory response. The time delays 11.7 +/- 8.1 and 6.4 +/- 6.8 (SD) s (obtained from mean values per cat) for the step into and out of hypercapnia, respectively, were not significantly different (P = 0.10) and were of the order of the transit time of the tubing from valve to brain stem. The steady-state CO2 sensitivities obtained from the on- and off-responses were also not significantly different (P = 0.10). The time constants 87 +/- 25 and 150 +/- 51 s, respectively, were significantly different (P = 0.0002). We conclude that the central chemoreflex is adequately modeled by a single component with a different time constant for on- and off-responses.

Ventilatory response of intact cats to carbon monoxide hypoxia

1983 ◽  
Vol 55 (4) ◽  
pp. 1064-1071 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora
Keyword(s):  
Carbon Monoxide ◽  
Brain Stem ◽  
Ventilatory Response ◽  
Hypoxic Hypoxia ◽  
Small Decrease ◽  
Low Concentrations ◽  
Initial Decrease ◽  
Respiratory Centers ◽  
Ventilatory Response To Co2

Adult intact conscious or anesthetized cats have been exposed to either hypoxia or low concentrations of CO in air. In addition, the ventilatory response to CO2 was studied in air, hypoxic hypoxia, and CO hypoxia. The results show that 1) in conscious cats, low concentrations of CO (0.15%) induce a slight decrease in ventilation and higher concentrations of CO (0.20%) induce first a small decrease in ventilation and then a characteristic tachypnea similar to the hypoxic tachypnea described in carotid-denervated cats; 2) in anesthetized cats, CO hypoxia induces only mild changes in ventilation; and 3) the ventilatory response to CO2 is increased in CO hypoxia in both conscious and anesthetized animals but differs from the increase observed during hypoxia. It is concluded that the initial decrease in ventilation may be caused by some brain stem depression of the respiratory centers with CO hypoxia, whereas the tachypnea originates probably at some suprapontine level. Conversely, the possible central acidosis may account for the potentiation of the ventilatory response to CO2 observed in either conscious or anesthetized animals.

Suprapontine mechanisms in regulation of respiration

1962 ◽  
Vol 202 (2) ◽  
pp. 217-220 ◽  
Author(s):  
B. R. Fink ◽  
R. Katz ◽  
H. Reinhold ◽  
A. Schoolman
Keyword(s):  
Brain Stem ◽  
Ventilatory Response ◽  
Regulation Of Respiration ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Reticular Activating System ◽  
The Brain ◽  
Frequency Of Respiration

The ventilation and blood acid-base balance of 19 cats were studied after supracollicular ablation of the forebrain and again after intercollicular transection of the brain stem. The first ablation caused a marked increase in the frequency of respiration, apparently unmasking a caudad facilitory influence through the removal of forebrain inhibition. Hypocapnic apnea could not be induced in this preparation. After intercollicular section there was a sudden fall in frequency, the ventilatory response to CO2 was diminished and hypocapnic apnea was easily induced. It is concluded that a tonic facilitory effect on respiration originates in the rostral midbrain and adjacent diencephalon, possibly in the reticular activating system.

Luft's syndrome: O2 cost of exercise and chemical control of breathing

1975 ◽  
Vol 39 (5) ◽  
pp. 857-859 ◽  
Author(s):  
N. H. Edelman ◽  
T. V. Santiago ◽  
H. L. Conn
Keyword(s):  
Chemical Control ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Control Of Breathing ◽  
O2 Consumption ◽  
Arterial Blood ◽  
Skeletal Muscle Mitochondria ◽  
Ventilatory Response To Co2

The oxygen cost of exercise and chemical control of breathing were studied in a subject with Luft's syndrome, a disorder in which skeletal muscle mitochondria have a high “resting” O2 consumption which is imcreased only slightly by stimulation with excess phosphate acceptor, but a normal P/O ratio. The O2 consumption was more than three times normal (1.05 1/min) at rest but could be doubled when stimulated by maximal exercise. The O2 cost of exercise was similar to that of normal subjects. At rest, arterial blood PCO2 and ventilatory response to CO2 were normal, while ventilatory response to hypoxia was four times the predicted value. The data 1) confirm, in vivo, the normal respiratory efficiency of skeletal muscles in this disorder; 2) suggest that in vitro estimates of the extent to which mitochondrial respiration can be stimulated may not correlate with in vivo determinations; and 3) suggests that hypermetabolism per se can cause the ventilatory adjustments which are associated with exercise in normal subjects.

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