Temperature and CO2 effect on phrenic activity and tracheal occlusion pressure

1977 ◽  
Vol 43 (3) ◽  
pp. 449-454 ◽  
Author(s):  
T. Trippenbach ◽  
J. Milic-Emili
Keyword(s):  
Body Temperature ◽  
Moving Average ◽  
Similar Increase ◽  
Occlusion Pressure ◽  
Tracheal Occlusion ◽  
Pentobarbital Sodium ◽  
Central Inspiratory Activity ◽  
Similar Index ◽  
Inspiratory Activity ◽  
Breathing Room

The present investigation was undertaken to study the interaction of CO2 and body temperature on phrenic activity (moving average) and tracheal occlusion pressure. Studies were performed on spontaneously ventilated cats anesthetized with pentobarbital sodium at different body temperatures (32–41 degrees C) while breathing room air, 2 and 4% CO2 in 50% O2. At any given chemical drive, increased body temperature caused a similar increase in rate of phrenic activity and tracheal occlusion pressure, while their peak values remained virtually unchanged. At any given body temperature, increased chemical drive caused an increase in both rate of rise and peak values of phrenic activity and tracheal occlusion pressure. These results confirm previous findings that body temperature affects the rate of rise of the central inspiratory activity (CIA), but not the inspiratory “off-switch” threshold, while CO2 increases both the rate of rise of CIA and off-switch threshold. In addition the results indicate that tracheal occlusion pressure provides a similar index of CIA as “integrated” phrenic activity.

A model for the relation between respiratory neural and mechanical outputs. III. Validation

1981 ◽  
Vol 51 (4) ◽  
pp. 990-1001 ◽  
Author(s):  
M. Younes ◽  
W. Riddle ◽  
J. Polacheck
Keyword(s):  
Respiratory System ◽  
Pressure Wave ◽  
Time Course ◽  
Present Report ◽  
Occlusion Pressure ◽  
Single Breath ◽  
Wave Forms ◽  
Inspiratory Activity ◽  
Good Agreement

In the preceding two communications we described a model for the relation between respiratory neural and mechanical outputs. In the present report we test the accuracy of the model in predicting volume and flow from occlusion pressure wave forms, and vice versa. We performed single-breath airway occlusions in 21 unconscious subjects and determined the time course of occlusion pressure. We also measured the passive properties of the respiratory system. The time course of volume and flow was predicted from the occlusion pressure wave forms, and the results were compared with the spontaneous breaths immediately preceding occlusion. Inspiratory duration, shape and amplitude of occlusion-pressure wave forms, and the passive properties of the respiratory system varied widely among subjects. There was good agreement between predicted and observed values in all cases. Except for some prolongation of inspiration (Hering-Breuer reflex), diaphragmatic activity did not change during occlusion. Since occlusion pressure is proportional to inspiratory activity, we conclude that the model described provides a good approximation of the relation between inspiratory activity and spirometric output.

Aminophylline effects on ventilatory response to hypoxia and hyperoxia in normal adults

1989 ◽  
Vol 67 (3) ◽  
pp. 1150-1156 ◽  
Author(s):  
D. Georgopoulos ◽  
S. G. Holtby ◽  
D. Berezanski ◽  
N. R. Anthonisen
Keyword(s):  
Moving Average ◽  
Minute Ventilation ◽  
Base Line ◽  
Breathing Patterns ◽  
Average Technique ◽  
Carotid Bodies ◽  
Before And After ◽  
Arterial O2 Saturation ◽  
Hyperoxic Ventilation ◽  
Breathing Room

In 10 normal young adults, ventilation was evaluated with and without pretreatment with aminophylline, an adenosine blocker, while they breathed pure O2 1) after breathing room air and 2) after 25 min of isocapnic hypoxia (arterial O2 saturation 80%). With and without aminophylline, 5 min of hyperoxia significantly increased inspiratory minute ventilation (VI) from the normoxic base line. In control experiments, with hypoxia, VI initially increased and then declined to levels that were slightly above the normoxic base line. Pretreatment with aminophylline significantly attenuated the hypoxic ventilatory decline. During transitions to pure O2 (cessation of carotid bodies' output), VI and breathing patterns were analyzed breath by breath with a moving-average technique, searching for nadirs before and after hyperoxia. On placebo days, at the end of hypoxia, hyperoxia produced nadirs that were significantly lower than those observed with room-air breathing and also significantly lower than when hyperoxia followed normoxia, averaging, respectively, 6.41 +/- 0.52, 8.07 +/- 0.32, and 8.04 +/- 0.39 (SE) l/min. This hypoxic depression was due to significant decrease in tidal volume and prolongation of expiratory time. Aminophylline partly prevented these alterations in breathing pattern; significant posthypoxic ventilatory depression was not observed. We conclude that aminophylline attenuated hypoxic central depression of ventilation, although it does not affect hyperoxic steady-state hyperventilation. Adenosine may play a modulatory role in hypoxic but not in hyperoxic ventilation.

Maturational effect of enkephalin on respiratory control in newborn rabbits

1982 ◽  
Vol 53 (5) ◽  
pp. 1063-1070 ◽  
Author(s):  
M. M. Grunstein ◽  
J. S. Grunstein
Keyword(s):  
Respiratory Control ◽  
Periodic Breathing ◽  
Opioid Peptide ◽  
Time Profile ◽  
Central Inspiratory Activity ◽  
Age Dependent ◽  
Inspiratory Activity ◽  
Afferent Influence ◽  
The Stability ◽  
Age Range

The respiratory responses to systemic infusion of the opioid peptide, [D-Ala2, D-Leu5]enkephalin (ENK) were determined in 39 unanesthetized tracheotomized rabbits (age range 1–20 days). At all ages, ventilation (VE), measured in a body plethysmograph, was depressed after ENK infusion in association with a decrease in CO2 elimination (VCO2) and body temperature. The degree of VE depression varied inversely with increasing age and was directly related to changes in mean inspiratory flow (i.e., VT/TI) while the ratio of inspiratory to total breath duration (TI/TT) was unaltered, except in rabbits under about 1 wk of age. Maturational differences in the VE response to ENK were related to age-dependent variation in the stability of the central inspiratory activity, which was manifested as periodic breathing with apnea in rabbits under about 5 days of age. Since the initial inspiratory volume-time profile was little affected by ENK and vagal afferent influence on respiration was not diminished, the depression in VE could be explained by an inhibition of the central inspiratory “off-switch” threshold and delay in central inspiratory “on-switching.” All effects of ENK were reversed by the opiate antagonist, naloxone.

Nasal and laryngeal reflex responses to negative upper airway pressure

1984 ◽  
Vol 56 (3) ◽  
pp. 746-752 ◽  
Author(s):  
E. van Lunteren ◽  
W. B. Van de Graaff ◽  
D. M. Parker ◽  
J. Mitra ◽  
M. A. Haxhiu ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Muscle Activity ◽  
Moving Average ◽  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Laryngeal Nerve ◽  
Topical Anesthesia ◽  
Inspiratory Activity ◽  
Posterior Cricoarytenoid ◽  
Upper Airway Muscles

The effects of negative pressure applied to just the upper airway on nasal and laryngeal muscle activity were studied in 14 spontaneously breathing anesthetized dogs. Moving average electromyograms were recorded from the alae nasi (AN) and posterior cricoarytenoid (PCA) muscles and compared with those of the genioglossus (GG) and diaphragm. The duration of inspiration and the length of inspiratory activity of all upper airway muscles was increased in a graded manner proportional to the amount of negative pressure applied. Phasic activation of upper airway muscles preceded inspiratory activity of the diaphragm under control conditions; upper airway negative pressure increased this amount of preactivation. Peak diaphragm activity was unchanged with negative pressure, although the rate of rise of muscle activity decreased. The average increases in peak upper airway muscle activity in response to all levels of negative pressure were 18 +/- 4% for the AN, 27 +/- 7% for the PCA, and 122 +/- 31% for the GG (P less than 0.001). Rates of rise of AN and PCA electrical activity increased at higher levels of negative pressure. Nasal negative pressure affected the AN more than the PCA, while laryngeal negative pressure had the opposite effect. The effects of nasal negative pressure could be abolished by topical anesthesia of the nasal passages, while the effects of laryngeal negative pressure could be abolished by either topical anesthesia of the larynx or section of the superior laryngeal nerve. Electrical stimulation of the superior laryngeal nerve caused depression of AN and PCA activity, and hence does not reproduce the effects of negative pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction between upper airway negative pressure pulses and CO2 on breathing pattern

1988 ◽  
Vol 65 (1) ◽  
pp. 205-209 ◽  
Author(s):  
D. L. Woodall ◽  
O. P. Mathew
Keyword(s):  
Closed System ◽  
Negative Pressure ◽  
Breathing Pattern ◽  
Upper Airway ◽  
System A ◽  
Pressure Pulses ◽  
Inspiratory Activity ◽  
Resultant Increase ◽  
Breathing Room ◽  
Spontaneously Breathing

The interaction between CO2 and negative pressure pulses on breathing pattern was investigated in 10 anesthetized, spontaneously breathing rabbits. The upper airway was functionally isolated into a closed system. A servo-respirator triggered by the inspiratory activity of the diaphragm was used to apply pressure pulses of -15 cmH2O to the isolated upper airway in early inspiration while the animal was breathing room air, 100% O2, 6% CO2 in O2, or 9% CO2 in O2. The negative pressure pulses produced a reversible inhibition of inspiration in most trials with resultant increase in inspiratory duration (TI); no change was observed in peak diaphragmatic electromyogram (Dia EMG) or expiratory duration, whereas a decrease was seen in mean inspiratory drive (peak Dia EMG/TI). This prolongation of inspiratory duration and decrease in mean inspiratory drive with negative pressure pulses persisted at higher levels of CO2; the slopes of the test breaths were not significantly different from that of control breaths. These results suggest that upper airway negative pressure pulses are equally effective in altering the breathing pattern at all levels of CO2.

Effect of Hypothermia of 2 to 24 Hours on Oxygen Consumption and Cardiac Output in the Dog

1957 ◽  
Vol 188 (3) ◽  
pp. 473-476 ◽  
Author(s):  
Bernard Fisher ◽  
Clem Russ ◽  
E. J. Fedor
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Body Temperature ◽  
The Body ◽  
Anesthetic Agent ◽  
Oxygen Utilization ◽  
Pentobarbital Sodium ◽  
Initial Decrease ◽  
Physiologic Parameters ◽  
Oxygen Difference

The changes occurring in cardiac output and oxygen consumption in short periods of hypothermia are the same when either ether or pentobarbital sodium is used as the anesthetic agent during the induction of hypothermia. Following an initial decrease in oxygen consumption, no further change occurred as long as the body temperature was maintained at a constant level. Cardiac output, arterial-venous oxygen difference, and coefficient of oxygen utilization remain unchanged for longer periods of time than most physiologic parameters studied during prolonged hypothermia at constant temperatures. After about 14 hours they also begin to alter so that by 24 hours the changes are profound. Stagnant anoxemia and marked increased in the coefficient of O2 utilization resulting from the markedly lowered cardiac output, which was 5% of the precooled controls, occurred.

Respiratory arrhythmias and airway CO2, lung receptors, and central inspiratory activity

1986 ◽  
Vol 60 (5) ◽  
pp. 1713-1721 ◽  
Author(s):  
R. L. Coon ◽  
E. J. Zuperku ◽  
J. P. Kampine
Keyword(s):  
Heart Rate ◽  
Cardiopulmonary Bypass ◽  
Breathing Frequency ◽  
Lung Inflation ◽  
Efferent Activity ◽  
Central Inspiratory Activity ◽  
Baroreceptor Stimulation ◽  
Inspiratory Activity ◽  
Lung Receptor

The purpose of this study was to determine whether hypocapnia affects heart rate secondary to an effect on pulmonary receptors. Dogs were anesthetized and placed on cardiopulmonary bypass. Interrelationships among airway CO2, central inspiratory activity, and lung receptor effects on respiratory-related heart rate changes (respiratory arrhythmias) were studied after vagal efferent activity was increased secondary to baroreceptor stimulation. Hypocapnia, isolated to the lungs, produced an increase in the magnitude of the respiratory arrhythmias observed. Two mechanisms may produce these results. Hypocapnia affects pulmonary receptors, which 1) reflexly alter heart rate and 2) modulate breathing frequency, thus altering the dynamics of the respiratory arrhythmias that were produced. The results also suggested that the reflex increase in heart rate in response to lung inflation and the Hering-Breuer expiratory-facilitatory reflex are either produced by different pulmonary receptors or by the same pulmonary receptors but may be mediated by different central mechanisms.

Phrenic nerve activity and occlusion pressure changes during CO2 rebreathing in cats

1976 ◽  
Vol 41 (4) ◽  
pp. 536-543 ◽  
Author(s):  
M. J. Evanich ◽  
M. Lopata ◽  
R. V. Lourenco
Keyword(s):  
Electrical Activity ◽  
Phrenic Nerve ◽  
Motor Nerve ◽  
Rate Of Change ◽  
Occlusion Pressure ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Co2 Rebreathing ◽  
Time Average ◽  
Breathing Room

Changes in phrenic nerve activity, quantified as a moving time average, PNG(t), were characterized during complete airway occlusion at functional residual capacity (FRC) and compared to simultaneously occurring changes in intratracheal pressure. In anesthetized cats breathing room air and during CO2 breathing, PNG(t) during occlusion was the same as that found during unobstructed breathing until it reached a value approximately corresponding to that at peak inspiration in the preceding unoccluded breath, the rate of change of PNG(t) usually remained the same but in a few cases (2 out of 11)increased. When intratracheal occlusion pressure was plotted as a function of PNG(t), both while breathing room air and during CO2 rebreathing, an approximately linear relationship was obtained. Thus, changes in intratracheasocclusion pressure obtained at FRC parallel changes in phrenic motor nerve activity. Quantification of electrical activity of respiratory nerves as a moving time average provides a means of characterizing changes in the average level of electrical activity during an inspiratory effort.

Active impedance of respiratory system in anesthetized cats

1982 ◽  
Vol 53 (1) ◽  
pp. 149-157 ◽  
Author(s):  
W. A. Zin ◽  
L. D. Pengelly ◽  
J. Milic-Emili
Keyword(s):  
Respiratory System ◽  
Pressure Wave ◽  
Flow Resistance ◽  
Time Course ◽  
Flow Volume ◽  
Occlusion Pressure ◽  
Inspiratory Activity ◽  
Measured Flow ◽  
Active Impedance ◽  
Flow Resistances

We have assessed the validity of the method of Siafakas et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 51: 10913;121, 1981) for determining active elastance (E'rs) and flow resistance (R'rs) of the respiratory system. In six cats anesthetized with pentobarbital sodium we have measured flow, volume, and tracheal occlusion pressure during spontaneous breathing. This allowed us to compute E'rs and R'rs. From these data and the occlusion pressure wave we predicted the time course of volume during inspirations with added linear flow resistances (delta R). These were compared to the actual loaded inspirograms. The agreement was generally good, except for small predictable discrepancies with the highest delta R values, which could be attributed to decompression of thoracic gas. These results indicate that the approach of Siakafas et al. to determine E'rs and R'rs is valid. In addition, we have quantified the “terminal inhibition” of inspiratory activity, which occurs toward the end of unoccluded breaths (both loaded and unloaded).

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