Maturation of steady-state CO2 sensitivity in vagotomized anesthetized lambs

1992 ◽  
Vol 72 (4) ◽  
pp. 1255-1260 ◽  
Author(s):  
A. H. Jansen ◽  
S. Ioffe ◽  
V. Chernick
Keyword(s):  
Steady State ◽  
Test Procedure ◽  
Nerve Section ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Co2 Sensitivity ◽  
Carotid Bodies ◽  
Before And After ◽  
End Tidal ◽  
Respiratory Sensitivity

The maturation of the respiratory sensitivity to CO2 was studied in three groups of anesthetized (ketamine, acepromazine) lambs 2–3, 14–16, and 21–22 days old. The lambs were tracheostomized, vagotomized, paralyzed, and ventilated with 100% O2. Phrenic nerve activity served as the measure of respiration. The lambs were hyperventilated to apneic threshold, and end-tidal PCO2 was raised in 0.5% steps for 5–7 min each to a maximum 7–8% and then decreased in similar steps to apneic threshold. The sinus nerves were cut, and the CO2 test procedure was repeated. Phrenic activity during the last 2 min of every step change was analyzed. The CO2 sensitivity before and after sinus nerve section was determined as change in percent minute phrenic output per Torr change in arterial PCO2 from apneic threshold. Mean apneic thresholds (arterial PCO2) were not significantly different among the groups: 34.8 +/- 2.08, 32.7 +/- 2.08, and 34.7 +/- 2.25 (SE) Torr for 2- to 3-, 14- to 16-, and 21- to 22-day-old lambs, respectively. After sinus denervation, apneic thresholds were raised in all groups [39.9 +/- 2.08, 40.9 +/- 2.08, and 45.3 +/- 2.25 (SE) Torr, respectively] but were not different from each other. CO2 response slopes did not change with age before or after sinus nerve section. We conclude that carotid bodies contribute to the CO2 response during hyperoxia by affecting the apneic threshold but do not affect the steady-state CO2 sensitivity and the central chemoreceptors are functionally mature shortly after birth.

End-tidal CO2 response to low levels of inspired CO2 in awake beagle dogs

1980 ◽  
Vol 48 (6) ◽  
pp. 1077-1082 ◽  
Author(s):  
P. Reischl ◽  
D. M. Stavert ◽  
S. M. Lewis ◽  
L. C. Murdock ◽  
B. J. O'Loughlin
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Resolving Power ◽  
Beagle Dogs ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Control Of Ventilation ◽  
Low Levels ◽  
End Tidal ◽  
End Tidal Co2

The steady-state end-tidal CO2 tension (PCO2) was examined during control and 1% CO2 inhalation periods in awake beagle dogs with an intact airway breathing through a low dead-space respiratory mask. A total of eight experiments were performed in four dogs, comprising 31 control observations and 23 CO2 inhalation observations. The 1% inhaled CO2 produced a significant increase in the steady-state end-tidal PCO2 comparable to the expected 1 Torr predicted from conventional CO2 control of ventilation. We conclude that 1% inhaled CO2 results in a hypercapnia. Any protocol that is to resolve the question of whether mechanisms are acting during low levels of inhaled CO2 such that ventilation increases without any change in arterial PCO2 must have sufficient resolving power to discriminate changes in gas tension in magnitude predicted from conventional (i.e., arterial PCO2) control of ventilation.

Validation of a maskless CO2-response test for sleep and infant studies

1988 ◽  
Vol 64 (1) ◽  
pp. 391-396 ◽  
Author(s):  
K. H. Naifeh ◽  
J. W. Severinghaus
Keyword(s):  
Steady State ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Response Test ◽  
Response Slope ◽  
Fractional Increase ◽  
The Subject ◽  
End Tidal ◽  
Co2 Electrode ◽  
Co2 Excretion

The Hazinski method is an indirect, noninvasive, and maskless CO2-response test useful in infants or during sleep. It measures the classic CO2-response slope (i.e., delta VI/delta PCO2) divided by resting ventilation Sr = (VI''--VI')/(VI'.delta PCO2) between low (')- and high ('')-inspired CO2 as the fractional increase of alveolar ventilation per Torr rise of PCO2. In steady states when CO2 excretion (VCO2') = VCO2'', Hazinski CO2-response slope (Sr) may be computed from the alveolar exchange equation as Sr = (PACO2'--PICO2')/(PACO2'--PICO2'') where PICO2 is inspired PCO2. To avoid use of a mask or mouthpiece, the subject breathes from a hood in which CO2 is mixed with inspired air and a transcutaneous CO2 electrode is used to estimate alveolar PCO2 (PACO2). To test the validity of this method, we compared the slopes measured simultaneously by the Hazinski and standard steady-state methods using a pneumotachograph, mask, and end-tidal, arterial, and four transcutaneous PCO2 samples in 15-min steady-state challenges at PICO2 23.5 +/- 4.5 and 37 +/- 4.1 Torr. Sr was computed using PACO2 and arterial PCO2 (PaCO2) as well as with the four skin PCO2 (PSCO2) values. After correction for apparatus dead space, the standard method was normalized to resting VI = 1, and its CO2 slope was designated directly measured normalized CO2 slope (Sx), permitting error to be calculated as Sr/Sx.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acute hyperbaric oxygenation on respiratory control in cats

1989 ◽  
Vol 67 (6) ◽  
pp. 2351-2356 ◽  
Author(s):  
D. Torbati ◽  
A. Mokashi ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Hyperbaric Oxygenation ◽  
Respiratory Control ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
End Tidal ◽  
Arterial Po2 ◽  
Hypercapnic Response

We studied ventilatory responsiveness to hypoxia and hypercapnia in anesthetized cats before and after exposure to 5 atmospheres absolute O2 for 90-135 min. The acute hyperbaric oxygenation (HBO) was terminated at the onset of slow labored breathing. Tracheal airflow, inspiratory (TI) and expiratory (TE) times, inspiratory tidal volume (VT), end-tidal PO2 and PCO2, and arterial blood pressure were recorded simultaneously before and after HBO. Steady-state ventilation (VI at three arterial PO2 (PaO2) levels of approximately 99, 67, and 47 Torr at a maintained arterial PCO2 (PaCO2, 28 Torr) was measured for the hypoxic response. Ventilation at three steady-state PaCO2 levels of approximately 27, 36, and 46 Torr during hyperoxia (PaO2 450 Torr) gave a hypercapnic response. Both chemical stimuli significantly stimulated VT, breathing frequency, and VI before and after HBO. VT, TI, and TE at a given stimulus were significantly greater after HBO without a significant change in VT/TI. The breathing pattern, however, was abnormal after HBO, often showing inspiratory apneusis. Bilateral vagotomy diminished apneusis and further prolonged TI and TE and increased VT. Thus a part of the respiratory effects of HBO is due to pulmonary mechanoreflex changes.

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1885-1892 ◽  
Author(s):  
C. Shindoh ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
And Control

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.

Ventilatory control during experimental maldistribution of VA/Q in the dog

1982 ◽  
Vol 52 (1) ◽  
pp. 245-253 ◽  
Author(s):  
C. E. Juratsch ◽  
B. J. Whipp ◽  
D. J. Huntsman ◽  
M. M. Laks ◽  
K. Wasserman
Keyword(s):  
Steady State ◽  
Early Phase ◽  
Main Pulmonary Artery ◽  
State Regulation ◽  
Balloon Inflation ◽  
Peripheral Chemoreceptors ◽  
Arterial Pco2 ◽  
Bilateral Carotid ◽  
End Tidal ◽  
Transient Elevation

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5–2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5–2.0 min) of acute maldistribution of VA/Q.

CO2 sensitivity of cat phrenic neurogram during hypoxic respiratory depression

1988 ◽  
Vol 65 (2) ◽  
pp. 736-743 ◽  
Author(s):  
J. E. Melton ◽  
J. A. Neubauer ◽  
N. H. Edelman
Keyword(s):  
Blood Pressure ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Respiratory Depression ◽  
Separate Group ◽  
Respiratory Neurons ◽  
Co2 Response ◽  
Co2 Sensitivity ◽  
Lactate Formation ◽  
End Tidal

The CO2 response of the phrenic neurogram before and during CO-induced isocapnic brain hypoxia was studied in peripherally chemodenervated, vagotomized, paralyzed, ventilated cats with blood pressure held constant. During inhalation of 0.5% CO in 40% O2, arterial O2 content (CaO2) was reduced to 40% and minute phrenic activity to 38.4 +/- 9.4% (SE; n = 9) of prehypoxic levels, primarily due to depression of peak phrenic amplitude (PP). CO2 response, defined as the slope of the plot of PP vs. end-tidal PCO2 during CO2 rebreathing, was unaffected by phrenic depression even to the point of total suppression of phrenic activity in two cats. The effect of the tissue metabolic acidosis associated with hypoxia on phrenic CO2 sensitivity was assessed in a separate group of cats by blocking lactate formation during hypoxia with dichloroacetate (DCA). Preventing lactic acidosis during hypoxia did not affect the CO2 response of the phrenic activity during hypoxia. We conclude that 1) hypoxic depression does not limit the ability of central respiratory neurons to respond to CO2, and 2) the failure of DCA to affect the CO2 response of the phrenic neurogram suggests that brain intracellular lactic acidosis does not modify the phrenic response to hypercapnia.

Factors Determining the Ventilatory Response to Carbon Dioxide in Chronic Obstructive Airways Disease

1970 ◽  
Vol 39 (5) ◽  
pp. 653-662 ◽  
Author(s):  
T. K. C. King ◽  
D. Yu
Keyword(s):  
Carbon Dioxide ◽  
Response Curve ◽  
Ventilatory Response ◽  
Chronic Obstructive ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Obstructive Airways Disease ◽  
End Tidal ◽  
Chronic Obstructive Airways Disease ◽  
Carbon Dioxide Response

1. The ventilatory response to carbon dioxide was measured in a group of patients with chronic obstructive airways disease using a rebreathing method. 2. The slope of the carbon dioxide response curve was obtained by plotting the ventilation at successive half minutes against the corresponding mean end tidal Pco2. 3. The slope of the carbon dioxide response curve was positively correlated with (a) the FEV1 and (b) the reciprocal of the resting arterial Pco2, both these correlations being statistically significant. 4. Reference to FEV1 alone could explain more than 80% of the variation in the slope of the CO2 response curve. This explained variation was not significantly improved by the additional consideration of the resting arterial Pco2. 5. It was suggested that whatever the underlying complex mechanisms that determine the response to CO2, the FEV1 can be used as an empirical factor for the prediction of this response in patients with chronic obstructive airways disease.

Influences of Morphine on the Ventilatory Response to Isocapnic Hypoxia 

1997 ◽  
Vol 86 (6) ◽  
pp. 1342-1349 ◽  
Author(s):  
Aad Berkenbosch ◽  
Luc J. Teppema ◽  
Cees N. Olievier ◽  
Albert Dahan
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Shape Parameter ◽  
Ventilatory Response ◽  
Depressant Effect ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
Ventilatory Response To Hypoxia ◽  
Carbon Dioxide Sensitivity

Background The ventilatory response to hypoxia is composed of the stimulatory activity from peripheral chemoreceptors and a depressant effect from within the central nervous system. Morphine induces respiratory depression by affecting the peripheral and central carbon dioxide chemoreflex loops. There are only few reports on its effect on the hypoxic response. Thus the authors assessed the effect of morphine on the isocapnic ventilatory response to hypoxia in eight cats anesthetized with alpha-chloralose-urethan and on the ventilatory carbon dioxide sensitivities of the central and peripheral chemoreflex loops. Methods The steady-state ventilatory responses to six levels of end-tidal oxygen tension (PO2) ranging from 375 to 45 mmHg were measured at constant end-tidal carbon dioxide tension (P[ET]CO2, 41 mmHg) before and after intravenous administration of morphine hydrochloride (0.15 mg/kg). Each oxygen response was fitted to an exponential function characterized by the hypoxic sensitivity and a shape parameter. The hypercapnic ventilatory responses, determined before and after administration of morphine hydrochloride, were separated into a slow central and a fast peripheral component characterized by a carbon dioxide sensitivity and a single offset B (apneic threshold). Results At constant P(ET)CO2, morphine decreased ventilation during hyperoxia from 1,260 +/- 140 ml/min to 530 +/- 110 ml/ min (P < 0.01). The hypoxic sensitivity and shape parameter did not differ from control. The ventilatory response to carbon dioxide was displaced to higher P(ET)CO2 levels, and the apneic threshold increased by 6 mmHg (P < 0.01). The central and peripheral carbon dioxide sensitivities decreased by about 30% (P < 0.01). Their ratio (peripheral carbon dioxide sensitivity:central carbon dioxide sensitivity) did not differ for the treatments (control = 0.165 +/- 0.105; morphine = 0.161 +/- 0.084). Conclusions Morphine depresses ventilation at hyperoxia but does not depress the steady-state increase in ventilation due to hypoxia. The authors speculate that morphine reduces the central depressant effect of hypoxia and the peripheral carbon dioxide sensitivity at hyperoxia.

The Effect of Bendrofluazide and Frusemide on the Ventilatory Response to Carbon Dioxide and Hypoxia in Normal Man

1974 ◽  
Vol 47 (4) ◽  
pp. 377-385 ◽  
Author(s):  
A. G. Leitch ◽  
L. Clancy ◽  
D. C. Flenley
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Co2 Response ◽  
Acute Exacerbations ◽  
Before And After ◽  
Ventilatory Failure ◽  
End Tidal ◽  
Response Line ◽  
The Right ◽  
End Tidal Co2

1. We have determined the ventilatory response to CO2 at two levels of end-tidal O2 tension in eight normal subjects before and after (1) 4 days of 0.242 mmol (80 mg) oral frusemide daily and (2) 4 days of 0.024 mmol (10 mg) bendrofluazide daily. 2. Frusemide produced no significant alkalosis, change in end-tidal CO2 tension or alteration in the CO2 response line. However, we did demonstrate a linear relationship between the change in plasma total CO2 content and the change in intercept of the CO2 response line in hyperoxia after frusemide. 3. Bendrofluazide produced a metabolic alkalosis with no significant change in end-tidal CO2 tension. The CO2 response line after the drug showed a decrease in slope in hyperoxia and a shift to the right of the intercept in hypoxia. There was no relationship between change in plasma total CO2 content and change in the intercept of the CO2 response line in hyperoxia. 4. If these results obtained on normal subjects are applicable to patients with chronic bronchitis and emphysema, frusemide might be the diuretic of choice for use with controlled oxygen therapy in the management of acute exacerbations of this disease when it is complicated by ventilatory failure.

Arterial CO2 response to low levels of inspired CO2 in awake beagle dogs

1982 ◽  
Vol 52 (3) ◽  
pp. 672-676 ◽  
Author(s):  
P. Reischl ◽  
D. M. Stavert
Keyword(s):  
Steady State ◽  
Experimental Design ◽  
Repeated Measures ◽  
Experimental Session ◽  
Beagle Dogs ◽  
Co2 Response ◽  
Low Level ◽  
Low Co2 ◽  
Time Period ◽  
End Tidal

We have previously shown, using a repeated-measures experimental design, that 1% inspired CO2 with a partial pressure of 7 Torr at sea level results in an increased end-tidal CO2 pressure (PETCO2) in awake beagle dogs (22), suggesting hypercapnia rather than the isocapnia found by some investigators in human and nonhuman subjects. Because PETCO2 may, not equal arterial PCO2 (PaCO2), we examined the steady-state PaCO2 during air and 1% CO2 inhalation periods in three awake beagle dogs having exteriorized carotid arterial loops and an intact airway, and breathing through a low dead-space respiratory mask. Six low-level CO2 inhalation experiments were performed in three dogs with two experimental sequences in each dog on separate days. An experimental session consisted of alternating control and CO2 inhalation states for up to 10 low-CO2 and 11 control conditions, resulting in a total of 75 control and 57 low-level CO2 inhalation observations. Ten minutes were allowed to reach steady state in each condition. Blood samples (1.5 ml) drawn anaerobically over a 0.5-min time period from an indwelling arterial catheter were immediately analyzed with a radiometer blood gas system. The 1% inhaled CO2 produced a significant increase of 0.88 Torr in the steady-state PaCO2, compared with bracketing controls (t = 5.82, P less than 0.05, df = 2). We conclude that 1% inhaled CO2 results in hypercapnia detectable by a repeated-measures experimental design.

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