Comparison of chemoreflex gains obtained with two different methods in cats

1985 ◽  
Vol 59 (1) ◽  
pp. 170-179 ◽  
Author(s):  
J. DeGoede ◽  
A. Berkenbosch ◽  
D. S. Ward ◽  
J. W. Bellville ◽  
C. N. Olievier
Keyword(s):  
Experimental Data ◽  
Ventilatory Response ◽  
Artificial Brain ◽  
Wide Range ◽  
End Tidal ◽  
Alpha Chloralose ◽  
Peripheral Chemoreflex ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2 ◽  
Co2 Forcing

This study investigates the correspondence between results of the ventilatory response to CO2 obtained using the technique of dynamic end-tidal CO2 forcing (DEF) and results obtained using the technique of artificial brain stem perfusion (ABP). The DEF technique separates the dynamic ventilatory response into a slow and fast component with gains g1 and g2 as well as the extrapolated CO2 tension at zero ventilation (Bk). The ABP technique results in steady-state central (Sc) and peripheral (Sp) chemoreflex gains and extrapolated CO2 tension at zero ventilation (B). Experiments were performed on 14 alpha-chloralose-urethan anesthetized cats. A wide range of relative peripheral chemosensitivities was obtained by subjecting eight cats to normoxic and three cats to hypoxic CO2 challenges and three cats to both conditions. Statistical analysis of the experimental data showed that the vectors (g1, g2, Bk) and (Sc, Sp, B) for each cat did not differ significantly (P = 0.56). This was also the case for the vectors [g2/(g1 + g2), Bk] and [Sp/(Sc + Sp), B] (P = 0.21). We conclude that in the DEF experiments the slow ventilatory response to isoxic changes in end-tidal CO2 can be equated with the central chemoreflex loop and the faster ventilatory response to the peripheral chemoreflex loop. The agreement between the two techniques is good.

Dynamic response of peripheral chemoreflex loop to changes in end-tidal CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1779-1785 ◽  
Author(s):  
A. Berkenbosch ◽  
J. DeGoede ◽  
D. S. Ward ◽  
C. N. Olievier ◽  
J. VanHartevelt
Keyword(s):  
Time Delay ◽  
Ventilatory Response ◽  
Neural Mechanism ◽  
Artificial Brain ◽  
End Tidal ◽  
Alpha Chloralose ◽  
Peripheral Chemoreflex ◽  
Mean Time ◽  
Arterial Po2 ◽  
End Tidal Co2

The dynamic ventilatory response of the peripheral chemoreflex loop after isoxic step changes in end-tidal PCO2 (PETCO2) (range 5–30 Torr) was studied in 12 alpha-chloralose-urethan-anesthetized cats. The technique of artificial brain stem perfusion allowed the response to be observed in isolation from the central chemoreflex loop. The data were fitted by an exponential with time delay. During normoxia the mean time constant and time delay (with SD) were 8.6 +/- 7.3 and 3.3 +/- 0.9 s, respectively (9 cats, 56 runs). During hypoxia [arterial PO2 (PaO2) approximately 60 Torr] these values were 6.0 +/- 4.5 and 2.9 +/- 0.9 s (6 cats, 38 runs). In 17 of the 94 runs an augmented breath occurred in the first three breaths after the stepwise increase in PETCO2. For these augmented breaths, tidal volume, inspiratory time, and expiratory time were not different from the next augmented breath occurring in the same run in the steady state. Neither a rate-sensitive component nor a central neural mechanism (central afterdischarge), with the property of maintaining an increased but slowly declining respiratory activity for some minutes after cessation of the PETCO2 challenge, was found. We conclude that the description of the ventilatory response of the peripheral chemoreflex loop to step changes in PETCO2 with a single exponential and time delay is adequate.

Dynamic response of the peripheral chemoreflex loop to changes in end-tidal O2

1991 ◽  
Vol 71 (3) ◽  
pp. 1123-1128 ◽  
Author(s):  
A. Berkenbosch ◽  
J. DeGoede ◽  
D. S. Ward ◽  
C. N. Olievier ◽  
J. VanHartevelt
Keyword(s):  
Time Constant ◽  
Ventilatory Response ◽  
Slow Component ◽  
Response Dynamics ◽  
Exponential Functions ◽  
End Tidal ◽  
Alpha Chloralose ◽  
Peripheral Chemoreflex ◽  
The Brain ◽  
End Tidal Co2

We studied the peripheral ventilatory response dynamics to changes in end-tidal O2 tension (PETO2) in 13 cats anesthetized with alpha-chloralose-urethan. The arterial O2 tension in the medulla oblongata was kept constant using the technique of artificial perfusion of the brain stem. At constant end-tidal CO2 tension, 72 ventilatory on-responses due to stepwise changes in PETO2 from hyperoxia (45–55 kPa) to hypoxia (4.7–9.0 kPa) and 62 ventilatory off-responses due to changes from hypoxia to hyperoxia were assessed. We fitted two exponential functions with the same time delay to the breath-by-breath ventilation and found a fast and a slow component in 85% of the ventilatory on-responses and in 76% of the off-responses. The time constant of the fast component of the ventilatory on-response was 1.6 +/- 1.5 (SD) s, and that of the off-response was 2.4 +/- 1.3 s; the gain of the on-response was smaller than that of the off-response (P = 0.020). For the slow component, the time constant of the on-response (72.6 +/- 36.4 s) was larger (P = 0.028) than that of the off-response (43.7 +/- 28.3 s), whereas the gain of the on-response exceeded that of the off-response (P = 0.031). We conclude that the ventilatory response of the peripheral chemoreflex loop to stepwise changes in PETO2 contains a fast and a slow component.

Postnatal maturation of peripheral chemoreceptor ventilatory response to O2 and CO2 in newborn lambs

1996 ◽  
Vol 80 (6) ◽  
pp. 1928-1933 ◽  
Author(s):  
E. Canet ◽  
I. Kianicka ◽  
J. P. Praud
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Time Frame ◽  
Peripheral Chemoreceptor ◽  
Postnatal Maturation ◽  
Time Courses ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
End Tidal Co2

Although studies on lambs have shown that carotid body sensitivity to O2 is reset postnatally, it is still unknown whether O2 and CO2 peripheral chemoreflexes undergo parallel postnatal maturation. The present study was designed to analyze maturation of O2 and CO2 peripheral chemoreflexes in 10 lambs at < 24 h and at 12 days of age. We measured the ventilatory (VE) response to three tidal breaths of pure N2 or 13% CO2 in air. Overall, the N2 peripheral chemoreflex increased significantly with maturation [VE/end-tidal O2 (ml.min-1.kg-1.Torr-1) = 2.94 +/- 0.91 at < 24 h vs. 5.13 +/- 0.59 at 12 days, P < 0.05], whereas the CO2 peripheral chemoreflex did not change (VE/end-tidal CO2 = 7.04 +/- 0.98 at < 24 h vs. 7.75 +/- 1.07 at 12 days, not significant). We conclude that the CO2 peripheral chemoreflex does not change in awake lambs within the time frame studied, in contrast to a marked postnatal maturation of the O2 peripheral chemoreflex. The different time courses of O2 and CO2 peripheral chemoreflex maturation support the concept that carotid body sensitivities to O2 and CO2 do not depend on the same basic mechanisms.

The Ventilatory Effects of Doxapram in Normal Man

1983 ◽  
Vol 65 (1) ◽  
pp. 65-69 ◽  
Author(s):  
P. M. A. Calverley ◽  
R. H. Robson ◽  
P. K. Wraith ◽  
L. F. Prescott ◽  
D. C. Flenley
Keyword(s):  
Oxygen Uptake ◽  
Ventilatory Response ◽  
Co2 Production ◽  
Central Action ◽  
Ventilatory Responses ◽  
Ventilatory Effects ◽  
Normal Man ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2

1. To determine the mode of action of doxapram in man we have measured ventilation, oxygen uptake, CO2 production, hypoxic and hypercapnic ventilatory responses in six healthy men before and during intravenous infusion to maintain a constant plasma level. 2. Doxapram changed neither resting oxygen uptake nor CO2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO2 studied. 3. Doxapram increased the ventilatory response to isocapnic hypoxia from − 0.8 ± 0.4 litre min−1 (%Sao2)−1 to −1.63 ± 0.9 litres min−1 (%Sao2)−1. This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO2 by 0.5 kPa without adding doxapram. 4. The slope of the ventilatory response to rebreathing CO2 rose from 11.6 ± 5.3 litres min−1 kPa−1 to 20,4 ± 9.8 litres min−1 kPa−1 during doxapram infusion. 5. The marked increase in the ventilatory response to CO2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanaesthetized subjects.

Ventilatory sensitivity to CO2 in hyperoxia and hypoxia in older aged humans

1993 ◽  
Vol 75 (5) ◽  
pp. 2209-2216 ◽  
Author(s):  
M. J. Poulin ◽  
D. A. Cunningham ◽  
D. H. Paterson ◽  
J. M. Kowalchuk ◽  
W. D. Smith
Keyword(s):  
Linear Equation ◽  
Response Curve ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Ventilatory Responses ◽  
Co2 Sensitivity ◽  
End Tidal ◽  
Effects Of Aging ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Co2

Findings from studies of the effects of aging on the human respiratory controller are equivocal. This study assessed the ventilatory response to CO2 in hyperoxia and hypoxia in groups of younger (YS) and older (OS) humans. Two protocols were used. In the first, end-tidal PCO2 (PETCO2) was clamped at 1–2 Torr above rest (eucapnia), and, in the second, PETCO2 was clamped at 7–8 torr above resting PETCO2 (moderate hypercapnia). End-tidal PO2 was clamped at 100 Torr throughout except for two 2-min periods at 500 and 50 Torr. The ventilatory responses for each subject at each PO2 were fitted to the linear equation, VE = S(PETCO2 - B), where VE is minute ventilation, S is the response curve slope, and B is the response curve threshold. In eucapnia, there were no differences in hypoxic and hyperoxic VE between YS and OS. In hypercapnia, hypoxic VE was 24% lower in OS [39.93 +/- 2.71 (SE) l/min] than in YS (52.16 +/- 3.17 l/min). In hypoxia, S was significantly lower in OS (3.25 +/- 0.38 l.min-1.Torr-1) than in YS (4.76 +/- 0.37 l.min-1.Torr-1). We conclude that, in older humans, VE is lower in hypoxia during moderate hypercapnia, resulting mainly from a decreased peripheral chemoreflex CO2 sensitivity.

Almitrine bismesylate and the central and peripheral ventilatory response to CO2

1987 ◽  
Vol 63 (1) ◽  
pp. 66-74 ◽  
Author(s):  
C. N. Olievier ◽  
A. Berkenbosch ◽  
J. Degoede ◽  
E. W. Kruyt
Keyword(s):  
Brain Stem ◽  
Ventilatory Response ◽  
Compartment Model ◽  
Almitrine Bismesylate ◽  
Co2 Sensitivity ◽  
Artificial Brain ◽  
Wave Change ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
The Brain

Effects of almitrine bismesylate on the peripheral and central chemoreflex to a CO2 challenge during normoxia were studied in nine alpha-chloralose-urethan anesthetized cats. With the dynamic end-tidal CO2 forcing technique the ventilatory response after a square-wave change in end-tidal PCO2 (PETCO2) was partitioned into a central and a peripheral part using a two-compartment model. With almitrine administered intravenously (0.6 mg/kg followed by a maintenance dose of 0.4 mg.kg-1 X h-1) the CO2 sensitivity of the peripheral chemoreflex increased on the average from 0.315 to 0.564 l.min-1 X kPa-1 (P less than 0.001, 6 cats, 73 runs), whereas the CO2 sensitivity of the central chemoreflex remained the same (P = 0.87). The extrapolated PETCO2 at zero ventilation (apneic threshold) of the (total) steady-state response curve decreased on the average from 3.50 to 2.36 kPa (P less than 0.001). With the artificial brain stem perfusion technique it was confirmed that almitrine did not affect ventilation by administering it to the blood perfusing the brain stem. We conclude that almitrine bismesylate during normoxia enhances the CO2 sensitivity of the peripheral chemoreflex loop and decreases the apneic threshold due to an action located outside the brain stem.

Adenosine infusion and periodic breathing during sleep

1992 ◽  
Vol 72 (3) ◽  
pp. 1004-1009 ◽  
Author(s):  
K. Gleeson ◽  
C. W. Zwillich
Keyword(s):  
Ventilatory Response ◽  
Correlation Coefficients ◽  
Periodic Breathing ◽  
Normal Subjects ◽  
Adenosine Infusion ◽  
Amplitude Maximum ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2

Intravenously administered adenosine may increase ventilation (VI) and the ventilatory response to CO2 (HCVR). Inasmuch as we have previously hypothesized that those with higher HCVR may be more prone to periodic breathing during sleep, we measured VI and HCVR and monitored ventilatory pattern in seven healthy subjects before and during an infusion of adenosine (80 micrograms.kg-1.min-1) during uninterrupted sleep. Adenosine increased the mean sleeping VI (7.6 +/- 0.4 vs. 6.5 +/- 0.4 l/min, P less than 0.05) and decreased mean end-tidal CO2 values (42.4 +/- 1.2 vs. 43.7 +/- 1.0 Torr, P = 0.06, paired t test) during stable breathing. In six of seven subjects, periodic breathing occurred during this infusion. The amplitude (maximum VI--mean VI) and period length of this periodic breathing was variable among subjects and not predicted by baseline HCVR [correlation coefficients (r) = 0.64, P = 0.17 and r = -0.1, P = 0.9, respectively]. Attempts to measure HCVR during adenosine infusion were unsuccessful because of frequent arousals and continued periodic breathing despite hyperoxic hypercapnia. We conclude that adenosine infusion increases VI and produces periodic breathing during sleep in most normal subjects studied.

The effect of Airway Anaesthesia on the Control of Breathing and the Sensation of Breathlessness in Man

1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Cough Reflex ◽  
Before And After ◽  
Median Diameter ◽  
Receptor Block ◽  
Normal Man ◽  
End Tidal ◽  
Ventilatory Response To Co2

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.

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.

Is hypercapnia necessary for the ventilatory response to exercise in man?

1987 ◽  
Vol 73 (6) ◽  
pp. 617-625 ◽  
Author(s):  
K. Murphy ◽  
R. P. Stidwill ◽  
Brenda A. Cross ◽  
Kathryn D. Leaver ◽  
E. Anastassiades ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Co2 Production ◽  
Moderate Exercise ◽  
Arterial Ph ◽  
Arteriovenous Shunts ◽  
Exercise Period ◽  
Leg Exercise ◽  
End Tidal ◽  
Response To Exercise ◽  
End Tidal Co2

1. Continuous recordings of arterial pH, ventilation, airway CO2 and heart rate were made during rest and during 3–4 min periods of rhythmic leg exercise in four renal patients with arteriovenous shunts. 2. The patients were anaemic (haemoglobin 6.5–9.0 g/dl) but had a normal ventilatory response to exercise as judged by the ratio of the change in ventilation to the change in CO2 production. 3. Breath-by-breath oscillations in arterial pH disappeared for the majority of the exercise period in each patient. 4. Changes in mean arterial pH and end-tidal CO2 tension with exercise were inconsistent between subjects but consistent within a given subject. On average, mean arterial pH rose by 0.011 pH unit. Changes in end-tidal CO2 tension reflected changes in mean pHa by falling on average by 1 mmHg (0.13 kPa). 5. Hypercapnia and acidaemia were not found to be necessary for the ventilatory response to moderate exercise.

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