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.

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.

Blood-gas equilibration of CO2 and O2 in lungs of awake dogs during prolonged rebreathing

1984 ◽  
Vol 57 (5) ◽  
pp. 1354-1359 ◽  
Author(s):  
P. Scotto ◽  
H. Rieke ◽  
H. J. Schmitt ◽  
M. Meyer ◽  
J. Piiper
Keyword(s):  
Carotid Artery ◽  
Transit Time ◽  
Gas Mixture ◽  
Blood Gas ◽  
Venous Admixture ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
The Mean ◽  
End Tidal ◽  
Arterial Po2

To reinvestigate the blood-gas CO2 equilibrium in lungs, rebreathing experiments were performed in five unanesthetized dogs prepared with a chronic tracheostomy and an exteriorized carotid loop. The rebreathing bag was initially filled with a gas mixture containing 6–8% CO2, 12, 21, or 39% O2, and 1% He in N2. During 4–6 min of rebreathing PO2 in the bag was kept constant by a controlled supply of O2 while PCO2 rose steadily from approximately 40 to 75 Torr. Spot samples of arterial blood were taken from the carotid loop; their PCO2 and PO2 were measured by electrodes and compared with the simultaneous values of end-tidal gas read from a mass spectrometer record. The mean end-tidal-to-arterial PO2 differences averaging 16, 4, and 0 Torr with bag PO2 about 260, 130, and 75 Torr, respectively, were in accordance with a venous admixture of about 1%. No substantial PCO2 differences between arterial blood and end-tidal gas (PaCO2 - PE'CO2) were found. The mean PaCO2 - PE'CO2 of 266 measurements in 70 rebreathing periods was -0.4 +/- 1.4 (SD) Torr. There was no correlation between PaCO2 - PE'CO2 and the level of arterial PCO2 or PO2. The mean PaCO2 - PE'CO2 became +0.1 Torr when the blood transit time from lungs to carotid artery (estimated at 6 s) and the rate of rise of bag PCO2 (4.5 Torr/min) were taken into account. These experimental results do not confirm the presence of significant PCO2 differences between arterial blood and alveolar gas in rebreathing equilibrium.

scholarly journals The association between end-tidal carbon dioxide and arterial partial pressure of carbon dioxide after cardiopulmonary bypass pumping in cyanotic children

2021 ◽  
Author(s):  
Behrang Nooralishahi ◽  
Rozhin Faroughi ◽  
Hooman Naghashian ◽  
Ashkan Taghizadeh ◽  
Mohammadjavad Mehrabanian ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Cardiopulmonary Bypass ◽  
Heart Diseases ◽  
Arterial Line ◽  
Blood Gas ◽  
Arterial Pco2 ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Before And After ◽  
End Tidal

Introduction: Evidence suggests the high capability of non-invasive assessment of the End-tidal carbondioxide (ETCO2) in predicting changes in arterial carbon dioxide pressure (PCO2) following major surgeries in children. We aimed to compare EtCO2 values measured by capnography with mainstream device and EtCO2 values assessed by arterial blood gas analysis before and after cardiopulmonary bypass pumping in cyanotic children. Methods: This cross-sectional study was performed on 32 children aged less than 12 years with ASA II suffering cyanotic heart diseases and undergoing elective cardiopulmonary bypass pumping. Arterial blood sample was prepared through arterial line before and after pumping and arterial blood gas (ABG)was analyzed. Simultaneously, the value of EtCO2 was measured by capnography with mainstream device. Results: A significant direct relationship was found between the changes in ETCO2 and arterialPCO2 (r = 0.529, P = 0.029) postoperatively. According to significant linear association between postoperative change in ETCO2 and arterial PCO2, we revealed a new linear formula between the two indices: ΔPCO2 = 0.89× ETCO2-0.54. The association between arterial PCO2 and ETCO2 remained significant adjusted for gender, age, and body weight. Conclusion: the value of ETCO2 can reliability estimate postoperative changes in arterial PCO2 in cyanotic children undergoing cardiopulmonary bypass pumping.

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.

The Study of Dynamic Response to Acute Hemorrhage by Pulse Spectrum Analysis

2006 ◽  
Vol 34 (03) ◽  
pp. 449-460 ◽  
Author(s):  
Yu Hsin Chang ◽  
Chia I Tsai ◽  
Jaung Geng Lin ◽  
Yue Der Lin ◽  
Tsai Chung Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Spectrum Analysis ◽  
Pulse Spectrum ◽  
Acute Hemorrhage ◽  
Arterial Blood ◽  
Percentage Difference ◽  
Before And After

Traditional Chinese Medicine (TCM) holds that Blood and Qi are fundamental substances in the human body for sustaining normal vital activity. The theory of Qi, Blood and Zang-Fu contribute the most important theoretical basis of human physiology in TCM. An animal model using conscious rats was employed in this study to further comprehend how organisms survive during acute hemorrhage by maintaining the functionalities of Qi and Blood through dynamically regulating visceral physiological conditions. Pulse waves of arterial blood pressure before and after the hemorrhage were taken in parallel to pulse spectrum analysis. Percentage differences of mean arterial blood pressure and harmonics were recorded in subsequent 5-minute intervals following the hemorrhage. Data were analyzed using a one-way analysis of variance (ANOVA) with Duncan's test for pairwise comparisons. Results showed that, within 30 minutes following the onset of acute hemorrhage,the reduction of mean arterial blood pressure was improved from 62% to 20%. Throughout the process, changes to the pulse spectrum appeared to result in a new balance over time. The percentage differences of the second and third harmonics, which were related to kidney and spleen, both increased significantly than baseline and towards another steady state. Apart from the steady state resulting from the previous stage, the percentage difference of the 4th harmonic decreased significantly to another steady state. The observed change could be attributed to the induction of functional Qi, and is a result of Qi-Blood balancing activity that organisms hold to survive against acute bleeding.

Arterial-alveolar CO2 equilibration in exercising dogs during prolonged rebreathing

1985 ◽  
Vol 58 (5) ◽  
pp. 1654-1658 ◽  
Author(s):  
J. A. Loeppky ◽  
P. Scotto ◽  
H. Rieke ◽  
M. Meyer ◽  
J. Piiper
Keyword(s):  
Steady State ◽  
Carotid Artery ◽  
Average Rate ◽  
Blood Gas ◽  
O2 Uptake ◽  
Full Agreement ◽  
Arterial Blood ◽  
Simultaneous Measurements ◽  
The Mean ◽  
End Tidal

Arterial-alveolar equilibration of CO2 during exercise was studied by normoxic CO2 rebreathing in six dogs prepared with a chronic tracheostomy and exteriorized carotid loop and trained to run on a treadmill. In 153 simultaneous measurements of PCO2 in arterial blood (PaCO2) and end-tidal gas (PE'CO2) obtained in 46 rebreathing periods at three levels of mild-to-moderate steady-state exercise, the mean PCO2 difference (PaCO2-PE'CO2) was -1.0 +/- 1.0 (SD) Torr and was not related to O2 uptake or to the level of PaCO2 (30–68 Torr). The small negative PaCO2-PE'CO2 is attributed to the lung-to-carotid artery transit time delay which must be taken into account when both PaCO2 and PE'CO2 are continuously rising during rebreathing (average rate 0.22 Torr/s). Assuming that blood-gas equilibrium for CO2 was complete, a lung-to-carotid artery circulation time of 4.6 s accounts for the observed uncorrected PaCO2-PE'CO2 of -1.0 Torr. The results are interpreted to indicate that in rebreathing equilibrium PCO2 in arterial blood and alveolar gas are essentially identical. This conclusion is at variance with previous studies in exercising humans during rebreathing but is in full agreement with our recent findings in resting dogs.

Arterial blood gas tensions during breath-hold diving in the Korean ama

1993 ◽  
Vol 75 (1) ◽  
pp. 285-293 ◽  
Author(s):  
J. Qvist ◽  
W. E. Hurford ◽  
Y. S. Park ◽  
P. Radermacher ◽  
K. J. Falke ◽  
...  
Keyword(s):  
Radial Artery ◽  
Breath Hold ◽  
Blood Gas ◽  
Arterial Pco2 ◽  
Blood Samples ◽  
Arterial Blood Gas ◽  
Time Limits ◽  
Arterial Blood ◽  
Normal Ranges ◽  
Arterial Po2

Korean female unassisted divers (cachido ama) breath-hold dive > 100 times to depths of 3–7 m during a work day. We sought to determine the extent of arterial hypoxemia during normal working dives and reasonable time limits for breath-hold diving by measuring radial artery blood gas tensions and pH in five cachido ama who dove to a fixed depth of 4–5 m and then continued to breath hold for various times after their return to the surface. Eighty-two blood samples were withdrawn from indwelling radial artery catheters during 37 ocean dives. We measured compression hyperoxia [arterial PO2 = 141 +/- 24 (SD) Torr] and hypercapnia (arterial PCO2 = 46.6 +/- 2.4 Torr) at depth. Mean arterial PO2 near the end of breath-hold dives lasting 32–95 s (62 +/- 14 s) was decreased (62.6 +/- 13.5 Torr). Mean arterial PCO2 reached 49.9 +/- 5.4 Torr. Complete return of these values to their baseline did not occur until 15–20 s after breathing was resumed. In dives of usual working duration (< 30 s), blood gas tensions remained within normal ranges. Detailed analysis of hemoglobin components and intrinsic oxygenation properties revealed no evidence for adaptive changes that could increase the tolerance of the ama to hypoxic or hypothermic conditions associated with repetitive diving.

The adrenocorticotropic hormone and arginine vasopressin responses to hypercapnia in fetal and maternal sheep

1993 ◽  
Vol 264 (2) ◽  
pp. R324-R330 ◽  
Author(s):  
H. G. Chen ◽  
C. E. Wood
Keyword(s):  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Bilateral Vagotomy ◽  
Pregnant Ewe

Previous studies have demonstrated that fetal adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP) are increased during periods of acidemia produced by infusion of acid intravenously or by acidemia secondary to hypovolemia. The purpose of this study was to quantify ACTH and AVP responses to hypercapnic acidemia and to test the role of the peripheral chemoreceptors in the control of these responses. Chronically catheterized fetal sheep were subjected to carotid sinus denervation and bilateral vagotomy or were studied intact. At least 5 days after surgery, fetuses were exposed to a 60-min period of normocapnia or hypercapnia, delivered via a polyethylene bag containing 5-8% CO2 in 21% O2 fitted over the head of the pregnant ewe. Hypercapnia significantly increased fetal arterial PCO2 to 55.2 +/- 1.8 and 55.9 +/- 2.2 mmHg and decreased arterial pH to 7.257 +/- 0.011 and 7.281 +/- 0.010 in intact and denervated fetuses, respectively. Fetal mean arterial blood pressure was decreased slightly in the denervated fetuses during hypercapnia. Fetal plasma AVP was increased in both groups equally, and plasma ACTH and cortisol were increased in the denervated fetuses only. Fetal heart rate was increased significantly in intact but not denervated fetuses. We conclude that respiratory acidemia is a mild stimulus to AVP secretion and that this response is not attenuated by peripheral chemodenervation.

Responses of ganglioglomerular nerve activity to respiratory stimuli in the cat

1986 ◽  
Vol 60 (2) ◽  
pp. 391-397 ◽  
Author(s):  
S. Lahiri ◽  
S. Matsumoto ◽  
A. Mokashi
Keyword(s):  
Steady State ◽  
Action Potentials ◽  
Respiratory Drive ◽  
Blood Gas ◽  
Intravascular Injection ◽  
Nerve Activity ◽  
State Response ◽  
Arterial Blood ◽  
Respiratory Rhythms ◽  
Arterial Po2

We studied the responses of the ganglioglomerular nerve (GGN) efferents to brief periods of hypoxia and hypercapnia and to several levels of steady-state arterial PO2 and PCO2 and to intravascular injection of cyanide in thirteen anesthetized cats. The cats breathed spontaneously. A branch of the GGN which was cut close to the carotid body was divided into several filaments, and the activity of each filament was tested until clean and identifiable action potentials were obtained. The GGN efferent activity, breath-by-breath inspiratory volume, tracheal PO2 and PCO2 and arterial blood pressure were recorded simultaneously. We found that the GGN contained spontaneously active fibers which showed a range of responses to the respiratory stimuli. Fifty-eight percent of the filaments with dominant cardiovascular rhythm showed the least response to blood gas stimuli. Forty-two percent showed clear responses to hypoxia and hypercapnia. These responses developed slowly with the onset of the stimulus but decreased promptly with the withdrawal of the stimulus. These GGN efferents were also promptly stimulated by sodium cyanide. The steady-state response curve to hypoxia was hyperbolic and to hypercapnia it was linear. Some of these fibers showed stronger respiratory rhythms than others. The responses of these GGN efferents were associated with the respiratory responses to hypoxia and hypercapnia. For the same respiratory drive, however, the steady-state hypoxic stimulus elicited a greater GGN response than did hypercapnia.

Ventilatory response to moderate and severe hypoxia in adult dogs: role of endorphins

1988 ◽  
Vol 65 (3) ◽  
pp. 1383-1388 ◽  
Author(s):  
J. I. Schaeffer ◽  
G. G. Haddad
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Moderate Hypoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Before And After ◽  
The Relationship ◽  
Arterial Po2

To determine the role of opioids in modulating the ventilatory response to moderate or severe hypoxia, we studied ventilation in six chronically instrumented awake adult dogs during hypoxia before and after naloxone administration. Parenteral naloxone (200 micrograms/kg) significantly increased instantaneous minute ventilation (VT/TT) during severe hypoxia, (inspired O2 fraction = 0.07, arterial PO2 = 28-35 Torr); however, consistent effects during moderate hypoxia (inspired O2 fraction = 0.12, arterial PO2 = 40-47 Torr) could not be demonstrated. Parenteral naloxone increased O2 consumption (VO2) in severe hypoxia as well. Despite significant increases in ventilation post-naloxone during severe hypoxia, arterial blood gas tensions remained the same. Control studies revealed that neither saline nor naloxone produced a respiratory effect during normoxia; also the preservative vehicle of naloxone induced no change in ventilation during severe hypoxia. These data suggest that, in adult dogs, endorphins are released and act to restrain ventilation during severe hypoxia; the relationship between endorphin release and moderate hypoxia is less consistent. The observed increase in ventilation post-naloxone during severe hypoxia is accompanied by an increase in metabolic rate, explaining the isocapnic response.

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