scholarly journals The effect of low-dose acetazolamide on the ventilatory CO2 response curve in the anaesthetized cat.

1996 ◽  
Vol 495 (1) ◽  
pp. 227-237 ◽  
Author(s):  
M Wagenaar ◽  
L Teppema ◽  
A Berkenbosch ◽  
C Olievier ◽  
H Folgering
Keyword(s):  
Response Curve ◽  
Low Dose ◽  
Co2 Response ◽  
Co2 Response Curve

Regulation of arterial PCO2 during intravenous CO2 loading

1975 ◽  
Vol 38 (4) ◽  
pp. 651-656 ◽  
Author(s):  
K. Wasserman ◽  
B. J. Whipp ◽  
R. Casaburi ◽  
D. J. Huntsman ◽  
J. Castagna ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Response Curve ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Control Value ◽  
Co2 Output ◽  
Anesthetized Dogs ◽  
Co2 Flow ◽  
Co2 Response Curve

Increased CO2 flow to the lung produced by increasing cardiac output (with constant PVCO2) results in hyperpnea with arterial PCO2 maintained at its control value (J. Appl. Physiol. 36: 457, 1974). To study if arterial PCO2 could be similarly regulated when CO2 flow was elevated by increasing PVCO2 (without changing cardiac output), we produced graded increases in PVCO2 (up to a mean of 69 mmHg) using an extracorporeal gas exchanger in five chloralose-urethan-anesthetized dogs. CO2 output increased up to fourfold. Ventilation increased in proportion to the additional CO2 flow to the lung with consequent regulation of arterial PCO2 at its control value. Comparable increases in VE produced by “conventional” airway loading resulted in arterial hypercapnia. The resulting CO2 response curve was similar to that found in unanesthetized dogs. We conclude that intravenous delivery of CO2 to the lung results in infinite “sensitivity” when computed as Delta VE/Delta paco2. These results provide evidence for a CO2-linked hyperpnea which is not mediated by measurable increases in mean arterial PCO2.

Dexmedetomidine Does Not Depress the CO2 Response Curve in Postoperative Patients

2002 ◽  
Vol 96 (Sup 2) ◽  
pp. A1335
Author(s):  
Michael A. Ramsay ◽  
Comeco C. Jones ◽  
Heike C. Knorpp ◽  
Tillmann H.A. Hein ◽  
Christian J. Singer
Keyword(s):  
Response Curve ◽  
Co2 Response ◽  
Co2 Response Curve

Effect of Aminophylline on Respiratory Center Activity and Metabolic Rate in Premature Infants With Idiopathic Apnea

PEDIATRICS ◽  
1979 ◽  
Vol 63 (4) ◽  
pp. 537-542 ◽  
Author(s):  
Tilo Gerhardt ◽  
Jeane McCarthy ◽  
Eduardo Bancalari
Keyword(s):  
Oxygen Consumption ◽  
Premature Infants ◽  
Response Curve ◽  
Pressure Change ◽  
Esophageal Pressure ◽  
Respiratory Center ◽  
Significant Shift ◽  
Co2 Response ◽  
The Mean ◽  
Co2 Response Curve

The effects of aminophylline on the respiratory center output were studied in 14 premature infants with idiopathic apnea. The mean birth weight was 1,052 gm, and the mean gestational age was 30.2 weeks. These infants had a normal expired volume per minute (Ve) [291 ml/(min x kg)] and a normal esophageal pressure change per breath (4.5 cm H2O); however, their alveolar ventilation per minute (Va) was decreased [89 ml/(min x kg)], resulting in an elevated end-tidal PCO2 (PAco2) [47.8 mm Hg]. The reasons for the elevated PAco2 were the relatively large anatomical dead spaces (Vd) found in these infants (3.4 ml/kg), and a decreased slope of the CO2 response curve [22.2 ml/ (mm x kg x mm Hg PAco2)], with a shift of the curve to the right. Oxygen consumption was normal [7.0 ml/( min x kg)]. Forty-eight hours after initiating treatment with aminophylline (2 mg/kg of body weight every six hours), the incidence of apneic episodes decreased from 29.7 to 4.4 per 24 hours, Va and PAco2 became normal secondary to a 33% increase in esophageal pressure change per breath, and the position of the CO2 response curve showed a significant shift to the left without change in slope. Oxygen consumption increased 20% from basal value. These findings support the hypothesis that apnea in premature infants is related to an immature respiratory center characterized by a decreased output. Aminophylline probably increases respiratory center output by lowering the threshold of the central chemorecepter to CO2.

Ventilatory responses to chemoreceptor stimulation after hypoxic acclimatization in awake goats

1990 ◽  
Vol 69 (4) ◽  
pp. 1236-1243 ◽  
Author(s):  
M. J. Engwall ◽  
G. E. Bisgard
Keyword(s):  
Response Curve ◽  
Time Course ◽  
Minute Ventilation ◽  
Hypoxic Exposure ◽  
Co2 Response ◽  
Ventilatory Responses ◽  
Before And After ◽  
Arterial Po2 ◽  
Co2 Response Curve

Our objective was to test the hypothesis that exposure to prolonged hypoxia results in altered responsiveness to chemoreceptor stimulation. Acclimatization to hypoxia occurs rapidly in the awake goat relative to other species. We tested the sensitivity of the central and peripheral chemoreceptors to chemical stimuli before and after 4 h of either isocapnic or poikilocapnic hypoxia (arterial PO2 40 Torr). We confirmed that arterial PCO2 decreased progressively, reaching a stable value after 4 h of hypoxic exposure (poikilocapnic group). In the isocapnic group, inspired minute ventilation increased over the same time course. Thus, acclimatization occurred in both groups. In goats, isocapnic hypoxia did not result in hyperventilation on return to normoxia, whereas poikilocapnic hypoxia did cause hyperventilation, indicating a different mechanism for acclimatization and the persistent hyperventilation on return to normoxia. Goats exposed to isocapnic hypoxia exhibited an increased slope of the CO2 response curve. Goats exposed to poikilocapnic hypoxia had no increase in slope but did exhibit a parallel leftward shift of the CO2 response curve. Neither group exhibited a significant change in response to bolus NaCN injections or dopamine infusions after prolonged hypoxia. However, both groups demonstrated a similar significant increase in the ventilatory response to subsequent acute exposure to isocapnic hypoxia. The increase in hypoxic ventilatory sensitivity, which was not dependent on the modality of hypoxic exposure (isocapnic vs. poikilocapnic), reinforces the key role of the carotid chemoreceptors in ventilatory acclimatization to hypoxia.

Effect of CO2 and whole-body vibration on ventilation

1965 ◽  
Vol 20 (5) ◽  
pp. 844-848
Author(s):  
W. A. Young ◽  
D. B. Shaw ◽  
J. Navach ◽  
H. Shizgal ◽  
N. Kowalsky
Keyword(s):  
Response Curve ◽  
Critical Level ◽  
Ventilatory Response ◽  
Whole Body Vibration ◽  
Additive Effect ◽  
Whole Body ◽  
Co2 Response ◽  
Body Vibration ◽  
Co2 Response Curve

The ventilatory response of six subjects to increasing levels of alveolar CO2 was measured at rest and during the hyperventilation induced by passive vibratory movements of the whole body. During vibration, addition of CO2 to the inspired air produced no increase in ventilation until the PaCOCO2 reached a critical level which coincided closely with the intersection of the vibration with the resting CO2 response curve. Above this level the vibration curve was almost superimposed on the resting one. There was no evidence of an additive effect of the two stimuli, and no increase in sensitivity to CO2 during vibration. In these respects the situation differs from that in which CO2 is combined with hypoxia or hyperthermia. The findings indicate that when respiration is stimulated by vibration and CO2 simultaneously, the resultant ventilation at any point is solely that produced by the stronger of the two stimuli. hyperventilation; PaCOCO2 and ventilation; CO2 response curve and vibration Submitted on July 30, 1964

Respiration and cerebrospinal fluid pH in metabolic acidosis and alkalosis

1965 ◽  
Vol 20 (5) ◽  
pp. 905-911 ◽  
Author(s):  
R. A. Mitchell ◽  
M. M. Singer
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Response Curve ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Peripheral Chemoreceptors ◽  
Arterial Ph ◽  
Slope Change ◽  
Acute Increase ◽  
Co2 Response Curve

An acute base deficit of 5 mm/liter (metabolic acidosis) was induced in one normal man by an initial oral dose of 20 g NH4Cl and sustained for 5 days by administering 3 g every 6 hr. pHa (arterial) decreased from 7.42 to 7.34 in 4 hr. Ve (minute ventilation) increased from 6.2 to 8.4 liters/min, PaCOCO2 decreased from 40 to 37 mm Hg, CSF pH increased from 7.32 to 7.34, and the CO2 response curve shifted –2.8 mm Hg Pco2 without slope change. At 24 hr, CSF pH was 7.32, with CSF Pco2 and HCO3 – reduced to 42 mm Hg and 21.0 mEq/liter, respectively (control 49 mm Hg, 24 mEq/liter). Ve increased to 9.8 liters/min, arterial pH increased to 7.37, PaCOCO2 fell to 36 mm Hg, and the CO2 response curve was –5.0 mm Hg from control. After 6 days of acidosis, acute increase in pHa to 7.45 in 2 hr by NaHCO3 ingestion decreased Ve to 6.8 liters/min, increased PaCOCO2 to 39 mm Hg, decreased CSF pH to 7.30, and shifted the CO2 response curve back to control. Results of this study are consistent with the hypothesis that the peripheral chemoreceptors initiate and sustain alterations in Ve in metabolic abnormalities in the following manner: 1) acute acidosis increases Ve by stimulating the peripheral chemoreceptors; 2) the PaCOCO2 falls and CSF pH increases, decreasing medullary (H+) chemoreceptor activity; and 3) active transport across the blood-CSF barrier restores CSF pH and the medullary (H+) chemoreceptor activity to normal, causing a further increase in ventilation that partially compensates for the metabolic acidosis. medullary respiratory chemoreceptors; peripheral chemoreceptors; blood-brain barrier; active transport Submitted on July 27, 1964

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