Relative peripheral and central chemosensory responses to metabolic alkalosis

1983 ◽  
Vol 245 (6) ◽  
pp. R873-R880 ◽  
Author(s):  
M. Pokorski ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Metabolic Alkalosis ◽  
Central Effect ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Relative Contribution ◽  
Before And After ◽  
Ventilatory Effect ◽  
Peripheral Effect ◽  
Steady State Levels

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.

Inhibition of aortic chemoreceptor responses by metabolic alkalosis in the cat

1982 ◽  
Vol 53 (1) ◽  
pp. 75-80 ◽  
Author(s):  
M. Pokorski ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Partial Pressure ◽  
Metabolic Alkalosis ◽  
Major Effect ◽  
Average Dose ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Arterial Ph ◽  
Before And After ◽  
Increased Activity

The responses of the same aortic chemoreceptor afferents to steady-state isocapnic hypoxia and to hypercapnia on hyperoxia, before and after the induction of metabolic alkalosis, were investigated in 12 anesthetized cats. Metabolic alkalosis was achieved by intravenous administration of sodium bicarbonate in the average dose of 7 mmol . kg-1. On the average, arterial pH (pHa) increased from 7.383 to 7.650 at an arterial CO2 partial pressure (PaCO2) of 30 Torr. The increase in pHa resulted in a decrease in chemoreceptor activity, the effect being greater at a lower arterial O2 partial pressure. Increases in PaCO2 during hyperoxia resulted in an increased activity of the chemoreceptors both before and after NaHCO3 injection. The stimulatory effect of hypercapnia, however, was attenuated by metabolic alkalosis. At a constant PaCO2, decreases in arterial [H+] by the NaHCO3 administration caused an approximately linear decrease in the chemoreceptor activity. At a constant arterial [H+], higher PaCO2 was associated with a slightly greater activity of the chemoreceptors. These results indicate that the major effect of CO2 is mediated by [H+], but there appears to be another mechanism, albeit small, for the effect of CO2.

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.

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.

scholarly journals The critical role of T cells in glucocorticoid-induced osteoporosis

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Lin Song ◽  
Lijuan Cao ◽  
Rui Liu ◽  
Hui Ma ◽  
Yanan Li ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Steady State ◽  
Side Effects ◽  
Critical Role ◽  
Wild Type ◽  
Receptor Activator ◽  
Steady State Levels ◽  
Induced Apoptosis

AbstractGlucocorticoids (GC) are widely used clinically, despite the presence of significant side effects, including glucocorticoid-induced osteoporosis (GIOP). While GC are believed to act directly on osteoblasts and osteoclasts to promote osteoporosis, the detailed underlying molecular mechanism of GC-induced osteoporosis is still not fully elucidated. Here, we show that lymphocytes play a pivotal role in regulating GC-induced osteoporosis. We show that GIOP could not be induced in SCID mice that lack T cells, but it could be re-established by adoptive transfer of splenic T cells from wild-type mice. As expected, T cells in the periphery are greatly reduced by GC; instead, they accumulate in the bone marrow where they are protected from GC-induced apoptosis. These bone marrow T cells in GC-treated mice express high steady-state levels of NF-κB receptor activator ligand (RANKL), which promotes the formation and maturation of osteoclasts and induces osteoporosis. Taken together, these findings reveal a critical role for T cells in GIOP.

Separation of carotid body chemoreceptor responses to O2 and CO2 by oligomycin and by antimycin A

1982 ◽  
Vol 242 (3) ◽  
pp. C200-C206 ◽  
Author(s):  
E. Mulligan ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Carbonic Anhydrase ◽  
Partial Pressure ◽  
Carotid Body ◽  
Body Tissue ◽  
Antimycin A ◽  
Tissue Ph ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Metabolic Hypothesis

The cat carotid chemoreceptor O2 and CO2 responses can be separated by oligomycin and by antimycin A. Both of these agents greatly diminish or abolish the chemoreceptor O2 response but not the nicotine or CO2 responses. After either oligomycin or antimycin, the responses to increases and decreases in arterial CO2 partial pressure (PaCO2) consisted of increases and decreases in activity characterized respectively by exaggerated overshoots and undershoots. These were eliminated by the carbonic anhydrase inhibitor, acetazolamide, suggesting that they resulted from changes in carotid body tissue pH. The steady-state PaCO2 response remaining after oligomycin was no longer dependent on arterial O2 partial pressure (PaO2). All effects of antimycin were readily reversible in about 20 min. The separation of the responses to O2 and CO2 indicates that there may be at least partially separate pathways of chemoreception for these two stimuli. The similarity of the oligomycin and antimycin results supports the metabolic hypothesis of chemoreception.

Sexual influence on the control of breathing

1983 ◽  
Vol 54 (4) ◽  
pp. 874-879 ◽  
Author(s):  
D. P. White ◽  
N. J. Douglas ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Co2 Production ◽  
Menstrual Phase ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Chemical Stimuli ◽  
Low Levels ◽  
Normal Women

Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.

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