Central Respiratory Chemo-sensitivity and its Relationship to Peripheral Nerve Carbon Dioxide-sensitivity

Nature ◽  
1962 ◽  
Vol 196 (4856) ◽  
pp. 779-780 ◽  
Author(s):  
I. P. PRIBAN
Keyword(s):  
Carbon Dioxide ◽  
Peripheral Nerve ◽  
Carbon Dioxide Sensitivity

scholarly journals P132 Carbon dioxide sensitivity in patients with hyperventilation syndrome

Thorax ◽  
2010 ◽  
Vol 65 (Suppl 4) ◽  
pp. A134-A134
Author(s):  
K. A. Bazin ◽  
S. Moosavi ◽  
K. Murphy ◽  
A. Perkins ◽  
M. Hickson ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Hyperventilation Syndrome ◽  
Carbon Dioxide Sensitivity

Carbon dioxide sensitivity of pulmonary receptors in the frog

1977 ◽  
Vol 33 (9) ◽  
pp. 1167-1168 ◽  
Author(s):  
W. K. Milsom ◽  
D. R. Jones
Keyword(s):  
Carbon Dioxide ◽  
Carbon Dioxide Sensitivity

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.

Amiloride modulation of carbon dioxide hypersensitivity and thermal nociceptive hypersensitivity induced by interference with early maternal environment

2018 ◽  
Vol 33 (1) ◽  
pp. 101-108 ◽  
Author(s):  
Marco Battaglia ◽  
Orlane Rossignol ◽  
Karine Bachand ◽  
Francesca R D’Amato ◽  
Yves De Koninck
Keyword(s):  
Carbon Dioxide ◽  
Anxiety Disorders ◽  
Ion Channel ◽  
Linear Models ◽  
Epigenetic Modification ◽  
Thermal Stimulation ◽  
Pain Syndromes ◽  
And Control ◽  
Cross Fostering ◽  
Carbon Dioxide Sensitivity

Background: Early life adversities are risk factors for anxiety disorders and for pain syndromes, which are, in turn, highly comorbid with anxiety disorders. Repeated cross-fostering mouse pups to adoptive lactating females induces epigenetic modification and heightened mRNA-expression of the acid-sensing-ion-channel-1 gene, altered nociception, and hypersensitivity to 6% carbon dioxide air mixtures, a trait marker of specific human anxiety disorders such as, most clearly and prominently, panic disorder. Aims: We hypothesized that the acid-sensing ion channel inhibitor amiloride can modulate repeated cross-fostering animals’ exaggerated responses to carbon dioxide and nociceptive thermal stimulation. Methods: Respiratory carbon dioxide sensitivity was assessed by plethysmography during 6% carbon dioxide air mixture challenges, and nociception was assessed by latency of paw withdrawal to thermal stimulation, in repeated cross-fostering and control animals. To circumvent the blood-brain barrier, prior to testing, amiloride was nebulized in a plethysmograph. Data were analyzed by general linear models. Results: Analyses of tidal volume responses to 6% carbon dioxide of animals pre-treated with nebulized amiloride/saline in a randomized crossover design showed significant modulatory effect of amiloride, and amiloride×repeated cross-fostering interaction. In contrast, repeated cross-fostering animals’ responses to 6% carbon dioxide after intraperitoneal amiloride, saline, or no treatment, were no different. Analyses of responses to thermal stimuli showed a significant modulatory effect of nebulized amiloride, and repeated cross-fostering×amiloride interaction. Conclusions: Single-dose nebulized amiloride decreased repeated cross-fostering animals’ carbon dioxide sensitivity and nociception indices to levels that were no different from those of control animals. Inasmuch as these results pertain to human anxiety and/or pain hypersensitivity, our findings provide a rationale for studying inhaled amiloride in some anxiety disorders and/or pain syndromes.

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