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Carotid body excision significantly changes ventilatory control in awake rats
E B Olson1, E H Vidruk, J A Dempsey
1John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, School of Medicine, University of Wisconsin, Madison 53705.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 1, 1988
Summary
Carotid body excision (CBX) in rats impairs eupneic ventilation and blunts responses to hypoxia. Carotid body chemoreceptors are vital for maintaining normal breathing and adapting to chronic low oxygen levels.
Area of Science:
- Physiology
- Respiratory Regulation
- Chemoreception
Background:
- The carotid bodies are peripheral chemoreceptors that sense blood oxygen levels.
- Their role in regulating ventilation, especially during hypoxia, is critical.
- Understanding their function is key to respiratory control research.
Purpose of the Study:
- To investigate the impact of carotid body excision (CBX) on resting ventilation and ventilatory responses to various oxygen conditions in rats.
- To elucidate the necessity of carotid body chemoreceptors for eupneic breathing and hypoxic acclimatization.
Main Methods:
- Unanesthetized rats underwent carotid body excision (CBX) or sham operations.
- Ventilatory responses were assessed using arterial blood gases (PaCO2) and ventilation/CO2 production ratios (VA/VCO2).
- Experiments involved eupnea, acute hypoxia, acute hyperoxia, and chronic hypoxia.
Main Results:
- CBX rats exhibited chronic hypoventilation and respiratory acidosis.
- They showed hyperventilation to hyperoxia, unlike intact controls.
- Responses to acute hypoxemia were attenuated, and ventilatory acclimatization to chronic hypoxia was abolished.
- Restoration of normoxia after hypoxia led to decreased PaCO2 in CBX rats, contrasting with controls.
Conclusions:
- Carotid body chemoreceptors are essential for maintaining normal resting ventilation in rats.
- These chemoreceptors are indispensable for the process of ventilatory acclimatization to chronic hypoxia.
- CBX significantly disrupts normal respiratory regulation and adaptation to environmental changes.