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Acute and chronic effects of carotid body denervation on ventilation and chemoreflexes in three rat strains
Author(s) -
Mouradian Jr Gary C.,
Forster Hubert V.,
Hodges Matthew R.
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2012.234658
Subject(s) - hypercapnia , carotid body , ventilation (architecture) , medicine , hypoventilation , hypoxia (environmental) , anesthesia , peripheral chemoreceptors , arterial blood , hypoxic ventilatory response , control of respiration , endocrinology , respiratory system , chemistry , oxygen , carotid arteries , mechanical engineering , organic chemistry , engineering
Key points• Carbon dioxide (CO 2 ) provides a major chemical stimulus to breathe, primarily through the activity of CO 2 /pH sensors called chemoreceptors in the brainstem and in the carotid body. • Carotid body denervation (CBD) causes hypoventilation at rest and reduces ventilatory sensitivity to CO 2 in multiple mammalian species, suggesting an important role of the carotid bodies in determining levels of ventilation relative to the CO 2 drive to breathe. • CBD in three strains of adult rats with large inherent differences in CO 2 sensitivity causes hypoventilation at rest but has no effect on CO 2 sensitivity. • These data from rats reinforce the concept that the carotid bodies provide a tonic facilitatory drive to breathe, but differ from other species suggesting a minimal contribution of the carotid bodies to CO 2 sensitivity in rats.Abstract Brown Norway (BN) rats have a relatively specific deficit in CO 2 sensitivity. This deficit could be due to an abnormally weak carotid body contribution to CO 2 sensitivity. Accordingly, we tested the hypothesis that CBD would have less of an effect on eupnoeic breathing and CO 2 sensitivity in the BN rats compared to other rat strains. We measured ventilation and blood gases at rest (eupnoea) and during hypoxia (= 0.12) or hypercapnia (= 0.07) before and up to 23 days after bilateral or Sham CBD in BN, Sprague–Dawley (SD) and Dahl Salt‐Sensitive (SS) rats. In all three rat strains, CBD elicited eupnoeic hypoventilation (Δ+8.7–11.0 mmHg) 1–2 days post‐CBD ( P < 0.05), and attenuated ventilatory responses to hypoxia ( P < 0.05) and venous sodium cyanide (NaCN; P < 0.05), while sham CBD had no effect on resting breathing, blood gases or chemoreflexes ( P > 0.05). In contrast, CBD had no effect on CO 2 sensitivity (Δ/Δ) in all strains ( P > 0.05). Eupnoeic returned to pre‐CBD values within 15–23 days post‐CBD. Thus, the effects of CBD in rats (1) further support an important role for the carotid bodies in eupnoeic blood gas regulation, (2) suggest that the carotid bodies are not a major determinant of CO 2 sensitivity in rats, and (3) may not support the concept of an interaction among the peripheral and central chemoreceptors in rats.