Acute and chronic effects of carotid body denervation on ventilation and chemoreflexes in three rat strains.

Brown Norway (BN) rats have a relatively specific deficit in CO2 sensitivity. This deficit could be due to an abnormally weak carotid body contribution to CO2 sensitivity. Accordingly, we tested the hypothesis that CBD would have less of an effect on eupnoeic breathing and CO2 sensitivity in the BN rats compared to other rat strains.We measured ventilation and blood gases at rest (eupnoea) and during hypoxia (FIO2 =0.12) or hypercapnia (FICO2 =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 (PaCO2 +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 CO2 sensitivity (˙VE/PaCO2) in all strains (P>0.05). Eupnoeic PaCO2 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 CO2 sensitivity in rats, and (3) may not support the concept of an interaction among the peripheral and central chemoreceptors in rats.