Ventilatory and Carotid Body Chemosensory Responses In Rats Exposed To Short‐Term Sustained Hypoxia

Abstract

Previous studies performed in in situ rat preparations reported that the exposure to short‐term (24 h) sustained hypoxia (SH) generates active expiration at rest, increases baseline sympathetic activity during expiration and enhances sympathetic responses to peripheral chemoreceptor stimulation. In the present study, we evaluated basal and hypoxic‐induced changes in ventilatory parameters of unanesthetized juvenile male Holtzman rats (80–90 g) previously exposed to SH (10% O2, 24 hs). In addition, we examined the chemosensory response of carotid body chemoreceptors of decerebrated, artificially‐perfused in situ preparations of juvenile rats (60–80 g) submitted to SH. At resting conditions, SH rats (n=12) exhibited augmented (P<0.05) respiratory frequency (109±2 vs 97±1 cpm), tidal volume (14±1 vs 10±1 ml/kg) and minute ventilation (1550±137 vs 979±114 ml/kg.min) compared to control rats (n=12). SH rats also showed greater tachypneic and hyperventilatory responses (P<0.05) to a new hypoxia episode (7% O2, 20 min) in comparison to control rats. The magnitude of increase in tidal volume was similar between groups. The in situ preparations of SH rats (n=8), but not controls (n=8), exhibited additional bursts in baseline abdominal motor activity, indicating the presence of active expiration at rest. Interestingly, basal afferent activity of carotid sinus nerve (CSN) was similar (0.67±0.18 vs 0.65±0.18 μV) between SH and control rats. Moreover, the CSN excitatory response to stimulation of peripheral chemoreceptors with potassium cyanide was not different between groups (ΔCSN: 1235±372 vs 922±278 %), although the in situ preparations of SH rats showed greater sympathoexcitatory reflex responses (P<0.05). Our findings indicate that augmented basal ventilation and enhanced ventilatory and sympathetic responses to hypoxia in rats exposed to SH are not dependent on increased basal and sensorial activity of carotid body chemoreceptors, but may rely on central mechanisms.Support or Funding InformationFAPESP (2013/17.251‐6) and CNPq