Water Deprivation Enhances the Late Expiratory Activity of Abdominal Nerve During Hypercapnia and Hypoxia in Rats

Abstract

It is known that osmolarity challenges produce reflex adjustments in cardiorespiratory function. Herein, we investigated whether 48 h of water deprivation (WD) modifies respiratory pattern under room air conditions and in response to either hypercapnia or hypoxia using male juvenile (60–90 g) and adults (280–320 g) Holtzman rats. Control rats (n=6–7/group) had continuous access to tap water and food, whereas water‐deprived (WD; n=6–8/group) rats had water, but not food removed for 48 h before the experiments. Adult unanesthetized rats were placed in whole‐body plethysmographic chamber (5 L) for recording oxygen consumption (VO2), carbon dioxide production (VCO2) and ventilatory parameters. VO2 and VCO2 were evaluated under baseline conditions (room air), whereas respiratory frequency (fR) and tidal volume (VT) were measured during baseline, hypercapnia (7% CO2 balanced in 93% O2, for 5 min) or hypoxia (7% O2 balanced in N2, for 5 min). Decorticated, arterially‐perfused in situ preparations of juvenile rats were also used for recording respiratory motor outputs during normocapnia (5% CO2), hypercapnia (8% CO2) and while potassium cyanide (KCN; 25 μg in 50 μL) was intra‐arterially infused. WD rats presented a reduction in VO2 (18 ± 0.5 mL.kg−1.min−1 STPD, vs. control: 23 ± 1.2 mL.kg−1.min−1 STPD; p<0.05) and VCO2 (17 ± 0.5 mL.kg−1.min−1 STPD, vs. control: 26 ± 1.5 mL.kg−1.min−1 STPD; p<0.05). At baseline, WD rats exhibited increased VT (9.7 ± 0.5 mL.kg−1, vs. control: 7.7 ± 0.3 mL.kg−1; p<0.05), but reduced fR (76 ± 2 breaths.min−1, vs. control: 103 ± 7 breaths.min−1; p<0.05), resulting in similar ventilation (VE) between groups (746 ± 54 mL.kg−1.min−1, vs. control: 799 ± 64 mL.kg−1.min−1). During hypercapnia, WD rats had a higher increase in VT (15.3 ± 1.1 mL.kg−1, vs. control: 10.2 ± 0.3 mL.kg−1; p<0.05) and VE (1745 ± 202 mL.kg−1.min−1, vs. control: 1239 ± 49 mL.kg−1.min−1; p<0.05) compared to control rats, with similar increase in fR (112 ± 5 breaths.min−1, vs. control: 122 ± 6 breaths.min−1). Under hypoxia, WD rats presented a greater increase in VT (12.2 ± 0.4 mL.kg−1, vs. control: 8.1 ± 0.8 mL.kg−1; p<0.05) and VE (1247 ± 71 mL.kg−1.min−1, vs. control: 991 ± 84 mL.kg−1.min−1; p<0.05) than control rats, with a lower increase in fR (102 ± 4 breaths.min−1, vs. control: 122 ± 3 breaths.min−1; p<0.05). In in situ preparations, the respiratory motor outputs at baseline were not modified by WD, however, WD produced a greater increase in late expiratory activity of abdominal (ABD) nerve during hypercapnia (22 ± 2 μV, vs. control: 15 ± 2 μV; p<0.05) and hypoxia (14 ± 2 μV, vs. control: 7 ± 1 μV; p<0.05). The results show that 48 h of WD produces a hypometabolic stated, modifies baseline VE and enhances the ventilatory response to hypercapnia and hypoxia in conscious rats. The increased ABD nerve activity might contribute to ventilatory response after WD.Support or Funding InformationCapes, CNPq, FAPESP (grant numbers: 2015/23467‐7; 2017/04649‐2)