Acid-base and ventilatory adaptation in conscious dogs during chronic hypercapnia.
Ventilation and cisternal cerebrospinal fluid (CSF) and arterial acid-base balance were measured in awake dogs during air control and from 1 h to 26 days of breathing 5% CO2 in air. Ventilation increased 4-fold during acute hypercapnia and then declined to a minimum at 5-10 days. Between 1-3 days and 16-26 days of hypercapnia ventilation was relatively stable at 2.5 times control. [HCO3-]CSF increased rapidly by 12 h of hypercapnia and in the steady-state [HCO3-]CSF was correlated with PCSFCO2. Between 1 h and 1.5 days of hypercapnia, increase in [HCO3-]CSF was also correlated with increase in [NH3]CSF. Despite increase in [HCO3-]CSF, there was no compensation of [H+]CSF throughout 26 days of hypercapnia. Hydrogen ion may have contributed to the control of ventilation during chronic hypercapnia since ventilation was correlated with [HCO3-]a and [HCO3-]CSF. However, a relationship between ventilation and [H+] of arterial blood and CSF during chronic hypercapnia was relatively poor or absent. Ventilatory adaptation to chronic hypercapnia could not be related to metabolism or to [NH3]CSF. The mechanism(s) by which the increase in PCO2 during chronic respiratory acidosis results in sustained elevation of ventilation remains to be resolved.
D000136:Acid-Base Equilibrium; D000142:Acidosis, Respiratory / Q000378:metabolism; D000641:Ammonia / Q000134:cerebrospinal fluid; D000818:Animals; D001639:Bicarbonates / Q000097:blood / Q000134:cerebrospinal fluid; D004285:Dogs; D006935:Hypercapnia / Q000097:blood / Q000134:cerebrospinal fluid / Q000503:physiopathology*; D008297:Male; D012119:Respiration
D001639:Bicarbonates; D000641:Ammonia