Arterial PCO2 response to intravenous CO2 in awake dogs unencumbered by external breathing apparatus.
The steady-state arterial CO2 tension (PaCO2) was examined during control and intravenous CO2 loading in awake dogs unencumbered by any breathing apparatus. The dogs inhaled air while undergoing intravenous CO2 loading, and we estimated the gain, delta VA/delta PACO2. CO2 was introduced into the systemic venous blood via a membrane gas exchanger in a femoral arteriovenous shunt circuit, and the extracorporeal blood flow was maintained constant at 0.5 l/min. A total of 11 experiments were performed in 3 dogs comprising 93 control observations and 83 CO2 loading observations. Intravenous CO2 produced a significant increase in the steady state PaCO2, a finding consistent with our previous study in tracheostomized awake dogs. We conclude that intravenous CO2 produces hypercapnia in the awake dog with an intact airway unencumbered by external respiratory apparatus.
D000142:Acidosis, Respiratory / Q000378:metabolism; D000818:Animals; D001158:Arteries / Q000378:metabolism; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000097:blood*; D004285:Dogs; D005260:Female; D006935:Hypercapnia / Q000378:metabolism; D007263:Infusions, Parenteral; D008433:Mathematics; D012119:Respiration; D014851:Wakefulness / Q000502:physiology*
D002245:Carbon Dioxide