We investigated the effects of carbon dioxide on the splanchnic visceral organs (liver and kidney) as well as skeletal muscle in the anesthetized dog. Thirty two adult mongrel dogs were anesthetized with sodium pentobarbital, intubated and ventilated mechanically with 100% oxygen to maintain normocapnia. After laparotomy, miniature Clark-type polarographic oxygen electrodes were placed on the surfaces of liver, kidney and rectus femoris muscle. Electromagnetic blood flow (BF) probes were also applied to hepatic artery (HA), portal vein (PV), left renal artery (RA) and left femoral artery (FA). After a stable normocapnic ventilation, the hypocapnia was produced by increasing respiratory rate, and the hypercapnia was induced by adding the exogenous carbon dioxide.
Results: Hyperventilation resulted in a significant decrease in HABF, PVBF, liver surface PO2 and kidney surface PO2 in parallel with the decreased PaCO2, but these parameters increased dose dependently when the carbon dioxide was added to the inspired gas (hypercapnic hyperventilation). On the contrary, FABF and skeletal muscle surface PO2 increased by hypocapnia and decreased during hypercapnia. Neither PaCO2 or cardiac output showed any significant change during the entire experiment. Arterial PCO2 appears to exert significant effects on both splanchnic and skeletal muscle perfusion as well as corresponding changes in tissue oxygenations. It is possible that injudicious and prolonged hypocapnic hyperventilation may seriously compromise splanchnic organ perfusion and oxygenation.