Effect of Non‐Carbonic Acidosis on Total Splanchnic Perfusion and Cardiac Output During Anaesthesia with O2‐N2O‐Barbiturate‐Relaxant

Seven dogs were anaesthetized using mebumal natrium‐O2‐N2O‐gallamoni jodidum. The Paco2 was kept at a constant level by means of mechanical ventilation, and non‐carbonic acidosis was induced with HCI infusion (0.3 normal). The arterial pH varied from 7.45 to 6.88. During this acidosis, a rising arterio‐venous oxygen difference was observed, with an unchanged total oxygen consumption. The pulse fell, but the mean pressures in the right atrium and aorta were unchanged. The peripheral resistance rose by 50%, whereas the fall in cardiac output of 20%, was non‐significant (0.10>P>0.05). The total splanchnic perfusion fell by 28%, and the change in flow wa correlated to the change in pH. Total splanchnic perfusion (ml min‐1) = ‐4078 + 655 x pH (N = 42, r = 0.67, P< 0.001). Total splanchnic perfusion as a fraction of the cardiac outpnt remained unchanged. The resistance in the splanchnic area rose by 50%. The oxygen saturation in the portal vein and mixed venous blood changed in parallel. It is concluded that contraction of the blood vessels is the most important effect on the circulation resulting from non‐carbonic acidosis during the anaesthesia employed liere.