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-gallamonijdidum. The PaCO2 was kept at a constant level by means of mechanical ventilation, and non-carbonic acidosis was induced with HCl 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 greater than P greater than 0.05). The total splanchnic perfusion fell by 28%, and the change in flow was correlated to the change in pH. Total splanchnic perfusion (ml min-1) = -4078+655x pH (N = 42, r = 0.67, P less than 0.001). Total splanchnic perfusion as a fraction of the cardiac output 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 here.
D000005:Abdomen / Q000098:blood supply*; D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000503:physiopathology*; D000771:Anesthesia, Intravenous; D000818:Animals; D002302:Cardiac Output; D004285:Dogs; D005260:Female; D005703:Gallamine Triethiodide; D006863:Hydrogen-Ion Concentration; D008102:Liver Circulation; D008297:Male; D009609:Nitrous Oxide; D010313:Partial Pressure; D010424:Pentobarbital; D014655:Vascular Resistance
D010424:Pentobarbital; D009609:Nitrous Oxide; D005703:Gallamine Triethiodide