Transient liver hypoxia after liver hilus dearterialization.

Dearterializaton of the liver causes changes which have been thought to be ischaemic in nature. Previous reports of direct measurements of liver tissue gas tensions have been confined only to the acute postoperative phase. In this study 15 dogs underwent a standardized and angiographically controlled liver hilus dearterialization with (6 dogs) or without (9 dogs) cholecystectomy. Six dogs underwent a sham operation and were used as controls. Liver respiratory gas tensions were measured with a Silastic tonometer intraoperatively during the first 90 minutes after dearterialization and on the first and seventh day postoperatively. Six dogs died, only one of these being in the dearterialization and cholecystectomy group. Liver pO2 decreased from the mean of 33.2 mmHg to a level of 15--20 mmHg in 20 minutes (p less than 0.05) during room air breathing. On the next day the liver pO2 values were normal. There was no difference in pO2-Values between the cholecystectomy and the noncholecystectomy groups. Liver pCO2 increased from the mean of 26.4 mmHg to 55--60 mmHg in the same time (p less than 0.05). However, on the first postoperative day normal values were seen only in the cholecystectomy group. 60% oxygen breathing prevented the changes in both liver pO2 and pCO2. No changes were noted in the liver gas tensions of the sham-operated dogs, not in the systemic arterial pO2 and pCO2 of the dearterialized animals. Thus a transient hypoxic state developed after this operation, which lasted for less than one day. This hypoxia may be prevented by 60% oxygen breathing postoperatively.