Splanchnic oxygen consumption and hepatic surface oxygen tensions during isoflurane anesthesia

Blood flow to and oxygen consumption of the splanchnic organs were determined together with hepatic surface oxygen tensions in 18 mongrel dogs anesthetized with the long-acting narcotic piritramid. Twelve animals also received 0.7 Vol% and 1.4 Vol% isoflurane; six time-related controls received piritramid only. Surgical preparation consisted of a left thoracotomy for inserting a catheter into the left atrium for microsphere injections and for gaining access to the hepatic surface through an incision in the diaphragm. Parameters in the animals receiving isoflurane were recorded at three stages: stage 1--piritramid anesthesia after surgical preparation; stage 2-60 min after addition of 0.7 Vol% (end-expiratory) isoflurane; stage 3-60 min after addition of 1.4 Vol% (end-expiratory) isoflurane. Hepatic surface oxygen tension was determined at each stage using an eight-channel oxygen sensitive electrode. Mean arterial pressure and cardiac output decreased during both stages with isoflurane; hepatic arterial inflow remained constant. Portal blood flow and, hence, total hepatic inflow decreased significantly. An unchanged splanchnic O2 consumption induced lower hepatic venous pO2 values: 40 +/- 1 mmHg at control, 35 +/- 2 mmHg, and 31 +/- 2 mmHg (mean +/- SEM; both P less than 0.05) during isoflurane. A concomitant decrease of hepatic surface pO2 values indicated an altered tissue oxygenation. The percentage of hepatic surface pO2 values in the lowest pO2 range (0-5 mmHg) increased significantly from 8.4 to 20.3% during 1.4 Vol% isoflurane; the percentage of values of 0 mmHg increased from 2.4 to 9.8% during 1.4 Vol.%. No changes of these parameters were detected in the control animals during the 3-h observation period.(ABSTRACT TRUNCATED AT 250 WORDS)