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A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care
Minerva Anestesiologica 2008 October;74(10):511-9
Xenon anesthesia impairs hepatic oxygenation and perfusion in healthy pigs
Iber T. 1*, Hecker K. 2*, Vagts D. A. 1, Roesner J. P. 1, Otto B. 2, Steinicke A. 1, Nöldge-Schomburg G. F. E. 1, Rossaint R. 2
1 Department of Anesthesiology and Intensive Care Medicine, University of Rostock, Rostock, Germany;
2 Department of Anesthesiology, RWTH Aachen, Aachen, Germany
Background. Over the last 15 years, there has been growing interest in the noble gas xenon as a new inhalational anesthetic. This is due to its favorable pharmacological properties such as short onset and offset, as well as its hemodynamic stability. However, most volatile anesthetics appear to play an important role in the multi-factorial etiology of perioperative liver injury by decreasing liver blood flow with a subsequent reduction of hepatic oxygen supply. However, the effects of the anesthetic gas xenon on hepatic perfusion and oxygenation have not been completely investigated.
Methods. Following ethical approval, 18 anesthetized and acutely monitored pigs were randomly assigned to the two following groups: 9 animals received xenon anesthesia in increasing inspiratory concentrations of 0%, 20%, 50%, and 65% in addition to their basic intravenous anesthesia; 9 animals served as a control group. Measurement points for systemic and regional hemodynamic and oxygenation parameters were performed 30 min after changing the xenon concentration.
Results. Xenon elicited dose-dependent systemic hemodynamic changes such that the mean arterial pressure did not change, while the heart rate and cardiac output decreased by about 30%, thereby indicating an increase in the systemic vascular resistance. Portal venous blood flow decreased, while hepatic arterial blood flow was unchanged. The oxygen supply of the liver was reduced, but not the rate of indocyanine plasma disappearance from the liver. Furthermore, the increase of liver surface pO2 to systemic hyperoxia was absent, and hepatic lactate uptake was reduced.
Conclusion. Xenon, in addition to basic intravenous anesthesia, elicited a decrease in heart rate and cardiac output and an increase in mean arterial pressure. Similar to volatile anesthetics, xenon does reduce portal venous flow and influences hepatic tissue oxygenation. In contrast, hepatic arterial blood flow remains stable in the presence of xenon, and no changes in the hepatic arterial buffer responses were evident. Xenon does affect hepatic perfusion and oxygenation.