PURPOSE: Sevoflurane and isoflurane have been reported to exert protective effects against ischemia-reperfusion injury (IRI) in various organs. To compare the effect of sevoflurane anesthesia on liver IRI with that of isoflurane anesthesia, we performed the present study in pigs. METHODS: Nineteen pigs were assigned to either the sevoflurane ( n = 9) or the isoflurane group ( n = 10). Hepatic warm ischemia was produced by 30-min hepatic artery and portal vein clamping beginning 90 min after the start of the inhalation anesthesia; this was followed by a 240-min reperfusion. To extend our evaluation, we evaluated the degree of IRI using various parameters (plasma alpha-glutathione-S-transferase [alpha-GST], lipid peroxide, and lactate concentrations), in addition to the conventionally used liver damage markers. RESULTS: The lactate level was significantly higher under isoflurane than under sevoflurane at 120 min after reperfusion (4.0 +/- 0.4 mmol.l(-1) vs 2.5 +/- 0.3 mmol.l(-1); P < 0.05). How-ever, this difference had disappeared after 240 min of reperfusion. No significant differences between the two groups were observed in values for alpha-GST, lipid peroxides, aspartate aminotransferase, alanine aminotransferase, or lactic dehydrogenase. CONCLUSION: The extent of the hepatic IRI seen under sevoflurane anesthesia in pigs did not differ significantly from that seen under isoflurane, as judged from measurements of a number of parameters over a 240-min reperfusion period.
PURPOSE:Sevoflurane and isoflurane have been reported to exert protective effects against ischemia-reperfusion injury (IRI) in various organs. To compare the effect of sevoflurane anesthesia on liver IRI with that of isoflurane anesthesia, we performed the present study in pigs. METHODS: Nineteen pigs were assigned to either the sevoflurane ( n = 9) or the isoflurane group ( n = 10). Hepatic warm ischemia was produced by 30-min hepatic artery and portal vein clamping beginning 90 min after the start of the inhalation anesthesia; this was followed by a 240-min reperfusion. To extend our evaluation, we evaluated the degree of IRI using various parameters (plasma alpha-glutathione-S-transferase [alpha-GST], lipid peroxide, and lactate concentrations), in addition to the conventionally used liver damage markers. RESULTS: The lactate level was significantly higher under isoflurane than under sevoflurane at 120 min after reperfusion (4.0 +/- 0.4 mmol.l(-1) vs 2.5 +/- 0.3 mmol.l(-1); P < 0.05). How-ever, this difference had disappeared after 240 min of reperfusion. No significant differences between the two groups were observed in values for alpha-GST, lipid peroxides, aspartate aminotransferase, alanine aminotransferase, or lactic dehydrogenase. CONCLUSION: The extent of the hepatic IRI seen under sevoflurane anesthesia in pigs did not differ significantly from that seen under isoflurane, as judged from measurements of a number of parameters over a 240-min reperfusion period.
Authors: Maria D I Manunta; Robin J McAnulty; Amy McDowell; Jing Jin; Deborah Ridout; John Fleming; Stephen E Bottoms; Livia Tossici-Bolt; Geoffrey J Laurent; Lorenzo Biassoni; Christopher O'Callaghan; Stephen L Hart Journal: Am J Respir Cell Mol Biol Date: 2013-09 Impact factor: 6.914