Mechanisms of the beneficial effect of sevoflurane in liver ischemia/reperfusion injury

• Published in: Acta cirurgica brasileira Vol. 30; no. 11; pp. 749 - 755
• Main Authors: Cavalcante, Fernanda Paula, Coelho, Ana Maria Mendonça, Machado, Marcel Cerqueira Cesar, Sampietre, Sandra Nassa, Patzina, Rosely Antunes, Diniz, Márcio Augusto, Chaib, Eleazar, D'Albuquerque, Luiz Augusto Carneiro
• Format: Journal Article
• Language: English
• Published: Brazil Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 01.11.2015
• Subjects: Alanine Transaminase - blood; Anesthetics, Inhalation - pharmacology; Animals; Aspartate Aminotransferases - blood; Capillary Permeability - drug effects; Cytokines; Cytokines - blood; Ischemia; Ischemia - pathology; Ischemia - prevention & control; Lipid Peroxidation; Liver; Liver - blood supply; Liver - pathology; Lung; Male; Methyl Ethers - pharmacology; Mitochondria, Liver - drug effects; Mitochondria, Liver - physiology; Necrosis; Phosphorylation; Rats; Rats, Wistar; Reperfusion; Reperfusion Injury - pathology; Reperfusion Injury - prevention & control; Reproducibility of Results; Time Factors
• ISSN: 0102-8650; 1678-2674; 0102-8650
• DOI: 10.1590/S0102-865020150110000005

To evaluate the underlying mechanisms by which sevoflurane protects the liver against ischemia/reperfusion injury evaluate the mechanism by which sevoflurane exerts this protective effect. Twenty-six rats were subjected to partial ischemia/reperfusion injury for 1h: one group received no treatment, one group received sevoflurane, and sham group of animals received laparotomy only. Four hours after reperfusion, levels of alanine and aspartate aminotransferases, tumor necrosis factor-a, and interleukins 6 and 10 were measured. Analyses of mitochondrial oxidation and phosphorylation, malondialdehyde content, histology, and pulmonary vascular permeability were performed. Serum levels of alanine and aspartate aminotransferases were significantly lower in the sevoflurane group compared to untreated controls (p<0.05). The sevoflurane group also showed preservation of liver mitochondrial function compared to untreated controls (p<0.05). Sevoflurane administration did not alter increases in serum levels of tumor necrosis factor-a, and interleukins 6 and 10. Sevoflurane treatment significantly reduced the coagulative necrosis induced by ischemia/reperfusion (p<0.05). Pulmonary vascular permeability was preserved in the sevoflurane group compared to untreated controls. Sevoflurane administration protects the liver against ischemia/reperfusion injury, via preservation of mitochondrial function, and also preserves lung vascular permeability.