Effect of heme oxygenase–endogenous carbon monoxide on mortality during septic shock in rats

• Published in: Irish journal of medical science Vol. 178; no. 4; pp. 491 - 496
• Main Authors: Yu, J.-b., Yao, S.-l.
• Format: Journal Article
• Language: English
• Published: London Springer-Verlag 01.12.2009
• Subjects: Alanine Transaminase - blood; Animals; Aspartate Aminotransferases - blood; Blood Urea Nitrogen; Carbon Monoxide - blood; Carbon Monoxide - physiology; Creatinine - blood; Family Medicine; General Practice; Heme Oxygenase (Decyclizing) - metabolism; Heme Oxygenase (Decyclizing) - physiology; Heme Oxygenase-1 - metabolism; Heme Oxygenase-1 - physiology; Hypotension - physiopathology; Internal Medicine; Lipopolysaccharides; Male; Malondialdehyde - metabolism; Medicine; Medicine & Public Health; Original; Original Article; Oxidative Stress - physiology; Protoporphyrins - pharmacology; Rats; Rats, Sprague-Dawley; RNA, Messenger - metabolism; Shock, Septic - chemically induced; Shock, Septic - physiopathology; Superoxide Dismutase - metabolism; Up-Regulation; Septic shock; Carbon monoxide; Mortality; Hypotension; Heme oxygenase
• ISSN: 0021-1265; 1863-4362
• DOI: 10.1007/s11845-008-0260-x

Aim To investigate the effect of HO–CO on mortality during septic shock in rats. Method Eighty rats were randomly divided into group-control, group ZnPP-IX, group SS, and group LZ. Results Death was significantly lower in group SS than in group LZ ( P  < 0.05). The MAP was significantly higher in the group LZ than in the group SS ( P  < 0.05). ALT, AST, Cr and BUN, MDA, and the lung EB contents, were significantly lower in the group SS than that in the group LZ (all P  < 0.05). And CO and SOD activities were significantly higher in group SS than that in the group LZ (all P  < 0.05). HO-1 mRNA, and HO-1 protein were significantly lower in the group LZ than in the group SS ( P  < 0.05), whereas HO-2 mRNA, and HO-2 protein were not significantly different among four groups (all P  > 0.05). Conclusion The increased oxidative stress and end-organ damage is related to mortality during septic shock; while the hypotension partly contributing to HO-1 protein and CO has no obvious relation with it.