Background And Objectives: Apoptosis occurs after thermal injury and may result from either ischaemic intestinal insult or inflammatory mediators released after burn injury. The aim of the study was to investigate the effects of propofol and ketamine on gut epithelium apoptosis after burn injury.
Methods: Sixty male Wistar Albino rats were randomly assigned into four groups. Anaesthesia was induced and maintained with propofol in Groups 1 and 2, and ketamine in Groups 3 and 4 over 12 h. Groups 2 and 4 received 30% total body surface area burn. Groups 1 and 3 had no burn injury. Mean arterial pressure was maintained within 10% of baseline levels in all animals. At 12 h postburn, animals were sacrificed and tissue samples were taken from small intestine for determination of lipid peroxidation, apoptosis and proliferation. Also blood samples were taken for measurement of serum tumor necrosis factor-alpha (TNF-alpha) levels.
Results: Ileal malondialdehyde (MDA) concentration (extent of lipid peroxidation) increased significantly in Group 4 (112.4 +/- 10.2 nmol g-1) compared to Group 3 (48.4 +/- 5.6 nmol g-1) and Group 2 (59.8 +/- 3.2 nmol g-1). The mean TNF-alpha level in Group 4 (118.9 +/- 10.5 pg mL-1) at 12 h postburn was significantly higher than the mean in Group 2 (56.4 +/- 4.3 pg mL-1). Group 4 had the highest mean TUNEL index (terminal deoxyuridine nick-end labelling--an index of extent of apoptosis) of all the groups (265/10). Also the mean TUNEL index value in Group 2 (53/10) was higher than that of Group 1 (3/10) and Group 3 (5/10). The proliferating cell nuclear antigen index (extent of proliferation) remained unchanged among groups.
Conclusions: Propofol could offer a protection against apoptosis of enterocytes with a stable tissue MDA and serum TNF-alpha level compared to ketamine anaesthesia in an animal model of burn injury.
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http://dx.doi.org/10.1017/S0265021506000986 | DOI Listing |
BMC Med Genomics
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Post-Graduate Program in Pharmaceutical Sciences, State University of Maringá, Maringá, Paraná, Brazil. Electronic address:
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