Biochemical Changes in Experimental Rat Model of Abdominal Compartment Syndrome.

BACKGROUND: Increased intra-abdominal pressure (IAP) causes tissue ischemia, subsequent hypoxia, and impairment of normal tissue metabolism. Elevation of IAP above 20 mmHg leads to progression of abdominal compartment syndrome (ACS) that is associated with organ dysfunction or failure not previously manifested. AIM: To evaluate the eff ects of diff erent grades and time of exposure to IAP on biochemical parameters and oxidative stress in organs aff ected by ischemia using previously developed rat model. RESULTS: Three experimental groups exposed to diff erent IAP and time frames were tested for liver, kidney, and pancreas injury by measuring the activities of tissue specifi c enzymes in blood serum. Elevated activities of aspartate aminotransferase, pancreatic amylase, lipase, and higher concentrations of D-lactate, urea, and creatinine were found in some of the experimental groups compared to a control group of animals not subjected to increased IAP. Increased levels of biomarkers of oxidative stress as well as decrease in concentration of the major cellular antioxidant glutathione indicated the presence of oxidative injury as a result of elevated IAP. CONCLUSIONS: The developed rat model is appropriate to study the mechanism and manifestation of tissue injury during diff erent grades of elevated IAP but also to test approaches aimed to attenuate the detrimental eff ects of ACS. This study also underlines the necessity of using not a single but a set of biochemical parameters in order to assess the severity of tissue injury during elevated IAP and progression to ACS.