Hepatic microvascular changes in rat abdominal compartment syndrome

Abstract

BackgroundAbdominal compartment syndrome (ACS) is associated with an increased rate of multiple organ dysfunction and is an independent marker for mortality. Our objective was to develop an animal model to study the mechanisms of tissue and microvascular injury associated with ACS at the microscopic level. Materials and methodsACS was established in rats with CO2 insufflation at 20 mm Hg for 2 h, with an abdominal cast. Sinusoidal perfusion, inflammatory response, and cell death were quantified in exteriorized livers. Respiratory and renal dysfunction were assessed biochemically and morphologically. Myeloperoxidase levels, a marker of neutrophil activation, were measured in the liver, lung, and small intestine. ResultsContinuously perfused sinusoids were significantly lower in the ACS group (81.4 ± 2.2% versus 99.6% ± 0.50), with an increase in nonperfused and intermittently perfused sinusoids (P < 0.05). Hepatocellular death and the number of activated leukocytes in postsinusoidal venules showed 7- and 18-fold increases, respectively, in the ACS group (P < 0.05). A significant increase in blood urea nitrogen levels in experimental rats was also observed. Myeloperoxidase levels were found to be 8-fold higher in lungs of ACS rats relative to control (P < 0.05), as well as statistically significant increase in the pCO2 and decrease in pH of ACS rats. ConclusionsWe have successfully developed a model of ACS with documented evidence of renal and respiratory dysfunction. In addition, we have microscopy-confirmed evidence of early inflammatory changes and perfusion deficits in the liver with a concomitant increase in cell death in the ACS group.