Biochemical Changes in Experimental Rat Model of Abdominal Compartment Syndrome

Abstract

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. BACKGROUND

Comparison of the Hypertransferasemic Effects of Erythropoietin and U-74389G on Aspartate Aminotransferase Levels

“…Wang et al found [31] that flavonol glycosides which are in high concentrations in Inula racemosa altered cellular morphology, and cytokines and AST were returned to near normal level in hepatic I/R injury. Ardasheva et al elevated the intra-abdominal pressure (IAP) above 20 mmHg which led [32] to progression of abdominal compartment syndrome that is associated with organ dysfunction or failure and elevated activities of AST found in some of the experimental groups than control ones of animals not subjected to increased IAP and time frame tested for liver. Zazueta et al found [33] that citicoline CDPcholine reduced ASTl in blood samples from reperfused rats in I/R rat livers.…”

Abdominal Compartment Syndrome in Acute Pancreatitis: A Narrative Review

“…An evaluation of serum or urinary biomarkers was performed both on experimental and human subjects to assess the possibility of an earlier diagnosis of intra-abdominal hypertension or abdominal compartment syndrome. Several biomarkers were examined: kidney dysfunction (BUN and creatinine), intestinal damage (D-lactate [77,78], D-dimer [79], Intestinal Fatty Acid Binding Protein, and I-FABP [80,81]), aspartate aminotransferase [80], oxidative stress biomarkers such as glutathione [82,83], superoxide dismutase isoenzymes [84], and fatty acid ethyl esters [85].…”

D-Lactic Acid as a Metabolite: Toxicology, Diagnosis, and Detection

“…D-Lactate can be overproduced by microbiota under specific circumstances like short bowel syndrome and jejunoileal bypass surgery further supported when a patient takes a meal with high sugar content [ 51 , 52 ]. Abdominal compartment syndrome, a multiorgan failure associated with fluid accumulation within the peritoneal and retroperitoneal spaces, is another risk factor for increased D-lactate concentration in blood [ 53 ]. The presence of D-lactate can follow poisoning to heavy metals despite the exact mechanism remaining unknown.…”