A Pathological Study On Kidney In Experimental Abdominal Compartment Syndrome

Purpose: The ACS, frequently encountered in surgical practice, is a well-known emergency resulting from the progressively and acutely increased IAP(or IAH), and have drawn much attention. As the main complication of the ACS, the impairments of renal functions have been seldom implored and the exact mechanism remains unclear. Therefore, animal model of ACS was established and the renal histopthological changes following ACS in rats were investigated in this study. Materials and Methods: 136 SD rats (25days to 1 month) were randomly divided into control group and experimental groups (I, II). The controls were intraperitoneally infused 3 ml normal saline (NS) for 16 rats or nothing for other 8 rats. Experimental group I (n=64) were infused NS until IAP reached the levels of 0.5KPa, 1.25KPa, 1.75KPa and 2. OKPa monitoring by MS302 measuring system, respectively. Experimental group TJ (n=48) were randomly divided into 3 groups (16 rats in each group) : left renal vein compression group(LRV), left renal parenchymal compression group (LRP) and both (LRV plus LRP) after the right kidney was incised for the control. After 2 and 4 hours observation the renal function (Bun and Cr) were assessed with blood sample, and the left kidney was removed for histopthological evaluation. Immunochemistry was performed with multiclonal antibodies HSP70 and Actin, and the expression was measured by image analysis.Results: Renal pathological changes in 1.25KPa group, renal vein compression group and renal vein plus parenchymal compression group were most prominent compared with other groups. The Ozer scores of renal tubular cell necrosis and serum Bun and Cr levels in these three groups significantly increased (vs the other groups, p <0.05) and the HSP70 expressions in these three groups was the strongest (vs the other Groups, p <0.05), while the expression of Actin was the weakest (vs the other groups p <0. 05). These changes become more and more prominent as the time of IAH prolonged. However, no significant difference was found among these three groups (p >0. 05). On the other hand, the renal pathological changes in 0. 5KPa group and parenchymal compression group were similar to that of the control groups (p >0. 05). The 1. 75Kpa and 2KPa groups were excluded from the experimental analysis because there was no enough sample due to high death rate (80-100%).Conclusions: The renal vein compression played a critical role in the impairments of renal function companying ACS, followed by the parenchymal and ureter compressions. The acute renal tubular necrosis was the primarypathological changes in the ACS, and may be the result of cellular Actin framework damage. At the same time, the significant higher expression of HSP70 may be a protective factor in the renal damage. Moreover, IAP above 1.25KPa (about 2.5 times of the renal vein pressure) may result in significant renal damage and 1. 75KPa (about 3. 5 times) may be a morbidity threshold.