| PurposeObstructive jaundice (OJ) is a common disease in general surgery, perioperative patients with obstructive jaundice always associated with various degrees of renal damage, and the incidence of renal dysfunction in obstructive jaundice is at average 9 percent, the mortality rate even reaches 68 percent. The enterogenic endotoxin plays an important role in perioperative renal damage pathophysiological changes of obstructive jaundice, and is also an important factor of the patient death. Endotoxic renal injury manifested mainly in the acute injury of collecting duct, and the injury of collecting duct structure and function is of the most serious influence to the renal function, thus affecting the stability of the human body internal environment. Regulation of the renal water reabsorption mainly is completed in the collecting duct, collecting duct water metabolism regulation mainly depends on the role of the water channel protein (aquaporin, AQP) on membrane, in which Aquaporin 2 (AQP2) is particularly important. Current clinical indicators of renal function is creatinine (Cr) and blood urea nitrogen (BUN), but when both of them changed the renal damage has been very serious, and it brings difficulties to the treatments. Previous research found that the expression of AQP2 decreases in renal damage with other causes, but AQP2 how to change when endotoxemia have not reported. This study was to further use the endotoxin injury animal model to study whether endotoxin control AQP2 protein expression, and compared with the changes of Cr and BUN which usually use for clinical; then discuss diagnostic value of the AQP on endotoxic renal injury, and this can make early detection of renal damage of obstructive jaundice perioperative, even early diagnosis and treatment and reduce complications and lower mortality. Method80 adult male Wistar rats were randomly divided into experimental and control groups. The experimental group and the control group was further divided into 3,5,7,10,14 days groups of eight. Intraperitoneal injection of endotoxin (50 ug / kg.d) made endotoxemia model, and with the control group (intraperitoneal injection of 0.9% NaCl 1ml) control, respectively at 3,5,7,10,14 days decapitated rats and collected caval vein blood 5 ml, collected the supernatant after centrifugation and detected Cr and BUN; transfer kidney medulla to -80℃cryopreserved freezer by liquid nitrogen, using immunohistochemical staining technique to detect expression of AQP2 in kidney collecting duct of experimental group and control group ,and take the pathology light microscopy observation of renal medulla.ResultsUnder light microscopy we can see the experimental group renal collecting duct cell swelling, with no regular arrange, water-like degeneration, exfoliated, while visible focal epithelial cell necrosis, cytoplasm collapsed, a large number of interstitial inflammatory cell infiltration. The AQP2 expression of experimental group injected endotoxin 5 days was significantly decreased than that of the control group (P <0.01), and with the endotoxin injection time extending the reduction is marked. When AQP2 changes, the renal damage can be confirmed by the morphological changes of renal collecting duct. Cr began to increase after injection of endotoxin 10 days, and BUN began to increase after the injection of endotoxin 14 days. With the time of endotoxin injection extending, renal damage aggravated, AQP2 expression reduced.Conclusion1. The expression of AQP2 of renal collecting duct in the experimental group has begun to cut down from the fifth days. Cr began to increase from injection of endotoxin 10 days, BUN began to increase after the injection of endotoxin 14 days.2. AQP2 reduction is ahead of the changes of Cr and BUN, so AQP2 can be used as early detection of renal dysfunction. 3. The change of Endotoxemia induced AQP2 and that of obstructive jaundice induced AQP2 are in a certain consistency.
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