Development of a peritoneal sclerosis rat model using a continuous-infusion pump.

OBJECTIVE: Encapsulating peritoneal sclerosis (EPS) is a serious complication of continuous ambulatory peritoneal dialysis. Previous studies have created peritoneal sclerosis rat models using daily intraperitoneal injection of chlorhexidine gluconate (CG), but this technique is cumbersome and thickening of the peritoneum makes it difficult to evaluate the injection site. We therefore aimed to make a rat model using a continuous-infusion pump. METHODS: Various concentrations of CG (5%, 8%, 10%, 12%, and 14%) in ethanol were dissolved in saline within the infusion pumps, each of which was placed in the lower abdominal cavity of a male Wister rat. After a peritoneal equilibration test was performed, the rats were sacrificed and the lower anterior parietal and visceral peritoneum was removed. Each excised peritoneum was analyzed by macroscopic and microscopic examinations, including immunohistochemistry for the expression of transforming growth factor-beta 1 (TGF-beta1), vascular endothelial growth factor (VEGF), and alpha-smooth muscle actin (alphaSMA). The results were compared with those of control rats injected with ethanol dissolved in saline within the infusion pump and with no-pump rats. RESULTS: Two of the 5 rats in the 12% CG group and 3 of the 5 rats in the 14% CG group died of ileus within 14 days. All the rats in the 5%, 8%, and 10% CG groups survived to 28 days. Macroscopic examination in the 10% CG group showed bowel dilatation, bowel adhesion, and bloody ascites, similar to those seen in human EPS patients. All rats in each CG group showed the same extent of thickening of the submesothelial compact zone, proliferation of collagen fibers, and presence of numerous cells and neovascularization. Within same CG groups, an equal degree of thickening was observed at all sites of the peritoneum. TGF-beta1, VEGF, and alphaSMA were highly expressed in the peritoneum of the 10% CG group. CONCLUSION: We developed a novel method of creating a peritoneal sclerosis rat model using a continuous-infusion pump. Our technique is simple and highly reproducible, and will be useful in the study of peritoneal sclerosis mechanisms.

Splenectomy protects the kidneys against ischemic reperfusion injury in the rat.

BACKGROUND: Ischemic reperfusion (I/R) injury of the kidney is closely associated with delayed graft function, increased acute rejection, and late allograft dysfunction. Splenectomy reduced hepatic I/R injury by inhibiting leukocyte infiltration in the liver, release of TNF-α, cell apoptosis, and expression of caspase-3. Thus, we investigated the effects of splenectomy on renal I/R injury in the rat. METHODS: Male Wistar rats were assigned to four groups: sham operation (sham group), sham operation+splenectomy (sham+SPLN group), right nephrectomy followed by clamping the left renal pedicle for 30min (I/R 30 group), and I/R 30+splenectomy (I/R 30+SPLN group). Renal function was determined by measuring the concentration of blood urea nitrogen (BUN) and serum creatinine (S-Cr). The serum level of tumor necrosis factor-α (TNF-α) was measured as the marker for inflammation. Left kidneys were obtained 24h after reperfusion. TUNEL assay was assessed for cell apoptosis. Spleens were obtained immediately (0-h group) and 3h after reperfusion (3-h group). The removed spleens were histologically evaluated. RESULTS: The BUN and S-Cr levels were significantly lower in the I/R 30+SPLN group than in the I/R 30 group (p<0.05 for both). Apoptotic cells were significantly lower in the I/R 30+SPLN group than in the I/R 30 group. The serum level of TNF-α, which was increased after I/R, was significantly lower in the I/R 30+SPLN group than in the I/R 30 group (p<0.05). Spleen weights were significantly lower in the 3-h group than in the 0-h group (p<0.05). CONCLUSION: These results suggest that splenectomy reduces renal I/R injury, and this effect may occur by an anti-inflammatory pathway and inhibition of cell apoptosis.