Results: In the HCD group total cholesterol levels were significantly higher than in the control group (148.1 +/- 18.9 vs. 55.7 +/- 8.1 mg/dl, p = 0.002). The detumescence time was significantly decreased after HCD compared to the control diet (19.3 +/- 3.6 vs. 78.6 +/- 12.8 s, p < 0.001). The decreases in the HCD group were also significant in terms of ICP (53.4 +/- 4.5 vs. 35.6 +/- 5.5 mm Hg; p < 0.05), ICP/MAP (55.9 +/- 3.9 vs. 38.2 +/- 5.2%; p < 0.05) and AUC (1,404 +/- 197.1

vs. 2,250 +/- 253.7, p < 0.05) values. There were no significant changes in maximum relaxation responses of the thoracic aorta to Ach. Conclusion: These results suggest that erectile functions were significantly damaged early in HCD rats. However, endothelial functions, evaluated in the thoracic aorta, were not affected

simultaneously with erectile functions in rats fed a low concentration of HCD. Copyright (C) 2010 S. Karger AG, Basel”
“Peritoneal dialysis (PD) CAL-101 supplier solution contains high concentrations of glucose and glucose degradation products (GDPs). One of several GDPs-3,4-dideoxyglucosone-3-ene (3,4-DGE)-was recently identified as the most reactive and toxic GDP in PD fluids. In vitro, 3,4-DGE has been shown to induce mesothelial cell damage; however, its role in peritoneal fibrosis in vivo remains unclear. In the present study, we intraperitoneally administered LY3039478 mouse chlorhexidine gluconate (CG) for mild peritoneal SAR302503 injury, and we then injected 3,4-DGE [38 mu mol/L (low concentration) or 145 mu mol/L (high concentration)] 5 times weekly for 4 weeks. Significant thickening of the parietal peritoneal membrane was observed only when treatment with low or high concentrations of 3,4-DGE occurred after CG administration, but not when either CG or 3,4-DGE alone was given. The

combination of CG and 3,4-DGE also caused upregulation of messenger RNA expression of transforming growth factor beta 1, connective tissue growth factor, fibronectin, collagen type 1 alpha 1 chain, alpha smooth muscle actin (alpha-SMA), vascular endothelial growth factor 164, NADPH oxidase 1 and 4, p22phox, p47phox, and gp91phox in peritoneal tissue. Treatment with CG alone was sufficient to cause significant F4/80-positive macrophage infiltration, appearance of alpha-SMA-positive cells, and vessel formation in the submesothelial layer. Addition of 3,4-DGE markedly enhanced those changes and induced apoptosis, mainly in leukocytes. The concentration of 3,4-DGE in the abdominal cavity declined more rapidly in CG-treated mice than in PBS-treated mice. Peritoneal membrane permeability determined by peritoneal equilibration test showed high transport conditions in peritoneum treated with both CG and 3,4-DGE. These results indicate that, when mild peritoneal damage is already present, 3,4-DGE causes peritoneal thickening and fibrosis, resulting in deterioration of peritoneal membrane function. Perit Dial Int 2013; 33(2):143-154 www.PDIConnect.