Experimental portal hypertensive enteropathy could have an inflammatory etiopathogenesis and, if so, it would produce intestinal remodeling. The aim of this study was to test this hypothesis.Male Wistar rats with portal hypertension (PHT) produced by partial portal vein ligation were divided into four groups: group I (control; n = 9), group II (PHT; n = 8) at 3 months after surgery, group III (control; n = 8), and group IV (PHT; n = 10) at 1 year after surgery. The density of duodenal goblet cells and ileal levels of tumor necrosis factor (TNF)alpha, interleukin (IL)-1beta, and IL-10 were studied using an ELISA method.At 3 months after surgery, rats with PHT showed an increase in the number of goblet cells in the small bowel (103.63 +/- 14.37 vs 99.42 +/- 19.19/1,000 microm2). This change was associated with an increase (p < 0.05) in ileal levels of TNFalpha (0.20 +/- 0.09 vs 0.08 +/- 0.02 pmol/mg protein), and IL-1beta (0.40 +/- 0.21 vs 0.19 +/- 0.09 pmol/mg protein), as well as with a decrease (p < 0.05) in ileal IL-10 levels (0.06 +/- 0.02 vs 0.12 +/- 0.03 pmol/mg protein). At 1 year after surgery, rats with PHT showed hyperplasia of goblet cells in the small bowel (172.79 +/- 40.46 vs 121.76 +/- 20.74 /1,000 microm2) (p < 0.01), associated with an increase in ileal levels of TNFalpha (0.37 +/- 0.18 vs 0.17 +/- 0.08 pmol/mg protein) (p < 0.05), IL-1beta (0.28 +/- 0.14 vs 0.205 +/- 0.05 pmol/mg protein), and IL-10 (0.25 +/- 0.14 vs 0.20 +/- 0.11 pmol/mg protein).The increase in TNFalpha and IL-1beta levels and the decrease in IL-10 level in the small bowel in rats with chronic prehepatic PHT suggest the existence of an inflammatory process related to goblet cell hyperplasia. This inflammation could be responsible for the intestinal epithelial remodeling that occurs in the long term in this experimental model.