Background: Enteropathy characterized by vascular and inflammatory alterations in the submucosa and mucosa has been described in patients with portal hypertension. Aims: To verify the theory of inflammatory etiopathogenesis in experimental portal hypertensive duodenopathy, a prehepatic portal hypertension model based on the development of a single and triple partial ligation of the portal vein was used in the rat. Methods: Five rats in each group (male Wistar, 230–255 g) were subjected to single (group II) or triple (group III) partial ligation of the portal vein and then compared to 5 control animals (group I, no operation). The animals were sacrificed 6 weeks later to analyze the histological parameters of the duodenal mucosa and submucosa, i.e., number, diameter and area of submucosal vessels, density of mast cells and mitotic cells. Body, liver and spleen weights and collateral circulation type were also assayed. Results: As was demonstrated by the collateral circulation in all of the animals, the partial portal ligation was successful. Compared to the controls, the number of vessels per microscopic field (25 ± 3.16 vs. 18.60 ± 1.52), their diameter (20.09 ± 2.90 vs. 12.61 ± 3.97 µm, p < 0.05) and consequently their total area (12,749.30 ± 2,298.26 vs. 3,455.82 ± 1,702.33 µm2) were increased in the animals with a single partial ligation (group II) as well as in animals receiving triple partial ligation (group III) (33 ± 12.88, p < 0.05; 22.92 ± 6.72 µm, p < 0.05 and 51,376.95 ± 43,732.24 µm2, p < 0.05, respectively). In addition, the density of mast cells increased from 3.26 ± 1.18 in controls to 10.74 ± 1.47, p < 0.01 and 22.50 ± 6.42, p < 0.01 in single and triple partial portal ligated animals, respectively. Mitosis was significantly induced in crypts of the duodenal mucosa of the single portal ligated animals (25.20 ± 1.78 vs. 17.40 ± 1.14, p < 0.01) but was inhibited in triple partial ligated animals (12.40 ± 5.12, p < 0.05). Compared to controls, both groups of rats developed liver atrophy with a greater decrease in the liver/body weight ratio in the single (2.71 ± 0.50%, p < 0.01) compared to the triple partial ligated animals (3.33 ± 0.09%, p < 0.01). Conclusions: The correlation of the degree of portal hypertension with the vascular changes and mast cell density suggests that both the hypertensive state and inflammation may play a role in the development of portal hypertensive intestinal vasculopathy. The inverse relation of portal hypertension with liver atrophy and mitosis rate in the crypts of the duodenal mucosa has not been clarified and should be investigated in future studies.
A surgical technique based on the development of a triple stenosing ligation is used to worsen the complications inherent to the prehepatic chronic portal hypertension. The results have been compared with those obtained in rats with a single-portal stenosing ligation. An increase (p <.05) in the body, liver, spleen, and kidney weights as well as a decrease (p <.001) in the testes weight to body weight ratio were produced in both groups of animals. In addition, the variability in the obtained weights, particularly in the liver weight, stands out. The incidence of portosystemic and portohepatic collateral circulation and of the mesenteric venous vasculopathy increases in the animals with triple-portal stenosing ligation. The new proposed technique is a valid alternative to the classic one that used single portal stenosing ligation.
Proinflammatory (TNF-α, IL-1β, and NO) and antiinflammatory (IL-10, CO) levels were assayed in serum, liver, and small bowel in order to verify a hypothetic inflammatory etiopathogeny of portal hypertension that could be the cause of its evolutive heterogeneity. Male Wistar rats were divided into one control group (n = 11) and one group with a triple stenosing ligation of the portal vein (n = 23) after 28 days of evolution. In one subgroup of portal hypertensive rats, portal pressure, collateral venous circulation, mesenteric vasculopathy, and liver and spleen weights were determined. In the remaining rats with portal hypertension TNF-α, IL-1β, and IL-10 were quantified in liver and ileum by enzyme-linked immunosorbent assay. NO synthase activity was studied in liver and ileum. CO and NO were measured in portal and systemic blood by spectrophotometry and Griess reaction, respectively. Portal hypertensive rats with mayor spleen weight show hepatomegaly and mayor development of collateral circulation. Ileum release of IL-10 (0.30 ± 0.12 versus 0.14 ± 0.02 pmol/mg protein; P < .01) is associated with a liver production of both proinflammatory mediators (TNF-α: 2 ± 0.21 versus 1.32 ± 0.60 pmol/mg protein; P < .05, IL-1β: 19.17 ± 2.87 versus 5.96 ± 1.84 pmol/mg protein; P = .005, and NO: 132.10 ± 34.72 versus 61.05 ± 8.30 nmol/mL; P = .005) and an antiinflammatory mediator (CO: 6.49 ± 2.99 versus 3.03 ± 1.59 pmol/mL; P = .005). In short-term prehepatic portal hypertension a gut-liver inflammatory loop, which could be fundamental in the regulation both of the portal pressure and of its complications, could be proposed.
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