Tipos evolutivos de hipertensión portal prehepática en la rata

Reyero, MA Aller; Fernández, Benjamı́n; Hidalgo, M.; Álvaro, Pedro Cuesta; García, Miguel Sánchez; Giménez-Rico, Hipólito José Durán; Matías, M. A. Llamas; Pérez, J. Arias

doi:10.4321/s0212-71992002000700004

Cited by 4 publications

(3 citation statements)

References 7 publications

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“…At 6 months portal hypertension is maintained by other factors, the most important of which is the resistance offered by the portosystemic collaterals to splanchnic venous flow [l4]. Owing to the persistence in the long term of the alterations related to portal hypertension [15], it can be deduced that the etiopathogenic factors that induce steatosis would also be maintained over this evolutionary period. Portal hypertension in the rat causes fatty liver [16]; and mitochondrial dysfunction [17][18][19] with megamitochondria formation [20][21][22][23] has been involved in its production.…”

mentioning

confidence: 99%

Tumor Necrosis Factor‐α, Interleukin‐1β and Nitric Oxide: Induction of Liver Megamitochondria in Prehepatic Portal Hypertensive Rats

et al. 2005

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It has been shown that portal hypertension in the rat causes microvesicular hepatocytic fatty infiltration. Formation of megamitochondria (MG) is one of the most prominent alterations in steatosis. Because nitric oxide (NO), tumor necrosis factor-alpha (TNFalpha), and interleukin-1beta (IL-1beta) impair mitochondrial function, these mediators have been studied in prehepatic portal hypertensive rats to verify their coexistence with MG and therefore with steatosis. Male Wistar rats were divided into two groups: a control group (n = 7) and a group with partial portal vein hgation (n = 19) at 6 weeks of evolution. TNFalpha and IL-1beta were quantified in liver by enzyme-linked immunosorbent assay, and NO was measured in the portal vein, suprahepatic inferior vena cava, and infrahepatic inferior vena cava by the Griess reaction. In portal hypertensive rats, the serum concentration of NO of hepatic origin increases (132.10 +/- 34.72 vs. 52.44 +/- 11.32 nmol/ml; p < 0.001), as do TNFalpha (2.02 +/- 0.20 vs. 1.12 +/- 0.43 micromol/mg protein) and IL-1beta (18.95 +/- 2.59 vs. 5.48 +/- 1.70 micromol/mg protein) (p = 0.005) in the liver. The most frequent hepatic histologic findings are the presence of MG (p < 0.001), steatosis, and hyperplasia. An increase in hepatic release of NO, TNFalpha and IL-1beta with MG formation is produced in rats with portal hypertension. Therefore these proinflammatory mediators and this morphologic mitochondrial alteration could both be involved in the etiopathogenesis of steatosis.

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confidence: 99%

Tumor Necrosis Factor‐α, Interleukin‐1β and Nitric Oxide: Induction of Liver Megamitochondria in Prehepatic Portal Hypertensive Rats

et al. 2005

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“…In relation to HO-2, the constitutive isoform of HO, the only chemical inducers identified are adrenal glucocorticoids [ 60 ]. We have previously demonstrated that there is an increase in plasma levels of corticosterone in rats with short-term PVL [ 13 ] and therefore, HO-2 could be activated by glucocorticoids in this experimental model.…”

Section: Discussionmentioning

confidence: 94%

“…Therefore, until now PHT in the rat has always been considered to be a hemodynamic impairment with much more homogeneous alterations than those described in human PHT because of a narrow range of PHT, grade of portosystemic shunts, and hepatic atrophy [ 12 ]. However, this evolutive uniformity could not be verified from our previous studies using a modified technique of PV calibrated stenosis in the rat since the degree of hepatic atrophy, splenomegaly, and portosystemic collateral circulation that developed were variable [ 13 ]. A possible inflammatory etiopathogeny of PHT could be one cause of this evolutive heterogeneity.…”

Section: Introductionmentioning

confidence: 99%

Proinflammatory Liver and Antiinflammatory Intestinal Mediators Involved in Portal Hypertensive Rats

Aller

Vara

Garcı́a

et al. 2005

Mediators of Inflammation

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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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The mast cell integrates the splanchnic and systemic inflammatory response in portal hypertension

2007

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Portal hypertension is a clinical syndrome that is difficult to study in an isolated manner since it is always associated with a greater or lesser degree of liver functional impairment. The aim of this review is to integrate the complications related to chronic liver disease by using both, the array of mast cell functions and mediators, since they possibly are involved in the pathophysiological mechanisms of these complications. The portal vein ligated rat is the experimental model most widely used to study this syndrome and it has been considered that a systemic inflammatory response is produced. This response is mediated among other inflammatory cells by mast cells and it evolves in three linked pathological functional systems. The nervous functional system presents ischemia-reperfusion and edema (oxidative stress) and would be responsible for hyperdynamic circulation; the immune functional system causes tissue infiltration by inflammatory cells, particularly mast cells and bacteria (enzymatic stress) and the endocrine functional system presents endothelial proliferation (antioxidative and antienzymatic stress) and angiogenesis. Mast cells could develop a key role in the expression of these three phenotypes because their mediators have the ability to produce all the aforementioned alterations, both at the splanchnic level (portal hypertensive enteropathy, mesenteric adenitis, liver steatosis) and the systemic level (portal hypertensive encephalopathy).This hypothetical splanchnic and systemic inflammatory response would be aggravated during the progression of the chronic liver disease, since the antioxidant ability of the body decreases. Thus, a critical state is produced, in which the appearance of noxious factors would favor the development of a dedifferentiation process protagonized by the nervous functional system. This system rapidly induces an ischemia-reperfusion phenotype with hydration and salinization of the body (hepatorenal syndrome, ascites) which, in turn would reduce the metabolic needs of the body and facilitate its temporary survival.

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Tipos evolutivos de hipertensión portal prehepática en la rata

Cited by 4 publications

References 7 publications

Tumor Necrosis Factor‐α, Interleukin‐1β and Nitric Oxide: Induction of Liver Megamitochondria in Prehepatic Portal Hypertensive Rats

Tumor Necrosis Factor‐α, Interleukin‐1β and Nitric Oxide: Induction of Liver Megamitochondria in Prehepatic Portal Hypertensive Rats

Proinflammatory Liver and Antiinflammatory Intestinal Mediators Involved in Portal Hypertensive Rats

The mast cell integrates the splanchnic and systemic inflammatory response in portal hypertension

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