Redistribución del peso lobular hepático en ratas con hipertensión portal prehepática crónica

Reyero, MA Aller; Hidalgo, M.; Mezquida, M.D. Palma; Álvarez, Lydia; Pérez, Jorge; Ameigeiras, Elena Vara; Pérez, J. Arias

doi:10.1016/s0009-739x(01)71889-1

Cited by 2 publications

(1 citation statement)

References 24 publications

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“…The existence of dilation and tortuosity of the superior mesenteric vein branches is referred to as mesenteric venous vasculopathy (MVV). Three grades of MMV were considered: grade 0, normal appearance of the superior mesenteric vein branches; grade I, dilation and tortuosity of the mentioned branches secondary to the Pringle maneuver; grade II, in which the dilation and tortuosity of the superior mesenteric vein branches were spontaneous [30].…”

Section: Gross Superior Mesenteric Vein Studymentioning

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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Section: Gross Superior Mesenteric Vein Studymentioning

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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Evolutive phases of experimental prehepatic portal hypertension

Aller¹,

Nava²,

Cuéllar³

et al. 2007

J of Gastro and Hepatol

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Partial portal vein ligation is the experimental model most frequently used to study prehepatic portal hypertension. Different systemic and splanchnic biochemical and histological alterations in short-term (28-45 days) and long-term (12-14 months) evolutive phases which has been described in this experimental model suggest the existence of different pathophysiological mechanisms involved in their production. The enteropathy produced could develop in three phases: an early or acute phase with vasomotor hemodynamic alterations (ischemia-reperfusion associated with intestinal hyperemia, edema and oxidative stress); an intermediate phase with immunological alterations (mesenteric lymphadenopathy, increased mucosal infiltration by mast cells and the hepato-intestinal release of pro-and anti-inflammatory mediators); and a late or chronic phase with intestinal remodeling (vascular and epithelial). The alterations which are produced in these three evolutive phases make it possible to propose an inflammatory etiopathogeny for hypertensive portal enteropathy.

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Redistribución del peso lobular hepático en ratas con hipertensión portal prehepática crónica

Cited by 2 publications

References 24 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

Evolutive phases of experimental prehepatic portal hypertension

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