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Tumor necrosis factor alpha: a major contributor to the hyperdynamic circulation in prehepatic portal-hypertensive rats.

Authors: Lopez-Talavera, J C  Merrill, W W  Groszmann, R J 
Citation: Lopez-Talavera JC, etal., Gastroenterology. 1995 Mar;108(3):761-7. doi: 10.1016/0016-5085(95)90449-2.
Pubmed: (View Article at PubMed) PMID:7875478
DOI: Full-text: DOI:10.1016/0016-5085(95)90449-2


BACKGROUND/AIMS: Portal hypertension is often accompanied by a hyperdynamic circulatory syndrome. Tumor necrosis factor (TNF) alpha causes vasodilatation and a hyperdynamic state in mammals by activating nitric oxide synthesis. The aim of this study was to investigate whether TNF-alpha plays a role in developing the hyperdynamic syndrome in portal hypertension.
METHODS: Portal-hypertensive rats, induced by partial ligation of the portal vein (PVL), were used. In experiment 1, rats that underwent PVL were treated with polyclonal anti-mouse TNF-alpha or placebo intravenously the same day of the PVL operation and 24 hours before hemodynamic studies. Hemodynamic studies were performed 5 days after PVL. In experiment 2, rats that underwent PVL received anti-TNF-alpha or placebo intravenously 3 days and 24 hours before hemodynamics as in experiment 1. Hemodynamics were performed 14 days after the PVL operation. TNF-alpha blood levels were measured using a bioassay.
RESULTS: Anti-TNF-alpha treatment induced a significant increase in mean arterial pressure, heart rate, and systemic vascular resistance and a significant decrease in cardiac index, portal pressure, and TNF-alpha levels in comparison with placebo animals. No significant effects were observed in sham rats.
CONCLUSIONS: Anti-TNF-alpha treatment in rats that underwent PVL significantly blunts the development of the hyperdynamic circulation and reduces portal pressure. TNF-alpha may play a role in the hemodynamic abnormalities of portal hypertension.

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CRRD Object Information
CRRD ID: 14975128
Created: 2019-09-27
Species: All species
Last Modified: 2019-09-27
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.