The Gastrointestinal Circulation

Lanciault, G.; Jacobson, Eugene D.

doi:10.1016/s0016-5085(76)80374-5

Cited by 93 publications

(31 citation statements)

References 229 publications

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“…Moreover, macrophages stimulated with IFN γ activate nuclear factor-kappa B (NF-Kb) and induce MCP-1 gene expression in HUVECs, which posits to a possible interaction between adipose inflammatory cells and vascular cells [36]. Mesenteric vasculature regulates total blood flow to the gut and mediates transport of nutrients in the circulation [24]. The mesenteric bed is surrounded by a variable volume of peri-vascular mesenteric adipose tissue, which plays an important role in sustaining an inflammation cascade in obesity and type 2 diabetes [14].…”

Section: Discussionmentioning

confidence: 99%

Interferon-gamma induced adipose tissue inflammation is linked to endothelial dysfunction in type 2 diabetic mice

et al. 2011

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Interferon-gamma (IFNγ) has previously been associated with immuno-mediated inflammation in diet-induced obesity and type 1 diabetes. This study sought to define the role of IFNγ-induced adipose tissue inflammation in endothelial dysfunction in type 2 diabetes. We examined mesenteric adipose tissue (MAT) inflammation, and endothelial function of small mesenteric artery (SMA) in control mice (m Leprdb), diabetic mice (Leprdb), m Leprdb treated with IFNγ, and Leprdb treated with anti-IFNγ or anti-monocyte chemoattractant protein-1 (anti-MCP-1). mRNA and protein expression of IFNγ and MCP-1 were increased in MAT of Leprdb, accompanied by increased T-lymphocyte and macrophage infiltration. Anti-IFNγ reduced MAT inflammatory cell infiltration and inflammatory cytokine expression in Leprdb, while IFNγ treatment showed the opposite effects in m Leprdb. Acetylcholine (ACh)-induced vasorelaxation of SMA was impaired in Leprdb versus m Leprdb, but sodium nitro-prusside (SNP)-induced vasorelaxation was comparable. Both anti-IFNγ and anti-MCP-1 improved endothelial function of Leprdb, while IFNγ treatment impaired endothelial function of m Leprdb. Superoxide production was higher in both MAT and SMA of Leprdb mice, and anti-IFNγ reduced MAT and SMA superoxide production. Macrophage accumulation in the adventitia of SMA, and mRNA expression of MCP-1 in SMA were increased in Leprdb and IFNγ-treated m Leprdb, but reduced in anti-IFNγ treated Leprdb. These findings suggest IFNγ has a key role in the regulation of visceral adipose tissue inflammatory response and endothelial dysfunction in type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Interferon-gamma induced adipose tissue inflammation is linked to endothelial dysfunction in type 2 diabetic mice

et al. 2011

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“…The gut receives about 20-25% of the resting and up to 35% of the postprandial cardiac output [9,11], ranging among the most intensively perfused organs at rest. Seventy percent of the mesenteric blood flow is directed to the mucosal and submucosal layers of the bowel, with the remainder supplying the muscularis and the serosal layers.…”

Section: Physiology Of Intestinal Perfusionmentioning

confidence: 99%

“…The parallel arrangement of vessels in the villus permits countercurrent blood flows through the central arteriole and capillaries or venules being only 15 to 20 μm apart [11] (Fig. 3).…”

Section: Physiology Of Intestinal Perfusionmentioning

confidence: 99%

Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences

Vollmar

Menger

2010

Langenbecks Arch Surg

228

153

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“…However, the conclusions with regard to this relationship are conflicting (14)(15)(16)(17). The present study was designed to determine whether inhibition of gastric acid secretion by omeprazole has any effect on the regional blood flow in the gastrointestinal tract.…”

mentioning

confidence: 99%

Effects of Omeprazole on Gastric Mucosal Blood Flow in the Conscious Rat

Mattsson¹,

Larsson²

1987

Scandinavian Journal of Gastroenterology

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Regional blood flow in the gastrointestinal tract (forestomach, corpus, antrum, duodenum, jejunum, and colon) was determined in the conscious rat by means of the microsphere technique. The effects on blood flow were determined after omeprazole (orally and intravenously) and cimetidine (intravenously) during both basal and pentagastrin-stimulated gastric acid secretion. Under basal conditions neither omeprazole nor cimetidine decreased the blood flow in the gastrointestinal tract in spite of pronounced inhibition of acid secretion. On the contrary, there was a tendency towards an increased blood flow in the mucosal layer of the corpus after the oral (80 mumol/kg) and the high intravenous (10 mumol/kg) dose of omeprazole. When omeprazole was given intravenously to rats during pentagastrin-stimulated acid secretion, blood flow in the gastric mucosa was unaffected in spite of complete or almost complete inhibition of acid secretion. In contrast, cimetidine decreased the mucosal blood flow, indicating that the pentagastrin-induced increase in blood flow to some extent is mediated by H2 receptors.

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The Gastrointestinal Circulation

Cited by 93 publications

References 229 publications

Interferon-gamma induced adipose tissue inflammation is linked to endothelial dysfunction in type 2 diabetic mice

Interferon-gamma induced adipose tissue inflammation is linked to endothelial dysfunction in type 2 diabetic mice

Intestinal ischemia/reperfusion: microcirculatory pathology and functional consequences

Effects of Omeprazole on Gastric Mucosal Blood Flow in the Conscious Rat

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