Mechanism of production of intestinal secretion by elevated venous pressure.

Yablonski, Michael E.; Lifson, Nathan

doi:10.1172/jci108367

Cited by 86 publications

(28 citation statements)

References 32 publications

(35 reference statements)

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“…The mechanism of protein loss in the absence of ulceration is not clear. Obstruction of lymphatic flow by inflammation and fibrosis in the lamina propria may increase tissue fluid pressure, and it has been shown that increased tissue pressure changes the permeability of the intestinal epithelium allowing leakage of protein [25]. Fluid pressures within the mucosa would also be likely to increase due to activity of vasoactive amines produced during immediate hypersensitivity reactions as is said to occur in paratuberculosis in cattle [14].…”

Section: Discussionmentioning

confidence: 99%

Chronic Eosinophilic Gastroenteritis in the Horse

1982

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Abstract. Four cases of chronic eosinophilic gastroenteritis in horses are described. The disease was manifested clinically by weight loss, malabsorption and diarrhea or soft, formless feces. A chronic inflammatory reaction, with diffuse and focal eosinophilic infiltrates, was present in the esophagus, stomach, small and large intestine, and mesenteric lymph nodes. The cause of the lesion was not determined but was thought to be due to an ingested allergen, as the lesion is indicative of an on-going, immediate hypersensitivity reaction. One horse had generalized acanthosis, hyperkeratosis, and ulcerative coronitis.Chronic enteric disease in the horse, characterized by weight loss with or without diarrhea, has been reported in several countries [3, 5, 15, 17, 211. The enteric lesion in these horses was a chronic granulomatous inflammation. This paper describes a chronic eosinophilic enteritis that is pathologically distinct from the previously described chronic enteritides of horses. Materials and MethodsFour young-adult horses with signs of weight loss, diarrhea, or both (table I) were presented to Murdoch University Veterinary Hospital over an 18-month period. The horses were unrelated and from different areas of Western Australia. Routine clinical, hematological, biochemical, and fecal examinations were done. Glucose absorption tests [20] were done on all horses and full-thickness intestinal biopsies were removed from two horses. The horses either died or were killed. At necropsy, tissues from all visceral organs and skin from horse 4 were fixed in 10% neutral buffered formalin, processed routinely in paraffin, and stained with hematoxylin and eosin (HE). Selected tissues also were stained with the periodic acid-Schiff technique, Gram-Twort, Ziehl-Neelsen, Warthin and Starry, Castaneda's, and toluidine blue stains.Several sections of duodenum, jejunum, ileum, cecum, colon, and mesenteric lymph nodes from two horses were fixed in 3% glutaraldehyde in 0.1 mol/l phosphate buffer at pH 7.4, were post-fixed in 1% osmium tetroxide in the same buffer and embedded in epon. Sections for light microscopy were cut 1-pm thick and stained with toluidine blue. Thin sections were cut from selected areas and stained with uranyl acetate and lead citrate for examination by electron microscopy.Intestinal contents, mesenteric lymph node, and liver from all horses were cultured aerobically on sheep blood agar and McConkey's agar. Intestinal mucosa and mesenteric lymph node from horse 4 were homogenized in normal saline following removal of surface contam-486

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Section: Discussionmentioning

confidence: 99%

Chronic Eosinophilic Gastroenteritis in the Horse

1982

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“…The observed flux ratio is computed by (lumen-to-plasma flux):(plasma-to-lumen flux). The calculated flux ratio for passive ion movement is derived from the PD and ion concentration in plasma and lumen according to Ussing's equation (20). With limitations described in the text, a significant difference between observed and calculated flux ratio suggests active transport.…”

Section: Discussionmentioning

confidence: 99%

“…We have also examined histological sections and protein output to look for evidence of filtration as an additional cause of intestinal secretion (20)(21)(22) an electrical gradient for the passive secretion of cations, while development of a high concentration of ions at the site of secretion (within crypts or within villous unstirred layer) would promote osmotic flow of water from plasma to lumen. Inspection of Fig.…”

Section: Discussionmentioning

confidence: 99%

Intestinal Secretion Induced by Vasoactive Intestinal Polypeptide

Krejs¹,

Barkley²,

Read³

et al. 1978

J. Clin. Invest.

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A B S T R A C T The effect of vasoactive intestinal polypeptide (VIP) on intestinal water and electrolyte transport and transmucosal potential difference was investigated in the dog jejunum in vivo and compared to secretion induced by cholera toxin. Isolated jejunal loops were perfused with a plasma-like electrolyte solution. VIP (0.08 ug/kg per min) was administered directly into the superior mesenteric artery by continuous infusion over 1 h. From a dye dilution method, it was estimated that a mean plasma VIP concentration of 12,460 pglml reached the loops. VIP caused secretion of water and electrolytes; for example, chloride: control, 8 ,ueq/cm per h absorption; VIP, 92 ,eq/ cm per h secretion. A marked increase in transmucosal potential difference (control, -1.0 mV; VIP, -5.9 mV, lumen negative) occurred within 1 min after starting VIP infusion. Analysis of unidirectional fluxes showed increased plasma-to-lumen flux of sodium and chloride and decreased lumen-to-plasma flux of sodium. Chloride and bicarbonate were actively secreted against an electrochemical gradient. Although sodium secretion occurred down an electrochemical gradient, flux ratio analysis suggested a component of active sodium secretion. VIP caused a slight increase in protein output into the loops; light microscopy revealed capillary dilatation and closed intercellular spaces. The effect of VIP was readily reversible. Except for the delayed onset of secretion, the effect of cholera toxin was qualitatively similar to VIP; however, capillary dilatation and increased protein output were not noted with cholera toxin.

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“…Lifson (14) showed in dogs that elevations of venous pressure as low as 4-6 cm H 2 O caused "secretory filtration" by both providing a driving force for secretion and increasing the hydraulic permeability of the epithelium, without which the driving force would be ineffective. The resulting pores, which are reminiscent of those induced by TNF and LIGHT, are large enough for proteins to pass.…”

Section: Figurementioning

confidence: 99%

T cell activation altersintestinal structure and function

Field¹

2006

Journal of Clinical Investigation

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Treatment with anti-CD3 antibody (anti-CD3) causes transient diarrhea. In this issue of the JCI, Clayburgh et al. show that, in jejunum of mice injected with anti-CD3 or with TNF, fluid accumulation and changes in epithelial phenotype develop, the latter including an increase in the passive permeability to proteins, smaller solutes, and water and the endocytosis of the brush border Na + /H + exchanger, thereby inhibiting Na + absorption (a second cytokine, LIGHT, has the former effect, but not the latter) (see the related article beginning on page 2682). These phenotypic changes, by themselves, do not, however, explain increased fluid secretion. Since active anion secretion is not stimulated (in fact it is inhibited), a non-epithelial cell-mediated driving force must be present -most likely an increase in interstitial pressure due to an effect of TNF on capillary permeability, smooth muscle contractility, or both.

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Mechanism of production of intestinal secretion by elevated venous pressure.

Cited by 86 publications

References 32 publications

Chronic Eosinophilic Gastroenteritis in the Horse

Chronic Eosinophilic Gastroenteritis in the Horse

Intestinal Secretion Induced by Vasoactive Intestinal Polypeptide

T cell activation altersintestinal structure and function

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