Two populations of sympathetic neurons project selectively to mesenteric artery or vein.
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The objective of this study was to determine whether sympathetic neurons of the inferior mesenteric ganglion (IMG) projecting to mesenteric arteries could be distinguished by their localization, neurochemical phenotype, and electrophysiological properties from neurons projecting to mesenteric veins. In an in vitro intact vasculature-IMG preparation, neurons were labeled following intraluminal injection of Fluoro-Gold or rhodamine beads into the inferior mesenteric artery (IMA) or vein (IMV). The somata of neurons projecting to IMA were localized in the central part of the IMG, whereas those projecting to IMV were localized more peripherally. None of the labeled neurons was doubly labeled. Neuropeptide Y immunoreactivity was found in 18.9% of neurons innervating the IMA, but not in neurons innervating the IMV. Identified neurons were dissociated and characterized using whole cell patch-clamp recording. After direct soma depolarization, all of the labeled arterial and venous neurons were classified as tonic firing, compared with only 40% of unlabeled neurons; the remaining 60% of unlabeled neurons were phasic firing. The results indicate that IMG neurons projecting to mesenteric arteries are distinct from neurons projecting to mesenteric veins. (+info)
Human eotaxin induces eosinophil extravasation through rat mesenteric venules: role of alpha4 integrins and vascular cell adhesion molecule-1.
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Eotaxin is a potent eosinophil-specific CC-chemokine, which has been shown to play a role in the selective induction of eosinophil accumulation in a number of allergic models of inflammation. Many aspects of the mechanism by which eotaxin induces eosinophil accumulation in vivo remain unresolved. In the present study, we investigated the direct effect of synthetic human eotaxin on leucocyte/endothelial cell interactions within rat mesenteric venules, as quantified by intravital microscopy. Topical eotaxin (30 pmol) induced rapid firm adhesion and extravasation of leucocytes within the rat mesentery, the extravasated leucocytes all being eosinophils, as determined by histological analysis. Whilst eotaxin was unable to stimulate the interaction of rat eosinophils with vascular cell adhesion molecule-1 (VCAM-1) under static conditions in vitro, eotaxin-induced responses in vivo were significantly suppressed by anti-alpha4 integrin and anti-VCAM-1 monoclonal antibodies (mAbs). The anti-alpha4 integrin mAb, HP2/1 (3.5 mg/kg), inhibited the eotaxin-induced firm adhesion and extravasation, 60 min postapplication of the chemokine, by 89% and 84%, respectively. In the same set of experiments, the anti-VCAM-1 mAb, 5F10 (3.5 mg/kg), inhibited leucocyte adhesion and extravasation by 61% and 63%, respectively. These results demonstrate that eotaxin-induced migration of eosinophils through rat mesenteric venules in vivo is dependent on an alpha4 integrin/VCAM-1 adhesion pathway, the significance of which may only be evident under flow conditions and/or following the ligation of other adhesion molecules expressed on eosinophils. (+info)
Segmental differentiations of cell junctions in the vascular endothelium. Arteries and veins.
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A systematic survey of endothelial junctions in elastic (aorta) and muscular (mesenteric) arteries and in medium (renal and mesenteric) and large (cava inferior) size veins has been carried out in the rat using freeze-cleaved preparations. The arterial endothelium is provided with a complex of occluding and communicating junctions (gap junctions) comparable to, though less elaborate than, that described in arterioles. The particles of the occluding junctions behave like "single unit" particles and have the tendency to remain on B faces upon membrane cleavage. In the venous endothelium the junctions take the form of long occluding junctions with few associated communicating junctions (maculae communicantes). As in arterial endothelium, the junctional particles appear preferentially on B faces in cleaved preparations. These structures, although continuous over long distances, are interrupted focally by areas in which the junctional elements are similar to those found in venules: the ridges and grooves are short, discontinuous, randomly distributed along the general line of cell contact, and often particle-free. In muscular arteries two unusual types of junctions are encountered. Both are disposed in loops over short distances along the perimeter of the cell. One type appears to be a strectched-out version of the usual combination of occluding and communcating junctions of the arterial endothelium (this type is also occasionally encountered in the venous endothelium). The other type is reminiscent of the septate junctions found in the epithelia of invertebrates but the apparent similarity remains to be checked by further work. (+info)
Phlebosclerosis of the colon with positive anti-centromere antibody.
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A 56-year-old woman with symptoms of chronic bowel disease presented a peculiar calcification of the mesenteric vein of the ascending to transverse colon on barium enema study. The resected colon was hard and black. Histo-pathologic examinations demonstrated fibrous change of the colon with a calcified and hyaline-deposited mesenteric vein. No cell infiltration was observed. These findings were compatible with phlebosclerosis and also with systemic sclerosis. Positive anti-centromere antibody and Raynaud's phenomenon, hallmarks of a variant systemic sclerosis, the CREST syndrome were observed. We therefore speculated that the pathogenesis of the phlebosclerosis of the colon is related to the CREST syndrome. (+info)
P-selectin expression by endothelial cells is decreased in neonatal rats and human premature infants.
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Decreased adhesion of neutrophils to endothelial cells and delayed transendothelial cell migration of neutrophils have been consistently reported in neonatal animals and humans and contribute to their susceptibility to infection. The delayed transmigration of neutrophils is especially prevalent in premature neonates. To define the nature of this defect, we used an in vivo animal model of inflammation and found that radiolabeled leukocytes from adult rats transmigrated into the peritoneum of other adult rats 5 times more efficiently than they did in neonatal rats (P =.05). This indicated that defects in neonatal neutrophils could not completely account for the delayed transmigration. Delayed transmigration in the neonatal rats correlated with a defect in the expression of P-selectin on the surface of their endothelial cells. We found a similar P-selectin deficiency in endothelial cells lining mesenteric venules and umbilical veins of human premature infants when compared with term human infants. The decreased P-selectin in premature infants was associated with decreased numbers of P-selectin storage granules and decreased P-selectin transcription. Decreased P-selectin expression on the surface of endothelial cells in preterm infants may contribute to delayed neutrophil transmigration and increased susceptibility to infection. (+info)
Resistance to praziquantel: direct evidence from Schistosoma mansoni isolated from Egyptian villagers.
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Recent evidence suggest that resistance to praziquantel (PZQ) may be developing. This would not be surprising in countries like Egypt where the drug has been used aggressively for more that 10 years. The classic phenotype of drug resistance is a significant increase in the 50% effective dose value of isolates retrieved from patients not responding to the drug. In a previous publication, we reported that such phenotypes have been isolated from humans infected with Schistosoma mansoni. Since the action of PZQ may be dependent upon the drug and host factors, most notably the immune system, we analyzed the quantitative effects of PZQ on single worms that differed in their response to PZQ when maintained in mice. Our hypothesis was that the in vitro action of the drug would correlate with it in vivo action. We confirmed this hypothesis and conclude that the in vitro action of the drug is related to its in vivo action. Knowing this relationship will assist in our ability to detect or survey for the PZQ resistant phenotype in human populations. (+info)
Superior mesenteric vein stenosis complicating Crohn's disease.
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BACKGROUND: Superior mesenteric vein stenosis as a consequence of mesenteric fibrosis, causing the development of small bowel varices, is an unrecognised association of Crohn's disease. CASE REPORTS: Two cases of gastrointestinal bleeding occurring in patients with Crohn's disease, and a third case, presenting with pain and diarrhoea, are described. In all three patients, visceral angiography showed superior mesenteric vein stenosis with dilatation of draining collateral veins in the small bowel. Overt gastrointestinal bleeding or iron deficiency anaemia resulting from mucosal ulceration is common in Crohn's disease, but acute or chronic bleeding from small bowel varices as a result of superior mesenteric vein stenosis due to fibrosis has not previously been reported. (+info)
Mesenteric and portal vein thrombosis in a young patient with protein S deficiency treated with urokinase via the superior mesenteric artery.
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A 32-year-old man, who was previously healthy, had acute abdominal pain without peritonitis. Diffuse mesenteric and portal vein thrombosis were shown by means of a computed tomography scan. A protein s deficiency was found by means of an extensive workup for hypercoagulable state. Successful treatment was achieved with urokinase infusion via the superior mesenteric artery without an operation. This represents an attractive alternative approach to treating patients with this disease. The previous standard of operative intervention(1) can now be reserved for complications, such as bowel infarction with peritonitis, or for those patients with absolute contraindications to thrombolytic therapy. (+info)