Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MESENTERIES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Morphological aspects and observations about the permeability of the rat mesentery to the lanthanium Nitrate. Some comparisons with the morphology of the human mesentery.

A review in the classic literature showed that many authors were interested about the permeability and structure of the mesentery. With the evolution of new techniques, this subject came back in different research areas. The purpose of this paper concentrates in the study of the permeability of the mesentery and of other small intestine layers of the rat to the lanthanium nitrate. Some comparisons are also made with the morphology of the human mesentery. Human and rat mesentery were used in different methods, and an ultrastructural study was performed. However, in all techniques employed in our paper, we could not observe a single area of the basement membrane that was penetrated by the lanthanium nitrate. We may conclude that the penetration of the lanthanium nitrate is impeded by the basement membrane and that this penetration is also impeded in the intercellular space of the mesothelial layer by the presence of a basal lamina, which is continuous with the basement membrane, as we can see in some of our sections.

Animals↗

Potassium permeability of the mesothelium of the frog mesentery.

The mesothelium of the mesentery is a single cell layer described to offer no or every little hindrance to diffusion of small water soluble solutes. We have measured the potassium permeability of the mesothelium of the frog mesentery both in vivo and in vitro. The permeability measured in vivo--using K+--sensitive microelectrodes is 2.4 X 10(-5) cm s-1. In vitro measurements using conventional tracer flux technique on isolated mesentery yields a K+-permeability of 5.7 X 10(-5) cm s-1. These values are 15--30 times smaller than values previously reported from in vitro experiments on rat and rabbit mesentery. Also, the permeability is 12--15 times lower than the K+-permeability of the capillary wall determined on single capillaries in the frog mesentery. In the frog mesentery the mesothelium thus represents an important diffusion barrier compared to the capillary wall. This may be critical in experiments where filtration and reflexion coefficients of the capillaries are determined from measurements of fluid exchange across the capillary wall in response to application of hypertonic solutions on the surface of the mesentery.

Animals↗

Distinct roles for the SgIGSF adhesion molecule and c-kit receptor tyrosine kinase in the interaction between mast cells and the mesentery.

Intraperitoneal injection of bone marrow-derived mast cells (BMMCs) has therapeutic efficacy against acute bacterial peritonitis. For this role, BMMCs need to settle down the mesentery from the peritoneal cavity. Interaction between BMMCs and the mesentery was examined by using mast cell deficient WBB6F1(F1)-W/Wv [c-kit receptor tyrosine kinase (KIT) mutant], F1-Sl/Sld [KIT ligand stem cell factor mutant], and F1-tg/tg [a practically microphthalmia transcription factor (MITF)-null mutant] mice. Three parameters were measured: the number of BMMCs: (1) developed in the mesentery 5 weeks after intraperitoneal injection into mast cell deficient mice, (2) adhered to mesenteric mesothelial cells, and (3) transmigrated across the mesenteric mesothelial cell monolayer when coculturing both cells for 3 and 18 h, respectively. After intraperitoneal injection, F1-wild type (+/+) BMMCs developed in the mesentery of F1-W/Wv mice but not in that of F1-Sl/Sld mice, while F1-tg/tg BMMCs did not develop, even in the mesentery of WBB6F1-W/Wv mice. In the coculture, WB-W/W BMMCs normally adhered to but poorly transmigrated across F1-+/+ mesothelial cells, and in accordance, F1-+/+ BMMCs normally adhered to but poorly transmigrated across F1-Sl/Sld mesothelial cells. F1-tg/tg BMMCs showed poor adhesion and transmigration, but both parameters were partially but significantly improved by ectopic expression of spermatogenic immunoglobulin superfamily (SgIGSF), a mast-cell adhesion molecule critically regulated by MITF. Since F1-tg/tg BMMCs expressed reduced levels of KIT, these results suggested that SgIGSF and KIT independently played a significant role in the transmigration. Among three parameters, development of mast cells in the mesentery well correlated with the transmigration. This process seemed important for mast cells to settle down from the peritoneal cavity to the mesentery.

Animals↗

Characterization of endothelium-dependent relaxations in mesenteries from transgenic hypertensive rats.

Endothelial dysfunction has been reported to be a feature of hypertension. We have investigated the relative contributions of nitric oxide (NO) and the endothelium-derived hyperpolarizing factor (EDHF) to endothelium-dependent relaxations in isolated mesenteries from (mREN-2)-27 transgenic hypertensive (TGH) rats and their normotensive controls (Hannover Sprague-Dawley). Relaxation to the endothelium-dependent relaxant, carbachol, was unimpaired in mesenteries from TGH rats compared to the Hannover Sprague-Dawley controls. Inhibition of NO synthase (with 100 microM Nomega-nitro-L-arginine methyl ester) had greater inhibitory effects against these relaxations in the mesenteries from Hannover Sprague-Dawley compared to TGH. Inhibition of EDHF activity with high K+ also had greater inhibitory effects against endothelium-dependent relaxations in the mesenteries from the Hannover Sprague-Dawley compared to TGH. The present results show that, although endothelium-dependent relaxation is unimpaired in mesenteries from TGH rats, there are differences in the relative contributions of NO and EDHF, such that inhibition of either NO or EDHF alone in TGH mesenteries has less impact compared to Hannover Sprague-Dawley. It is suggested that the recently identified reciprocal relationship between NO and EDHF is upregulated in the mesenteries from the TGH rats.

Animals↗

Solitary neurofibroma of the mesentery: report of a case and review of the literature.

Neurofibromas of the gastrointestinal tract are usually associated with neurofibromatosis type 1 (Nfl), or they are exclusive manifestations of the so-called "familial intestinal neurofibromatosis". Gastrointestinal neurofibromas can rarely occur as sporadic lesions in the jejunum and stomach, and only exceptionally in the mesentery. A critical review of the literature revealed that only seven cases of solitary neurofibromas (SNFs) of the mesentery (six in the ileal mesentery; one in the gastrocolic mesentery) have been reported in patients without stigmata of Nf1. We report the clinicopathologic features of an additional case of SNF of the ileal mesentery, incidentally found in a patient with an advanced gastric carcinoma. Since there is increasing evidence that some patients may have some features of Nf1, including dermal or nodular SNFs alone - limited to one or more body segments - (segmental Nf1), the possibility that SNFs of the mesentery may also represent a segmental manifestation of Nf1 is postulated.

Adenocarcinoma↗

Hyperplasia of the mesenterial windows precedes that of the small gut in the streptozotocin-diabetic rat.

Hyperplastic growth of the mesenterial windows abutting the small gut occurs in lactating rats (Bergström and Norrby 1988) and chronically diabetic rats (Norrby et al. 1983). In the present study, early events in the mesenterial windows and the small gut in streptozotocin-diabetic rats were examined. The area of the mesenterial windows had already increased significantly on day 1 and hyperplasia in terms of increased DNA content, as well as an increase in histamine content (a mast-cell marker), was established from day 2 of diabetes. The increase in total mesenterial window content of DNA, histamine and protein was roughly linear and parallel from day 2 to day 19. The small-gut circumference increased transiently on day 1, but the small-gut mucosal volume was unaffected on days 1 and 2. The small-gut wet weight increased significantly from day 5, whereas elongation was not observed until day 19. The difference in time between the appearance of hyperplasia and the growth of the mesenterial windows and their adjoining gut and the rate with which the hyperplasia proceeds in the two tissues indicate that the regulatory mechanisms of early hyperplastic growth in these tissues are not identical. The factor(s) causing mesenterial window growth and hyperplasia is/are as yet unknown.

Animals↗

Simultaneous measurement of pressure in the interstitium and the terminal lymphatics of the cat mesentery.

1. Simultaneous measurements of the pressure in terminal lymphatics and interstitial tissue have been made in the exteriorized cat mesentery superfused with either physiological salt solution (Krebs solution) or a water-immiscible fluorocarbon, FC-80. 2. The pressures within individual terminal lymphatics were measured using glass micropipettes attached to a servo pressure-measuring system. Tissue pressures were recorded using saline-filled cotton-wool wicks. 3. Mean pressure recorded in the terminal lymphatics of the Krebs-superfused mesentery were slightly above atmospheric (+0.2 mmHg, n = 45), while those recorded in the FC-80-superfused mesentery were slightly below atmospheric (-0.2 mmHg, n = 46). 4. Tissue pressures were also slightly subatmospheric in the in situ mesentery, and the recently exposed tissue. Continuous superfusion with Krebs solution caused the tissue pressure to rise to atmospheric pressure or above; with FC-80-superfusion the tissue pressure also rose, but never to above atmospheric pressure. 5. Isolated strips of mesentery immersed in Krebs solutions of different concentrations gained weight, but when immersed in FC-80 no change in weight was detected. 6. It was concluded that the interstitial gel of the mesentery is normally unsaturated and that superfusion with Krebs solution leads to tissue oedema. This tendency is less marked in FC-80-superfused preparations. Possible mechanisms for lymph formation and propulsion are discussed.

Animals↗

Strain differences in the facilitatory action of angiotensin on noradrenergic transmission in the rat mesentery.

The isolated perfused rat mesenteric vasculature preparation was used to assess the contributions of presynaptic as well as postsynaptic mechanisms in the adrenergic potentiating action of angiotensin II in different rat strains. Angiotensin II (3 ng/ml; 2.5 x 10(12) M) potentiated vasoconstrictor responses to periarterial nerve stimulation in mesentery obtained from Sprague-Dawley (SD) rats by 102.5 +/- 6.2% (p less than .05) but did not significantly affect responses in mesentery from Wistar (W) rats. Responses to nerve stimulation were increased in W rats by 22.6 +/- 12.9% (p less than .05) at higher concentrations of angiotensin II (10 ng/ml; 8.5 x 10(12) M). The facilitatory actions of angiotensin II on nerve stimulation responses were antagonized by saralasin. Angiotensin II (2.5 or 8.5 x 10(12) M) had little or no effect on responses to norepinephrine in mesentery from either SD or W rats. Blockade or neuronal and extraneuronal uptake potentiated the effects of angiotensin II on the responses to nerve stimulation in mesentery from W rats but not in mesentery from SD rats. The data suggest that angiotensin II increases norepinephrine release during nerve stimulation in mesentery obtained from SD and W rats. However, due to differences in the ability of the two strains of rats to compensate for the effect through increased neurotransmitter reuptake, the net effect on nerve stimulation responses is a large increase (100-110%) in SD rats as opposed to only a slight increase (15-20%) in W rats.

Angiotensin II↗

A comparison of micro- and macrocirculation of the isolated rat mesentery preparation.

To allow a comparison of microcirculatory perfusion and whole organ blood flow, pressure-flow curves were established in the isolated rat mesentery preparation at two different hematocrit values (5%; 35 +/- 4%). Besides whole organ volume flow, red blood cell (RBC) flow velocity in capillaries of the mesentery membrane, and RBC-flux in fat tissue along the mesentery arteries as well as in small intestine were simultaneously measured. The arterio-venous pressure difference over the tissue was varied from 20-100 mmHg (2.7-13.3 kPa). It could be shown, that the pressure-flow curves in the mesentery membrane as well as in fat demonstrate autoregulation over a pressure range of 30-70 mmHg (4-9.3 kPa), whereas flow through the small intestine and whole organ responded passively to pressure changes. At constant pressure differences an increase in hematocrit value from about 5% to 35 +/- 4% reduced whole organ blood flow as well as flow velocity in capillaries of the mesentery membrane by 50% over the pressure range applied. It is concluded that in a heterogeneous tissue like the isolated rat mesentery preparation the pressure-flow-relationship in tissue components with a low flow fraction might be disparate from that of the whole organ volume flow. Furthermore, despite differences in the pressure flow relationship for the whole and microcirculation, a changed blood viscosity can be quantified in both circulations.

Adipose Tissue↗

Lengthening of the mesentery using the marginal vascular arcade of the right colon as the blood supply to the ileal pouch.

PURPOSE: Creation of a safe ileal pouch requires a tension-free anastomosis. The aim of this study was to evaluate a technical procedure that increases the length of the mesentery while preserving the blood supply to the ileal pouch. HYPOTHESIS: Preservation of the marginal vascular arcade (MVA) of the right colon will allow ligation of more mesenteric vessels and increase the mesenteric length. METHODS: Six fresh cadavers were dissected. Measurement of the apex of the terminal ileum was done in relation to the pubic symphysis. Measurements were taken after 1) complete mobilization of the terminal ileum, right colon, and hepatic flexure; 2) vascular ligation between colon wall and the MVA, preserving the latter from the right branch of the middle colic artery to the ileal branch of the ileocolic artery (ICA); 3) ligation of the distal third of the superior mesenteric artery; 4) ligation of the ICA at its origin; 5) ligation of the right colon artery; and 6) division of the terminal ileal mesentery. RESULTS: This technique enabled complete division of the terminal ileal mesentery, adding a mean additional 3.6 (range, 2.5 - 5.0) cm (36.5 +/- 16.5 percent) in length to the mesentery, compared with superior mesenteric artery, ICA, and right colic artery ligation. CONCLUSION: Patients who have a shorter mesentery and concern of excessive mesenteric tension should have colectomy performed, preserving the MVA from the middle colic artery to the ileal branch of the ICA. The preserved MVA can be a reliable alternative blood supply to the pouch if more mesenteric vessel ligations are necessary.

Anastomosis, Surgical↗

Partial abdominal evisceration, ex vivo resection, and intestinal autotransplantation for the treatment of pathologic lesions of the root of the mesentery.

BACKGROUND: Resection of lesions of the root of the mesentery with established techniques is difficult and at times impossible because of their proximity to the blood supply of the intestine. Damage of the superior mesenteric vessels necessitates resection of the intestine, resulting in short bowel syndrome and intestinal failure. STUDY DESIGN: We describe a surgical technique drawn from our experience in intestinal transplantation in which the root of the mesentery (including the lesion) and the head or the entire pancreas, duodenum, small intestine, and part of the colon are excised en bloc and preserved in a cold solution. Resection of the lesion is performed in a bloodless field ex vivo, and the salvaged intestine is reimplanted in the abdominal cavity. We performed this procedure in four patients, two adult and two pediatric, who had extensive neoplasms of the root of the mesentery. Their underlying diseases were mesenteric fibroma, vascular dysplasia of the root of the mesentery, pancreatic cancer, and desmoid tumor. RESULTS: Local control of the lesions was achieved in all four cases, preserving at the same time enough small intestine to avoid short bowel syndrome. All patients survived the operation and live on enteral nutrition 6 to 49.5 months after the procedure. CONCLUSIONS: The procedure of partial abdominal exenteration, ex vivo resection, and autotransplantation is an extension of our experience with intestinal transplantation. In selected cases, this technique may be useful in the treatment of extensive, otherwise unresectable lesions of the root of the mesentery.

Abdominal Pain↗

Expression of hydrophilic surfactant proteins by mesentery cells in rat and man.

Human peritoneal dialysis effluent (PDE) contains a phosphatidylcholine-rich compound similar to the surfactant that lines lung alveoli. This material is secreted by mesothelial cells. Lung surfactant is also characterized by four proteins essential to its function. After having long been considered as lung-specific, some of them have been found in gastric and intestinal epithelial cells. To explore further the similarity between lung and peritoneal surfactants, we investigated whether mesothelial cells also produce surfactant proteins. We used rat transparent mesentery, human visceral peritoneum biopsies and PDE. Surfactant proteins were searched for after one- and two-dimensional SDS/PAGE and Western blotting. On a one-dimensional Western blot, bands at 38 and 66 kDa in rat mesentery, and at 38 and 66 kDa in human peritoneal mesothelial cells (in vivo and in vitro) and PDE, corresponded to monomeric and dimeric forms of lung surfactant protein A (SP-A). On two-dimensional Western blots, the 32 and 38 kDa spots in mesentery and PDE localized at the acidic pH appropriate to the SP-A monomer's isoelectric point. SP-D was also identified at the same 43 kDa molecular mass as in lung. SP-B was not detected in mesenteric samples. Expression of SP mRNA species was also assessed by reverse transcriptase-PCR, which was performed with specific primers of surfactant protein cDNA sequences. With primers of SP-A and SP-D, DNA fragments of the same size were amplified in lung and mesentery, indicating the presence of SP-A and SP-D mRNA species. These fragments were labelled by appropriate probes in a Southern blot. No amplification was obtained for SP-B. These results show that mesentery cells produce SP-A and SP-D, although they are of embryonic origin (mesodermal) and are different from those of the lung and digestive tract (endodermal) that secrete these surfactants.

Animals↗

Induction by endotoxin of nitric oxide synthase in the rat mesentery: lack of effect on action of vasoconstrictors.

1. Male Sprague-Dawley or Wistar rats were injected with bacterial lipopolysaccharide (LPS; 5 mg kg-1, i.p.) and killed after 1, 3, 6, 15, and 24 h. The brains, mesenteries, spleens, lungs, livers, kidneys, hearts, aortae and diaphragms were removed and frozen immediately. Control rats were injected with sterile saline and killed after 6 h. 2. The organs were homogenized in a semi-frozen state and NO synthase (NOS) activity measured in tissues from both LPS-treated and saline-treated groups by the ability of homogenates to convert [3H]-L-arginine to [3H]-L-citrulline in a NADPH-dependent manner. 3. The NOS activity in all organs taken from control animals was found to be calcium-dependent, with the highest activity being in the brain. After LPS-treatment an induced calcium-independent NOS was detected in all tissues tested, with the exception of the brain. The spleen, lung, mesentery and liver had the highest amounts of LPS-induced NOS activity. No induction of calcium-dependent NOS was detected. 4. Induction of NOS was maximum 6 h after administration of LPS and had returned to control levels in 24 h. 5. The constitutive NOS in brain and mesentery and the LPS-induced activities in the spleen, lung, liver and mesentery were inhibited by NG-monomethyl-L-arginine (L-NMMA) or NG-nitro-L-arginine methyl ester (L-NAME) according to concentration. The IC50 for L-NAME was 2.5 microM against the constitutive NOS from brain, and 20-25 microM against the inducible NOS. For L-NMMA the IC50 was 20-25 microM against either NOS isoform. 7. The vascular responses to endothelin-I (ET-1), the thromboxane A2-mimetic 11 alpha,9 alpha-epoxymethanoprostaglandin F2alpha (U46619), phenylephrine (PE) or 5-hydroxytryptamine (5-HT) were measured in the simultaneously perfused arterial and venous mesenteric vascular beds from both control and LPS-treated(6 h) rats. Vasoconstrictor responses to all agonists tested were unaffected by LPS treatment. In the presence of L-NAME (100 microM) vasoconstrictor responses were potentiated in both the arterial and venous portion of the mesenteric beds from both control and LPS-treated rats. The potentiation of responses to U46619 was significantly greater in beds from LPS-treated rats.8. Injection of LPS i.p. is associated with induction of NOS in all organs tested, except for the brain. In the mesentery this is not accompanied by a hyporesponsiveness to constrictor agents suggesting an increased sensitivity, particularly to U46619. This may explain the poor perfusion and tissue damage in the splanchnic circulation associated with sepsis.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

On mast cell-mediated mitogenesis in normal and hyperplastic mesenterial windows in female rats.

The outcome of the mast cell-mediated mitogenesis in hyperplastic membranous mesenterial windows of lactating rats as well as in normal mesenterial windows of age-matched and young virgin female rats was studied quantitatively in vivo and in organ culture. Besides elucidating the effect of age and tissue hyperplasia on mitogenic responsiveness, this approach should provide some insight into the pathogenic mechanics of the previously reported supranormal mast cell-mediated mitogenic reaction that emerges in similarly hyperplastic mesenterial windows of diabetic rats. Mast cell secretion was elicited by Compound 48/80 and the histamine release, which was quantified fluorometrically, was unaffected by lactation. The young female rats showed a statistically significant mast cell-dependent mitogenesis taken as the mitotic index and the fraction of the predominating fibroblasts and mesothelial cells in the (S+G2) cell cycle phases after Feulgen-DNA absorption analysis of the cells in situ. Although there was an age-dependent decrease in mitogenesis, the older lactating and non-lactating virgin control rats also showed mast cell-mediated mitogenesis measured as the specific DNA activity. The hyperplastic mesenterial tissue of the lactating animals showed a virtually normal mitogenic reactivity following local mast cell secretion, but at a lower level than in the age-matched controls. This finding suggests that the supranormal mast cell-mediated mitogenesis previously found in the hyperplastic mesenterial windows of diabetic animals is causally related to the diabetic condition rather than to the hyperplastic state of the test tissue.

Animals↗

Anatomic CT demonstration of the peritoneal spaces, ligaments, and mesenteries: normal and pathologic processes.

Computed tomography (CT) has become increasingly useful in the detection of intraabdominal disease. Owing to the widespread use of CT, it is essential that radiologists have a thorough understanding of the peritoneal spaces and the ligaments and mesenteries that form their boundaries. The majority of ligaments and mesenteries in the abdomen are formed from remnants of the ventral and dorsal mesenteries, which suspend the primitive gut. Unlike the abdominal ligaments, the pelvic ligaments are mainly formed by reflections of peritoneum over the pelvic organs or structures. The mesenteries and ligaments form the boundaries of the peritoneal spaces; this knowledge aids in localizing fluid collections, allowing the differential diagnosis to be narrowed. The ability to localize fluid collections accurately is also important if percutaneous or surgical drainage is to be performed. In addition, neoplasms can be more accurately staged when the pathway of spread through adjacent ligaments and mesenteries is understood.

Abdomen↗

Segmental misty mesentery: analysis of CT features and primary causes.

PURPOSE: To review the computed tomographic (CT) features of segmental misty mesentery (SMM) in 29 patients and assess the primary causes of this CT finding. MATERIALS AND METHODS: The authors analyzed the medical records and CT features of SMM in 29 patients. CT images were evaluated for the site, thickness, and vascular changes of the involved mesentery; bowel wall changes; lymphadenopathy; and the fat ring sign. The primary cause of SMM in five patients was determined at histopathologic examination, that in three patients was determined at surgical observation of the mesentery, and that in nine patients was determined on the basis of follow-up CT and clinical data. The primary cause of SMM in 12 patients was unknown. RESULTS: Twenty-five of the 29 patients had various underlying diseases. Fourteen (48%) patients had a malignancy: 11 had intraabdominal cancer and three had extraabdominal cancer. Jejunal mesentery was more commonly involved than was ileal mesentery (P <.05). The mean thickness of the SMM was 4.0 cm. Mesenteric vessels were dilated in 27 patients (93%): 19 with venous dilatation and eight with either arterial dilatation only or both arterial and venous dilatation. At CT, seven (24%) patients had a thickened bowel wall; nine (31%) patients, lymphadenopathy; and two (7%) patients, the fat ring sign. The primary cause of SMM was edema in eight, malignant neoplasm in four, inflammation and/or fibrosis in five, and idiopathic in 12 patients. CONCLUSION: At CT, SMM appears as a result of malignant neoplasms, inflammation, or vascular disorders.

Adolescent↗