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The normal appearances of 14 peritoneal ligaments and mesenteries were demonstrated by magnetic resonance imaging (MRI). Antegrade or retrograde air introduction was employed to distend and mark the gastrointestinal tract. Delineation of these ligaments and mesenteries was helped by the presence of ascites and air-distended bowel loops. The different intraperitoneal compartments are also demonstrated.
A mast-cell activator, compound 48/80, causes proliferation of mesenchymal cells in the mesentery of rats. Its effect on W/Wv mice deficient in mast cells was tested to determine whether the proliferation is mediated in the degranulation of mast cells. Incorporation of [3H]thymidine into mesenchymal cells in the mesentery of these mice with or without compound 48/80 was very small compared to their normal litter mates. However, bone marrow transplantation markedly enhanced the effect of compound 48/80, and resulted in an incorporation of [3H]thymidine almost comparable to that observed in normal mice. Our results provide evidence that mesenchymal cell proliferation is caused by a product secreted by mast cells when stimulated by compound 48/80.
The mesentery preparation of normotensive rats (NR) (Pcarotis97 +/- 4 mm Hg) and of spontaneously hypertensive rats (SHR) (161 +/- 2 mm Hg) of comparable age (20 +/- 3 weeks) was used to study morphological changes of the microvasculature in established hypertension. The arterioles, classified according to their branching order, had an increased inner diameter in SHR (by 20%). The smooth muscle hypertrophy decreased with smaller vessel size. Pre- and postcapillary vessels were shorter in SHR than in NR by 17 to 35%. The number of these vessels related to the number of the feeding terminal arterioles was found to be reduced by nearly 50% in SHR. The data suggest a lowered arteriolar flow resistance in individual vessels of the hypertensive group concomitant with a gradually disappearing smooth muscle hypertrophy towards the capillary bed. The elevation of the resistance to blood flow in the hypertensive rats is obviously caused by a reduced number of resistance vessels, as seen in the mesentery vascular bed. Similar results were obtained in the true capillaries, which showed greater inner diameters (SHR vs NR:7.2 micron vs 6.4 micron), shortened lengths (141 vs 170 micron) and a reduced number (50 vs 70). Red cell velocity in true capillaries did not differ (0.51 mm/s vs 0.49 mm/s). Arterio-venous shunt vessels were described with an average inner diameter of 11 micron. In SHR these vessels were shorter (424 vs 654 micron) and increased in number. The 'hydraulic hindrance' of AV-shunt vessels and true capillaries together was decreased in SHR; the surface area did not differ between SHR (55.7 . 10(3) micron2) and NR (50.1 . 10(3) micron2) suggesting no major variation in the exchange functions.
The vasculature of rat isolated mesentery and small intestine was perfused with a gelatin-containing physiological salt solution (GPSS). When 5-hydroxytryptamine (5HT, 1 x 10(-4) M), or the calcium ionophore A23187 (1 x 10(-4) M), or 12-deoxyphorbol 13-phenylacetate (DOPPA, 1 x 10(-6) M), or 12-deoxyphorbol 13-phenylacetate 20-acetate (DOPPAA, 1 x 10(-6) M) or thymeleatoxin (TMX, 1 x 10(-6) M) was added to the GPSS for 5 min there was a gradual rise in perfusion pressure, whereas resiniferatoxin (RFX, 1 x 10(-6) M) was without effect. Pre-treatment of the tissue with the protein kinase C (PKC) inhibitor Ro 31-8220 (1 x 10(-6) M) significantly reduced the rise in perfusion pressure in response to 5HT, DOPPA, DOPPAA and TMX, but not that to A23187. Platelet-activating factor (PAF, 5 x 10(-6) M) caused an almost immediate but transient rise in perfusion pressure, followed by a more gradual rise, neither response being blocked by Ro 31-8220. When blood vessels of the mesentery alone were perfused with gelatin-free PSS, PAF caused a transient rise in perfusion pressure, but with no subsequent gradual rise over 5 min. After Ca(2+)-depletion this transient response was also absent. In contrast, when blood vessels were perfused with gelatin-free PSS, DOPPA and TMX still caused gradual rises in perfusion pressure, which were totally abolished by Ro 31-8220. TMX had no effect at all when the tissue was depleted of Ca2+, whereas the response to DOPPA was only partially reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
Cystic lymphangioma of the small-bowel mesentery is a rare manifestation of an intraabdominal tumor in elderly patients. We present a case of a small-bowel mesentery lymphangioma, causing fever and chills and present clinical and pathologic features. Furthermore, etiology and differential diagnosis of this tumor are discussed.
BACKGROUND: Peritoneal involvement by Wilms' tumor indicates stage III disease. CT is the single preferred modality in determining the extent and staging of Wilms' tumor; however, the CT appearances of Wilms' tumor involvement of the peritoneum have not been specifically addressed in the literature. OBJECTIVE: The objective of this study was to demonstrate the CT manifestations when there is involvement of the peritoneum, mesentery and/or omentum in Wilms' tumor. MATERIALS AND METHODS: Four cases of Wilms' tumor form the basis of this report. They were examined on Elscint CT scanners. RESULTS: Masses ("dropped metastases") in the pelvis were present in all four patients. Three patients had masses in the mesentery of the small bowel and sigmoid colon. Infiltration of the greater omentum was identified in two patients as a mantle of tumor separating bowel from the anterior abdominal wall. Ascites was present in two patients. In one patient broad-based solid masses of varying sizes were noted on the parietal and on the visceral surfaces of the peritoneum, and in a different patient a discrete mass was noted in the lesser omentum. CONCLUSION: The peritoneal spaces, recesses, ligaments and folds are invisible unless invaded by disease which is well demonstrated on CT.
The peritoneum is the largest and most complexly arranged serous membrane in the body. The potential peritoneal spaces, the peritoneal reflections forming peritoneal ligaments, mesenteries, omenta and the natural flow of peritoneal fluid determine the route of spread of intraperitoneal fluid and, consequently, disease processes within the abdominal cavity. The peritoneal ligaments, mesenteries and omenta also serve as boundaries for disease processes and conduits for disease spread. The peritoneal cavity and its reflections are frequently involved by infectious, inflammatory, neoplastic and traumatic processes. Before the introduction of cross-sectional imaging, the peritoneum and its reflections could only be imaged with difficulty, often requiring invasive techniques. Computed tomography and, to a lesser extent, sonography and MR imaging allow the accurate examination of the complex anatomy of the peritoneal cavity, which is the key to understanding the pathological processes affecting it. This article reviews the normal peritoneal anatomy and its disease processes.
Cystic tumors of the retroperitoneum, omentum, and mesentery are extremely rare lesions. We report a case of one such lesion in the mesentery of the left hemicolon that was mistaken on imaging to be an ovarian tumor. Development of this tumor at this site has been described only twice before in the literature.
A malignant rhabdoid tumor is very rare and its prognosis is extremely poor. It was first described as a distinctive and highly malignant neoplasm of the infant kidney. Tumors with a similar appearance have been reported in various extrarenal sites. We herein report a case of a 41-year-old man who was admitted to our hospital complaining of a lower abdominal mass. After one series of examinations, the patient underwent a laparotomy. Most such tumors are situated in the mesentery and involve the small intestine, and thus we diagnosed it to originate from mesentery. This tumor could not be resected and only an excisional biopsy was done. It was histologically composed of a solid sheet arrangement with ovoid, round, and lateralized nuclei and mild acidophilic cytoplasm. Inclusion body-like structures were found in the cytoplasm. Immunohistochemically, the tumor cells were positive for cytokeratin, epithelial membrane antigen, vimentin, and CAM5.2. The patient died 2 weeks after operation due to multiple organ failure.
Two newborn infants with duodenal and jejunal atresia and agenesis of the dorsal mesentery represent our surgical experience with "apple peel" small bowel or "christmas tree" demormity. The first patient had the typical appearance of this condition. The postoperative course was complicated by hyperbilirubinemia, septicemia, and disseminated intravascular coagulation. The infant is in satisfactory condition 1.5 years after operation. The second patient had agenesis of the dorsal mesentery without spiraling of the bowel around its vascular stalk. The child died after 1 month, with complete absence of extrahepatic bile ducts as seen at a second laparotomy. Neither child had been subjected to gastrostomy.
In the perfused rat mesentery, when adrenergic nerves were blocked with guanethidine and vascular smooth muscle tone was increased with methoxamine, transmural field stimulation caused a dilator response. Bradykinin significantly suppressed vasodilator responses to a transmural field stimulation in a concentration-dependent manner. After pretreatment with saponin to damage endothelial cells, bradykinin still suppressed vasodilator responses to transmural field stimulation. The effect of bradykinin was unaltered by indomethacin. N omega-Nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis, abolished the inhibition of vasodilator responses to transmural field stimulation elicited by bradykinin. However, in the presence of L-arginine and L-NAME the inhibitory effect of bradykinin reappeared. Furthermore, methylene blue itself caused potentiation of vasodilator responses to transmural field stimulation and reversed the effect of bradykinin. These findings suggest that bradykinin can produce an inhibitory modulation of the actions of sensory nerves in the perfused rat mesentery and that the effect of bradykinin may be mediated by nitric oxide released from non-adrenergic, non-cholinergic nerves.
Rat cytokine-induced neutrophil chemoattractant (CINC) is a member of the IL-8 family, and its human counterpart is gro/MGSA but not IL-8. We ascertained that chemically synthesized CINC was comparable to native CINC/gro with regard to chemotactic activity for rat neutrophils and studied the effect of synthesized CINC/gro on circulating leukocytes in microvascular vessels of rat mesentery. Exposure of rat mesentery to 10(-8)M authentic CINC/gro induced neutrophil adherence to and extravasation from postcapillary venules (PCVs) but not from capillaries or arterioles. CINC/gro concentrations as low as 10(-10) M were effective in causing neutrophil adherence. Neutrophils adhered to thin PCVs (mean diameter, approximately 25 microns) after exposure to CINC/gro for 15 min. The mean diameters of the PCV with adherence of neutrophils after exposure to CINC/gro for 30 and 60 min were 37 and 43 microns, respectively. The diameters of PCV with extravasation of neutrophils also increased in a time-dependent manner. The starting position of adherence of neutrophils was approximately 25-50 microns away from the upper junction of two vessels and remained virtually unchanged during exposure to CINC/gro for 60 min. However, the distance from the start to the end of neutrophil adherence increased in a time-dependent manner. The effect of CINC/gro on adherence and extravasation of leukocytes was neutrophil specific since other leukocytes such as lymphocytes and monocytes were not identified among the adherent and extravasated leukocytes.
Epidermal growth factor (EGF) has been reported to stimulate healing of wounds in skin, cornea, and gastric mucosa. In the present study, we further investigate the effect of endogenous and exogenous EGF in healing of connective tissue wounds using the rat perforated mesentery model. Healing of mesenteric perforations is accomplished by the connective tissue fibroblasts since there are no interfering variables such as interactions of epithelial cells, desiccation, or foreign materials such as sutures or subcutaneous implants. We performed laparotomy in 114 adult male Sprague-Dawley rats and made 20 standardized perforations in the mesentery of each rat with a scalpel. Rats were randomly assigned to five groups. Group I received no treatment after surgery; Group II received intraperitoneal injections of phosphate-buffered saline (PBS) after surgery and then twice daily for the following 3 days; Group III received 10 micrograms of EGF in the PBS injections according to the same regimen as Group II; Group IV had sham exploration of the submandibular salivary glands; and Group V animals had excision of the submandibular glands 3 days before laparotomy to deprive the main source of EGF in rat. On Days 4 through 10 after surgery rats were sacrificed and the percentage of perforations in each rat which were closed was determined. The curves for the time course of wound closure for Groups IV and V were not different indicating that endogenous submandibular EGF does not play a role in healing of mesenteric wounds.(ABSTRACT TRUNCATED AT 250 WORDS)
Prejunctional effects of opioids were examined in the perfused mesentery of two species: the rat and rabbit. Use of agonists selective for subtypes of mu, delta, and kappa opioid receptors produced no effect on contractile responses to adrenergic nerve stimulation in the rat perfused mesentery, except for small effects of the kappa agonist EKC, which may be non specific. In contrast, mu, delta and kappa receptors appear to be present in the rabbit. The mu selective agonist, DAMGO, kappa agonist, ethylketocyclazocine, and delta agonists, DPDPE and [Leu5]-enkephalin, all produced significant inhibition of contractile responses to transmural nerve stimulation. The inhibitory effect was greatest for ethylketocyclazocine. To test the possibility that prejunctional activation of alpha 2 adrenoceptors with endogenous norepinephrine might decrease the activity of prejunctional opioid receptors in the rabbit, inhibitory effects of delta and kappa selective agonists were tested in the presence of 10(-7) M yohimbine. Inhibitory responses of the kappa selective agonist ethylketocyclazocine were enhanced, while that of delta selective agonists [Leu5]-enkephalin and DPDPE remained unchanged when yohimbine was present. Thus, the effects of opioids vary and depend on the tissue and receptor subtypes they act upon. Furthermore, the enhanced inhibitory effect of opioid receptor activation in the presence of yohimbine is not found for all opioid receptors.
Injuries to the bowel and mesentery are found in approximately 5% of all patients undergoing laparotomy after blunt abdominal trauma. Bowel and mesenteric injuries are often subtle and difficult to diagnose, and a delay in the diagnosis is associated with increased mortality and morbidity. CT is the best imaging method for diagnosing injuries to the bowel and mesentery. With meticulous scanning techniques, most significant bowel and mesenteric injuries can be reliably identified with CT preoperatively, and associated injuries to other abdominal viscera can be confirmed.
Opioids, alpha(2)-adrenoceptor agonists and blockers of voltage-gated calcium channels (VGCCs) have been attributed antinociceptive activity in various experimental set-ups. The present study tested the ability of morphine, clonidine and drugs acting at various VGCCs to inhibit the transmission of noxious stimuli from the mesentery at the level of the spinal cord. In rats under barbiturate anaesthesia traction of 20 g was applied to a bundle of mesenteric blood vessels. This caused immediate transient changes of mean arterial pressure that were taken as indication of nociception. Similar reflexes were elicited by applying 0.6% acetic acid to the same bundle of vessels. The reflexes were dose-dependently reduced by intrathecal administration of morphine or clonidine, but were left unaltered by intrathecal administration of verapamil, Bay-K 8644 or omega-conotoxin MVIIA. Neither verapamil nor Bay-K 8644 influenced clonidine-induced analgesia. Conotoxin markedly enhanced the effectiveness of all doses of clonidine against both types of mesenteric stimuli. Verapamil, Bay-K 8644, as well as conotoxin reduced the ability of morphine to inhibit mechanically evoked reflexes, while there was no statistically significant effect in chemonociception. These data suggest that, at the spinal level, both morphine and clonidine are effective drugs to decrease the cardiovascular changes caused by acute mesenteric pain. In the dorsal spinal cord neither L-type nor N-type VGCCs are responsible on their own for the transmission of noxious stimuli from the mesentery. Inhibition of N-type channels markedly augments the action of clonidine, whereas blocking either VGCC seems to inhibit antinociceptive mechanisms induced by morphine. It is suggested that in patients the combined administration of clonidine with omega-conotoxin MVIIA might lead to effective pain control with reduced side effects.
We present two cases of malignant fibrous histiocytoma (MFH) of the mesentery. A whorled internal structure observed on sonogram and large feeding and draining vessels demonstrated on color Doppler sonogram in these cases were worth noticing. When sonography reveals an abdominal tumor with such findings, although very rare, the possibility of a MFH of the mesentery must be considered. We also review briefly the literature.
1. The main objective of this study was to analyse the role and mode of action of the mast cell mediator histamine in leukocyte-endothelium interactions in small venules in vivo. For this purpose, we used a histological approach (combined with intravital microscopy) that allows studies of rapid mediator-induced venular leukocyte accumulation, reflecting leukocyte rolling, in the undisturbed microcirculation of the rat mesentery where rolling is normally absent. 2. We first examined the relative importance of histamine and 5-hydroxytryptamine (5-HT) in acute mast cell-dependent leukocyte recruitment. The mast cell secretagogue compound 48/80 (i.p. for 15 min) induced a marked venular accumulation of polymorphonuclear leukocytes (PMNL) which was almost abolished by combined histamine1 (H1)- and histamine2 (H2)-receptor blockade. In contrast, the 5-HT-receptor antagonist methysergide was inactive in this regard. Moreover, exogenous 5-HT was less active than exogenous histamine in evoking venular PMNL accumulation (histamine response dose-dependent; 5-HT response bell shaped). Prostaglandin D2 did not cause PMNL accumulation. 3. The venular PMNL response to exogenous histamine peaked between 15 min and 1 h, was still significantly elevated at 2 h, and then returned to prechallenge values after 3 h. At all time points, the histamine-induced PMNL accumulation was nearly abolished by i.v. treatment with the polysaccharide fucoidin (which blocks rolling but not firm adhesion per se), suggesting that the PMNL response to histamine was due to rolling rather than firm adhesion over the entire 3 h period. At no time point did histamine trigger accumulation of mononuclear leukocytes (MNL). 4. To examine the role of histamine-receptors in the histamine-induced PMNL accumulation (i.e. rolling), the animals were pretreated with diphenhydramine (H1-receptor antagonist), cimetidine, or ranitidine (H2-receptor antagonists). Diphenhydramine alone inhibited the venular PMNL response to histamine by 52%, while both H2-receptor antagonists were completely inactive. However, the combination of cimetidine and diphenhydramine reduced the histamine-induced PMNL rolling by 82%. Furthermore, in contrast to an H3-receptor agonist, challenge with either the H1-receptor agonist 2-thiazolylethylamine or two different H2-receptor agonists (impromidine, dimaprit) was sufficient to provoke significant venular PMNL accumulation. 5. Treatment with the nitric oxide-synthase inhibitor L-NAME did not affect the histamine-induced PMNL rolling. On the other hand, 3 h pretreatment with dexamethasone reduced the PMNL response to histamine by 73%, and flow cytometric analysis showed that the dexamethasone treatment almost completely inhibited binding of soluble P-selectin to rat isolated PMNLs. 6. We conclude that initial leukocyte recruitment after mast cell activation in the rat mesentery is critically dependent on histamine release. The cellular response to histamine was specifically due to PMNL rolling, involved activation of both H1- and H2-receptors, and lasted for 2 3 h. Moreover, the histamine-induced PMNL rolling was not dependent on nitric oxide synthesis, but was sensitive to glucocorticoid treatment, possibly via inhibition of expression or function of leukocytic P-selectin ligand(s).