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At least 631 records · Page 35Linked to original sources
PubMed1997

Follicular dendritic cell tumor of the mesentery.

Follicular dendritic cell (FDC) tumor is an exceedingly rare malignant neoplasm and occurs mainly in the cervical lymph nodes. We report a mesenteric FDC tumor occurring in a 66-year-old female, that manifested with intraabdominal multifocal recurrence 7 years after resection of the primary tumor. Histologically, both primary and recurrent tumors were composed of oval to spindle cells with paley eosinophilic cytoplasms, indistinct cell borders, round to elongated nuclei with clear or finely dispersed chromatin, and medium to large nucleoli. Characteristically, the tumor cells were growing in sheets, fascicles, and sometimes in whorls and a storiform pattern. In addition, focal necrosis, nuclear pleomorphism and abnormal mitoses were also observed. The neoplastic cells were intimately admixed with small lymphocytes. The diagnosis was confirmed by positive immunoreactivity with CD21 and CD35 antibodies and by ultrastructural demonstration of convoluted interdigitating cell processes connected by scattered desmosome-like junctions. Although our case showed a low proliferative activity evaluated by MIB-1, multifocal recurrence has occurred. The clinicopathologic features and differential diagnosis of FDC tumors are discussed with the review of the literature.

Aged↗
PubMed1997

Evidence that the substance P-induced enhancement of pacemaking in lymphatics of the guinea-pig mesentery occurs through endothelial release of thromboxane A2.

1. In vitro studies were performed to examine the mechanisms underlying substance P-induced enhancement of constriction rate in guinea-pig mesenteric lymphatic vessels. 2. Substance P caused an endothelium-dependent increase in lymphatic constriction frequency which was first significant at a concentration of 1 nM (115 +/- 3% of control, n = 11) with 1 microM, the highest concentration tested, increasing the rate to 153 +/- 4% of control (n = 9). 3. Repetitive 5 min applications of substance P (1 microM) caused tachyphylaxis with tissue responsiveness tending to decrease (by an average of 23%) and significantly decreasing (by 72%) for application at intervals of 30 and 10 min, respectively. 4. The competitive antagonist of tachykinin receptors, spantide (5 microM) and the specific NK1 receptor antagonist, WIN51708 (10 microM) both prevented the enhancement of constriction rate induced by 1 microM substance P. 5. Endothelial cells loaded with the Ca2+ sensing fluophore, fluo 3/AM did not display a detectable change in [Ca2+]i upon application of 1 microM substance P. 6. Inhibition of nitric oxide synthase by NG nitro-L-arginine (L-NOARG; 100 microM) had no significant effect on the response induced by 1 microM substance P. 7. The enhancement of constriction rate induced by 1 microM substance P was prevented by the cyclooxygenase inhibitor, indomethacin (3 microM), the thromboxane A2 synthase inhibitor, imidazole (50 microM), and the thromboxane A2 receptor antagonist, SQ29548 (0.3 microM). 8. The stable analogue of thromboxane A2, U46619 (0.1 microM) significantly increased the constriction rate of lymphangions with or without endothelium, an effect which was prevented by SQ29548 (0.3 microM). 9. Treatment with pertussis toxin (PTx; 100 ng ml-1) completely abolished the response to 1 microM substance P without inhibiting either the perfusion-induced constriction or the U46619-induced enhancement of constriction rate. 10. Application of the phospholipase A2 inhibitor, antiflammin-1 (1 nM) prevented the enhancement of lymphatic pumping induced by substance P (1 microM), without inhibiting the response to either U46619 (0.1 microM) or acetylcholine (10 microM). 11. The data support the hypothesis that the substance P-induced increase in pumping rate is mediated via the endothelium through NK1 receptors coupled by a PTx sensitive G-protein to phospholipase A2 and resulting in generation of the arachidonic acid metabolite, thromboxane A2 this serving as the diffusible activator.

Androstanes↗
PubMed2002

ATP-induced endothelium-independent enhancement of lymphatic vasomotion in guinea-pig mesentery involves P2X and P2Y receptors.

1. The present study has investigated mechanisms underlying ATP-induced endothelium-independent enhancement of vasomotion in guinea-pig mesenteric lymphatic vessels. 2. Lymphatic vasomotion, vessel tone and smooth muscle [Ca(2+)](i) showed similar ATP concentration-response curves. 3. ATP, at 0.1 mM, caused a biphasic increase in tonic [Ca(2+)](i) and superimposed vasomotion-associated Ca(2+) transients. All ATP-induced [Ca(2+)](i) changes were abolished by incubating the smooth muscle with suramin (0.1 mM). 4. alpha,beta-MeATP (0.1 mM) and UTP (0.1 mM) caused similar changes in [Ca(2+)](i) but the responses to these agonists were smaller than to ATP. 5. The actions of alpha,beta-MeATP (0.1 mM) were inhibited by suramin (0.1 mM) and PPADS (30 micro M) but not by reactive blue 2 (30 micro M). 6. In the presence of alpha,beta-MeATP (0.1 mM), the increases in tonic [Ca(2+)](i) and vasomotion-associated Ca(2+) transients induced by ATP (0.1 mM) were inhibited by U73122 (5 micro M), CPA (20 micro M) and heparin, whereas U73343 (5 micro M) and pre-treatment with PTx (100 ng ml(-1)) had no significant effects. 7. Depletion of the intracellular stores with CPA (20 micro M) caused an increase in [Ca(2+)](i), which was not blocked by desensitization of P(2X) receptors with alpha,beta-MeATP. 8. The data indicate that ATP, at relatively high concentrations increases lymphatic smooth muscle [Ca(2+)](i) and vasomotion through activation of P(2X1) and P(2Y2) purinoceptors present on lymphatic smooth muscle. The increase in [Ca(2+)](i) is likely to result from Ca(2+) release from inositol-1,4,5-trisphosphate-sensitive stores as well as Ca(2+) influx through store-operated channels and P(2X)-gated channels.

Adenosine Triphosphate↗
PubMed2003

ET-1-associated vasomotion and vasospasm in lymphatic vessels of the guinea-pig mesentery.

In vitro experiments were performed to investigate the actions of endothelin-1 (ET-1) on vasomotion and vasospasm in guinea-pig mesenteric lymphatics. ET-1 modulated lymphatic vasomotion independent of the endothelium, with lower concentrations ( or=100 nm) causing vasospasm. ET-1-induced increases in vasomotion were accompanied by an increase in tonic [Ca2+]i. These actions were inhibited by the ETA receptor antagonist BQ-123 (1 microm), the phospholipase C (PLC) inhibitor U73122 (5 microm), removal of extracellular Ca2+, chelation of intracellular Ca2+ with BAPTA/AM (10 microm), the store Ca2+-ATPase inhibitor thapsigargin (1 microm), caffeine (10 mm) and the inositol 1,4,5-trisphosphate (IP3) receptor blocker heparin and 2-APB (30 microm). In contrast, the ETB receptor antagonist BQ-788 (1 microm), ryanodine (1 & 20 microm), pertussis toxin (PTx) or Cs+ had no significant actions on vasomotion or the magnitude of increase in tonic [Ca2+]i. ET-1-induced vasospasm was accompanied by a transient increase in smooth muscle [Ca2+]i followed by a sustained plateau, an action that was abolished by removal of extracellular Ca2+, but only marginally inhibited by nifedipine (1 microm). Caffeine (10 mm), SKF 96165 (30 microm) or U73122 (5 microm) together with nifedipine (1 microm) abolished ET-1-induced vasospasm and increase in [Ca2+]i. These results indicate that ET-1 increases lymphatic vasomotion by acting on smooth muscle ETA receptors and activation of G-protein-PLC-IP3 cascade, which is known to cause pacemaker Ca2+ release and resultant pacemaker potentials. High concentrations of ET-1 cause a failure in Ca2+ homeostasis causing vasospasm, triggered by excessive Ca2+ influx primarily through store-operated channels (SOCs) with l-Ca2+ voltage-operated channels (VOCs) also contributing, but to a much lesser extent.

Animals↗
PubMed2002

Extravascular transport of fluorescently labeled albumins in the rat mesentery.

OBJECTIVE: Fluorescently labeled albumin is used frequently as a tracer when monitoring microvascular permeability. Several fluorescent dyes are available for labeling protein, including fluorescein isothiocyanate (FITC) and Texas Red (TR). Because differences in leakage of dye-labeled proteins have been reported, the objective of the present study was to compare the accumulation of these two tracers in interstitium and lymph after the inflammatory event of ischemia-reperfusion. METHODS: Anesthetized rats were injected intravenously with FITC-labeled albumin (FITC-alb) and TR-labeled albumin (TR-alb) before 30 minutes of mesenteric ischemia. Because the tracers leaked out of the microcirculation after reperfusion, accumulation in the surrounding buffer-superfused tissue, and in separate experiments, accumulation in lymph vessels, was defined as the ratio of tissue-to-plasma and lymph-to-plasma fluorescence. RESULTS: Reperfusion induced a significant increase in tissue-to-plasma fluorescence of FITC-alb; however, no increase was observed for TR-alb. In contrast, lymph-to-plasma fluorescence of TR-alb tended to be greater than FITC-alb. Reperfusion-induced increases in tissue-to-plasma fluorescence of TR-alb occurred only when the superfusate was replaced with mineral oil, in which case tissue-to-plasma TR-alb fluorescence tended to be greater than FITC-alb. CONCLUSIONS: Measurement of fluorescently labeled albumin leakage from mesenteric venules depends on the dye used to label the albumin and requires an assessment of losses from the extravascular measuring region.

Albumins↗