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Results for “Microvessels”

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PubMed1986

[Features of the dynamics of blood flow in the microvessels of the brain and muscles of the rat].

Disruption of the erythrocyte flow occurred more frequently in microvessels of the brain (2-3/sec) than in those of muscles (1/sec), and the amplitude of the blood flow oscillations was greater in the former (150-450 mu/sec) than in the latter (0-300 mu/sec). Besides, the average blood flow velocity was greater in the brain microvessels (1830 +/- 680 mu/sec) than in those of muscles (1460 +/- 630 mu/sec), the diameter of the erythrocyte flow being about 5-8 mu in the former and about 10-13 mu in the latter. The differences seem to be due to different spatial organization of the microvessel beds.

Animals↗

PubMed1985

Hexitol production by canine retinal microvessels.

Hexitol-producing activity has been quantitated in microvessels isolated from retina and cerebral cortex of dogs, a species known to develop a retinopathy similar to that seen in diabetic patients. Both the retinal and cerebral microvessels produce galactitol from galactose, but at a rate several-fold less than that seen in canine lens epithelium. This hexitol-producing activity of the microvessels is not an artifact of erythrocyte contamination and can be inhibited by the aldose reductase inhibitor, Sorbinil.

Animals↗

PubMed1984

Chronic ethanol treatment changes the number of beta-receptors in rat brain microvessels.

The effect of chronic ethanol consumption on the binding (125I)-iodohydroxybenzylpindolol to beta-adrenergic receptors in rat brain microvessels has been studied. The results show that chronic ethanol treatment increases the number of beta-receptors present in brain microvessels without changing the binding affinity of the binding site for the beta-adrenoceptor ligand. This effect is apparently not associated with changes in peripheral adrenergic tone, since no differences in platelet epinephrine or norepinephrine concentrations were found between ethanol-treated and control animals. An increase in beta-receptor density in brain microvessels might contribute to the alterations of cerebral blood flow and oxygen consumption reported during chronic ethanol intoxication.

Animals↗

PubMed1984

[Mesenteric microvessel reactivity in rats in mesenteric shock].

Reactivity of rat mesenterial microvessels was studied during mesenterial shock. The development of the shock was discovered to involve two phases in the changes of microvascular reactivity. The sensitivity of microvessels to adrenaline was increased at the beginning of the shock whereupon it started descending. This phenomenon evidences that vasodilatation occurring at the late stages of the shock development is determined not only by a reduction in the concentration of endogenous adrenaline and noradrenaline but also by a decrease in the sensitivity of microvessels to these agents. The data obtained make it possible to explain the mechanism of steady vasodilatation in response to injection of exogenous adrenaline and noradrenaline, which is seen at the late stages of mesenterial shock.

Animals↗

PubMed1995

Mixed culture of pericytes and endothelial cells from fetal microvessels of the human placenta.

To explore the role of perivascular cells in angiogenesis and vasomotricity, placental cultures of perivascular cells were performed from calibrated villi excised from term placentas. Microvessels were isolated using repeated digestion of villi by collagenase-dispase and purification by Percoll gradients. Plated on Petri dishes, the microvessels became adherent to the gelatin matrix permitting to cells to proliferate. Cells were harvested and subcultured. Endothelial and pericyte cell lines were identified by phase contrast microscopy. Pericyte number predominated rapidly, the endothelial cells remaining visible. After seven days, cells started to cluster, thus piled up and built numerous nodules. Medium-size oval endothelial cells were stained by anti-von Willebrand factor and anti-IgG coupled to fluorescein. Large cells with irregular border reacted to smooth muscle anti-alpha-actin and anti-IgG coupled to fluorescein. There was no cross-reaction of these two cell types with the antibodies. In contrast, nodules were stained by both immunostainings. Endothelial cells reacting to von Willebrand factor antibody were frequently associated to the nodule. The isolation of microvessels from the human placenta described in this study allowed the establishment of cultures of endothelial cells and pericytes that show: i) rapid predominance of pericytes over endothelial cells, ii) formation of nodules, iii) participation of endothelial cells and pericytes to nodules formation.

Actins↗

PubMedDate not supplied

Phospholipid base-exchange in brain microvessels.

The capillary endothelium of cerebral microvessels plays an important role in homeostasis within the central nervous system. The flux of fluids and solutes takes place through the lipid matrix of plasma membranes and the maintenance of their structural composition is necessary for cell membrane permeability and the cellular transport systems. Few studies have been carried out to clarify the relationships between brain microvessel lipid metabolism and the role of this metabolism. We have studied a particular aspect of the phospholipid metabolism, i.e. their hydrosoluble head group exchange with free choline, ethanolamine or serine, in capillaries from brains of both 4 month- old and 24 month-old rats. The results obtained indicate that microvessels possess the biochemical machinery of base-exchange reaction, whose activity rate appears unaffected by age.

Aging↗

PubMed1994

Congestive gastropathy: factors influencing development, endoscopic features, Helicobacter pylori infection, and microvessel changes.

OBJECTIVES: To study 1) the factors influencing the development of congestive gastropathy (CG) in patients with portal hypertension (PHT), 2) the changes in gastric microvessels in patients with PHT with and without CG, and 3) to determine whether Helicobacter pylori plays any role in the pathogenesis of CG. METHODS: One hundred eighteen patients with PHT (102 cirrhosis, 16 noncirrhotic portal fibrosis) were evaluated by videogastroscopic examination. Antral biopsy tissue was examined for microvessel changes, histological gastritis, and H. pylori infection in 85 of 118 patients and 45 controls. Portal venous pressure (PVP) was determined by hepatic venous pressure gradient in 17 patients with CG. RESULTS: CG was present in 71 (60%) patients with PHT, of whom 41 (58%) had mild and 30 (42%) had severe CG. CG was observed with equal frequency in cirrhosis (63%) and noncirrhotic portal fibrosis (44%). The incidence of CG was higher in patients with severe liver disease, a past history of hemetemesis, in those with esophageal varices, and in those with gastric varices. Severe CG was commonly observed in patients with large size esophageal varices and in those with gastric varices. There was significant dilation of gastric mucosal vessels in patients with PHT, but in this regard there was no significant difference between patients with and without CG. The presence of H. pylori, histological gastritis, degree of PVP, or degree of capillary dilation did not influence the severity of CG. CONCLUSIONS: CG occurs commonly in patients with PHT, especially those with severe liver disease, past history of hemetemesis, and esophagogastric varices. Patients with PHT have significant gastric microvessel changes. The severity of CG appears to be independent of PVP, capillary dilation, H. pylori infection, or histological gastritis.

Adolescent↗

PubMed1994

[A quantitative observation of erythrocyte flow dynamics in microvessels of isolated rabbit mesentery].

Erythrocyte flow dynamics in microvessels was quantitatively observed with an isolated rabbit mesentery. The flow resistance in the microvascular bed was analyzed with respect to the thickness of a cell-free layer along the inner vessel wall and the suspension viscosity of erythrocytes (in terms of hematocrit and erythrocyte deformability). The thickness of cell-free layer increased with the increase in the inner diameter of microvessels, by lowering the hematocrit, and by increasing the erythrocyte velocity, but it was constant in capillary region. The thickness decreased by decreasing the erythrocyte deformability with diamide, while it increased by accelerating the erythrocyte aggregation with dextran. The flow resistance in the microvascular bed was not simply related to the thickness of a cell-free layer, but it was well correlated to the viscosity of erythrocyte suspension. In the flow pattern of erythrocytes, the maximum inner diameter of microvessel required to induce parachute-like deformation decreased by decreasing the erythrocyte deformability. Moreover, the flow of erythrocytes became inhomogeneous and intermittent by accelerating the erythrocyte aggregation.

Animals↗

PubMed1993

Differential activation of Th1 and Th2 CD4+ cells by murine brain microvessel endothelial cells and smooth muscle/pericytes.

CD4+ Th cell infiltration into the brain and the activation by cellular elements of the central nervous system (CNS) are thought to be important steps in the initiation of CNS autoimmune diseases. T cell activation requires Ag-specific stimulation and additional costimulatory signals provided by the APC. Here we describe how murine brain microvessel endothelial (En) cells and smooth muscle/pericytes (SM/P) selectively induce the Ag-specific activation of different Th1 and Th2 CD4+ T cell clones. Th1 and Th2 cell clones were used that were specific for the same peptide Ag in the context of the same class II allotype. SM/P preferentially activated Th1 cell clones, whereas En cells activated Th2 cell clones better, as reflected by cell proliferation and production of IL-2 by SM/P-activated Th1 clones and IL-4 by Th2 clones. There was no difference in the level of expression of CD4, CD2, or LFA-1 molecules between these Th cell clones, and anti-CD4, CD2, LFA-1 or ICAM-1 mAb did not differentially affect Ag-induced proliferation among the clones. Moreover, antibody to CD28 did not influence Ag presentation by brain microvessel En or SM/P cells to Ag-specific Th1 and Th2 clones. These results suggest that: 1) different The subsets might require different signals for their activation; 2) different APC might provide different costimulatory signals for Th cell subsets; and 3) brain microvessel En and SM/P might play a differential role in induction of autoreactive T cell responses in the CNS.

Animals↗

PubMed1996

Fibronectin overexpression in retinal microvessels of patients with diabetes.

PURPOSE: To examine whether fibronectin is synthesized in the adult human retina and whether diabetes alters its amount, level of expression, and pattern of splicing. METHODS: Retinas were obtained after death from 24 patients (age, 64 +/- 6 years) with 8 +/- 5 years of diabetes and 24 age-matched control subjects. Retinal localization of fibronectin and its amount in retinal vessels were examined with the immunoperoxidase technique. Fibronectin mRNA in the total retina was studied with reverse transcriptase-polymerase chain reaction using primers encompassing the alternatively spliced exon ED-A. The levels of fibronectin mRNA were measured relative to an internal standard (beta-actin mRNA). To detect and measure fibronectin expression in microvessels, retinal trypsin digests were studied by in situ hybridization. RESULTS: In the adult human retina, fibronectin is present exclusively in the walls of the vessels, including capillaries, and in the internal limiting membrane. In diabetic vessels, immunoreactive fibronectin was increased 1.4-fold over levels in control vessels (P = 0.05). Fibronectin is synthesized locally, and the predominant mRNA species excludes the ED-A region. The splicing pattern was not altered by diabetes. However, in the retinas of patients with diabetes, the levels of fibronectin mRNA were increased 1.3-fold over levels in control retinas (P = 0.028), whereas actin mRNA levels were similar in the two groups. Levels of fibronectin mRNA showed a substantial increase in the microvessels of patients with diabetes (0.49 +/- 0.18 grains/cell versus 0.15 +/- 0.12 grains/cell in control microvessels; P = 0.009. CONCLUSIONS: Fibronectin is synthesized in the adult human retina. Diabetes increases the amount of fibronectin in retinal vessels and upregulates its expression without changing the splicing pattern of the ED-A segment. Increased synthesis and deposition of fibronectin by microvascular cells may modify the interactions of cells and matrix with functional consequences relevant to the lesions of retinopathy.

Aged↗

PubMed1996

Increased brain tumor microvessel permeability after intracarotid bradykinin infusion is mediated by nitric oxide.

Nitric oxide (NO), a free radical gas implicated in a wide variety of biological reactions, is a novel signaling molecule that may regulate vasodilation, cerebral blood flow, and vascular permeability. This study was performed to determine whether NO mediates the selective increase in brain tumor microvessel permeability after intracarotid infusion of bradykinin in the RG2 rat glioma model. Intracarotid infusion of bradykinin selectively increased the transport of radiolabeled alpha-aminoisobutyric acid and dextran into brain tumors. Transport into normal brain was not increased. The administration of an NO synthase inhibitor, NG-nitro-L-arginine methyl ester, significantly inhibited the increased transport into tumors for both tracers. The inhibitory effect of NG-nitro-L-arginine methyl ester on the response to bradykinin was reversed by L-arginine. The expression of two NO synthase (NOS) isoforms in cultured RG2 glioma cell lines and intracerebral RG2 glioma was examined by immunohistochemistry and Western blot analysis. High levels of expression of neuronal NOS were detected in cultured and intracerebral RG2 cells but not in normal brain tissue, except in rare neuronal cells. The endothelial form of NOS was also expressed in cultured RG2 cells, but not as strongly as neuronal NOS expression. In intracerebral RG2 gliomas, expression of endothelial NOS in the tumor was detected at higher levels than in normal brain. These findings indicate that RG2 rat gliomas express high levels of NOS, which regulate the production of NO, compared with normal brain. We suggest that the selective permeability increase in brain tumor microvessels after bradykinin infusion is mediated by NO. Furthermore, the absence of high levels of NOS in normal brain may account for the attenuated permeability response to bradykinin in normal brain microvessels.

Aminoisobutyric Acids↗

PubMed1997

[The comparative morphology of the specific endothelial granules in the microvessels of the hypertrophied myocardium in patients with congenital heart defects and in experimental animals].

Specific endothelial granules of myocardial microvessels were studied in both patients, suffering from different congenital heart pathology, and dogs, before and during hyperthermia. In the intact myocardium of dogs we found two morphological varieties of granules, dark and light ones. The ultrastructural polymorphism of these granules was due presumably to hyperthermia. In cases of heart disease, a third morphological form of granules was revealed in the endothelium of myocardium microvessels in the hemodynamic overloaded heart compartments. These granules were larger and had a lighter matrix and a lesser amount of tubes. The granules are considered to be ultrastructural characters of structural reconstruction in the wall of hypertrophied myocardium microvessels at the endothelial level.

Animals↗

PubMed1998

The prognostic significance of microvessel density and thymidine phosphorylase expression in squamous cell carcinoma of the esophagus.

BACKGROUND: Squamous cell carcinoma (SCC) of the esophagus is among the most malignant of neoplasms and is associated with a dismal prognosis. Although tumor microvessel density (MVD) is an important prognostic factor in several carcinomas, its role in SCC of the esophagus is still controversial. Also, the role of thymidine phosphorylase (dThdPase), a key angiogenic growth factor, is yet to be delineated in this disease. METHODS: Immunohistochemical staining using monoclonal antibodies was used to quantify microvessel and dThdPase expression in archival tissue specimens from 93 patients with SCC of the esophagus. RESULTS: High dThdPase expression and high MVD were associated with tumor progression (size and stage) and lymph node metastasis, but only MVD was a predictor of survival. dThdPase expression was significantly correlated with depth of tumor invasion (P = 0.015). In multivariate analysis, MVD was an independent predictor of survival in the lymph node negative cases. A significant correlation was noted between MVD and dThdPase expression, with a correlation coefficient of 0.083 (P = 0.002). CONCLUSIONS: MVD is an independent factor in determining the prognoses of lymph node negative patients with SCC of the esophagus. dThdPase could be a key factor in the angiogenesis of this disease and may be responsible for its aggressive behavior.

Adult↗

PubMed1998

Involvement of vascular endothelial growth factor and urokinase-type plasminogen activator receptor in microvessel invasion in human colorectal cancers.

To evaluate the association among known angiogenic growth factors or factors related to the plasminogen activation system and clinicopathological factors in patients with colorectal cancer, we examined the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor-alpha (TGF-alpha), urokinase-type plasminogen activator (u-PA), u-PA receptor (u-PA-R) and plasminogen activator inhibitor-1 (PAI-1) in clinical specimens of colorectal cancers by Northern blot analysis. In comparison with the expression of these angiogenesis-related genes in 7 paired samples of colorectal cancers and the adjacent normal mucosa, VEGF mRNA level was significantly higher in the cancer tissues than in the adjacent normal mucosa (p < 0.05). We analyzed expression of these genes in 44 cases of primary colorectal cancers. Among the 3 angiogenic growth factors we examined, VEGF mRNA expression was significantly higher in the cancer tissues with blood vessel invasion or with lymphatic vessel invasion than in those without, respectively (p < 0.05). On the other hand, u-PA-R mRNA expression was significantly higher in the cancers with blood vessel invasion than in those without (p < 0.05). In addition, there was a correlation between the expression levels of VEGF and u-PA-R mRNA in the cancer tissues we have examined. Using immunohistochemistry, strong staining of VEGF or u-PA-R was observed in the cancer cells invading the microvessels. Our findings suggest that malignant transformation might accompany the upregulation of VEGF expression in colorectal cancers and that VEGF and u-PA-R might contribute cooperatively to increase angiogenesis around the tumor as well as the metastasis via microvessels.

Adult↗

PubMed1996

Effects of basic fibroblast growth factor on human microvessel endothelial cell migration on collagen I correlates inversely with adhesion and is cell density dependent.

Angiogenesis, new vessel growth from existing vessels, is critical to tissue development and healing. Much is known about the molecular and cellular elements of angiogenesis, such as the effects of growth factors and matrix molecules on proliferation and migration. However, it is not clear how these elements are coordinated to produce specific microvascular beds. To address this, the effects of basic fibroblast growth factor (bFGF) on beta 1 integrin-mediated adhesion relative to migration in human microvessel endothelial cells (HMVEC) was examined. Using two assays of migration that differ in the density of cells being examined, bFGF stimulated single cell migration and reduced cell migration from a confluent monolayer on collagen I. Adhesion to collagen I of HMVEC treated at low density (2-4 x 10(4) cells/cm2) with bFGF for 22 h was reduced, while bFGF increased cell adhesion of HMVEC treated at high density (6-8 x 10(4) cells/cm2). Adhesion of both bFGF-treated and untreated HMVEC was mediated by the beta 1 integrin matrix receptor. Basic FGF treatment did not significantly alter surface expression of the beta 1 integrin subunit. Reduction in bFGF-mediated adhesion correlated with delayed cell spreading and altered organization of beta 1 integrin into substrate contacts. Thus, integrin-mediated cell adhesion in microvessel endothelial cells is sensitive to regulation by a growth factor. Furthermore, the nature of the response to this signal depends on another cell regulator, cell density. In addition, modulation of cell adhesion by a growth factor may be a central regulatory feature in controlling endothelial cell migration.

Antibodies↗

PubMed2000

Prognostic value of DNA cytometry in 281 premenopausal patients with lymph node negative breast carcinoma randomized in a control trial: multivariate analysis with Ki-67 index, mitotic count, and microvessel density.

BACKGROUND: The clinical relevance of DNA image cytometry (ICM) and flow cytometry (FCM) remains under investigation in breast carcinoma. The objective of the current work was to study the prognostic value of DNA ICM and FCM in a series of patients randomized in a control trial. A multivariate analysis has been performed including other factors still under investigation such as Ki-67 index, mitotic count, microvessel density, and P53 and Bcl-2 expression. METHODS: Two hundred and eighty-one patients were randomized in the European Organization for Research and Treatment of Cancer 10854 trial comparing surgery followed by one course of perioperative chemotherapy versus surgery alone. Tumor parameters studied were pT, multicentricity, tumor grading according to modified Scarff-Bloom-Richardson, estrogen receptors, mitotic count per 1.7 mm(2), MIB-1, and BCL-2 scores, microvessel density, and p53 expression. ICM DNA parameters studied from paraffin embedded specimens, were DNA ploidy, proliferative index, 2c deviation index, malignancy grade, and Auer-Baldetorp typing. FCM DNA parameters analyzed on the same samples were ploidy and S-phase fraction statistics. The influence of tumor parameters, and DNA parameters on overall survival (OS), disease free survival (DFS), and metastasis-free survival (MFS) was evaluated using the Cox model. Median follow-up was 82 months. RESULTS: For OS, the prognostic parameters retained were pathologic tumor size (pT) and mitotic index (MI). Overall survival was 94% and 68% for tumors pT1/MI less than 10 and pT2-3 MI greater than or equal to 10, respectively. For DFS, age, multicentricity, and grading according to modified Scarff and Bloom were predicting factors with the same relative risk. Disease free survival was 96%, 78% and 68% respectively, when 1, 2, or 3 of those factors were present. For MFS, the only retained predicting factor was MI. MFS was 97% and 73% when MI was less than 10 and MI was greater than or equal to 10, respectively. CONCLUSIONS: Evaluation of proliferative compartment was the most important predicting factor for OS and MFS in the current series of premenopausal lymph node negative patients with breast invasive carcinoma. When working on paraffin embedded tissue, the best way of assessing it was MI count. ICM DNA analysis results were not selected in multivariate analysis. DNA analysis by FCM should be considered as an unsuitable technique when working on paraffin embedded tissue.

Aneuploidy↗

PubMed1990

Immunohistochemical study of cerebral amyloid angiopathy. III. Widespread Alzheimer A4 peptide in cerebral microvessel walls colocalizes with gamma trace in patients with leukoencephalopathy.

Brain tissue from 11 patients with cerebral amyloid angiopathy, changes of Alzheimer's disease, and variable degrees of subcortical leukoencephalopathy was examined by immunohistochemical methods, using primary antibodies to peptide segments representing portions of the Alzheimer A4 (beta-) peptide or gamma-trace peptide (seen most commonly in Icelandic patients with cerebral hemorrhage (hereditary cerebral hemorrhage with amyloidosis [HCHWA-I]). Variable A4 immunostaining was seen within cortical (and rarely white matter) parenchyma in the form of senile plaques (with or without central cores), and within capillary and arteriolar walls. Within individual patients, A4 deposits were often primarily parenchymal or vascular, and when they were vascular they tended to be more prominent in arteriolar than in capillary wall segments. Perivascular A4 deposits were often detected around strongly immunoreactive microvessels. Gamma-trace immunoreactivity was noted in many A4-positive microvessel walls, but staining was always less intense than with the anti-A4 antibody. We conclude that patients with severe cerebral amyloid angiopathy may show wide variation in the severity and topography of A4 deposits within brain parenchyma. A4 may colocalize with gamma-trace peptide, suggesting that A4 and gamma-trace forms of cerebral amyloid angiopathy may not be as biochemically distinctive as has been suggested. Other proteases or protease inhibitors may contribute to the pathogenesis of cerebral amyloid angiopathy or cerebral amyloid angiopathy-related stroke syndromes.

Amyloid↗

PubMed1992

Carnitine acetyltransferase activity in the human brain and its microvessels is decreased in Alzheimer's disease.

L-Carnitine and acetyl-L-carnitine facilitate mitochondrial beta-oxidation of fatty acids. In the brain, they may also have a role in acetylcholine synthesis. Carnitine acetyltransferase catalyzes the interchange between L-carnitine and acetyl-L-carnitine. Recently, acetyl-L-carnitine was reported to have a beneficial effect in patients with Alzheimer's disease. We therefore assessed carnitine acetyl-transferase activity in selected brain regions and in isolated cerebral microvessels obtained at autopsy from patients with Alzheimer's disease and from age-matched control subjects. We found a 25 to 40% decrease in carnitine acetyltransferase activity in patients with Alzheimer's disease, which attained statistical significance in most brain regions and in cerebral microvessels. These findings document another neurochemical abnormality in patients with Alzheimer's disease and provide a rationale for the use of acetyl-L-carnitine in the treatment of patients with Alzheimer's disease.

Aged↗