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  • 1
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 27 (2000), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Chronic inflammation is associated with blood vessel remodelling, including vessel proliferation and enlargement, and changes in vessel phenotype. We sought to characterize these changes in chronic airway inflammation and to determine whether corticosteroids that inhibit inflammation, such as dexamethasone, can also reduce microvascular remodelling.2. Chronic airway inflammation was induced in C3H mice by infection with Mycoplasma pulmonis and the tracheal vessels were examined in whole mounts after Lycopersicon esculentum lectin staining.3. Neither the number nor the length of vessels changed in C3H mice after infection with M. pulmonis. Instead, vessel diameter and endothelial cell number doubled.4. Immunoreactivity for P-selectin, a marker of venular endothelial cells, also increased after infection, indicating that the proportion of venules doubled with a corresponding decrease in capillaries.5. Whereas the average diameter of tracheal capillaries doubled in mice inoculated 10 days earlier (mean (±SEM) diameter in infected and pathogen-free mice of 20.8±1.6 and 9.0±0.7 μm, respectively), dexamethasone treatment (0.2 mg/day, i.p.) for 7 days beginning 4 days after infection significantly decreased capillary diameter (13.0±0.7 μm). The treatment also decreased the immunoreactivity for P-selectin and the number of adherent leucocytes (595±203 vs 2024±393 cells/ mm 2 in treated and non-treated infected mice, respectively).6. We conclude that microvascular enlargement and changes in vessel phenotype are features of some types of chronic inflammation and, furthermore, that dexamethasone reverses the microvascular enlargement, changes in vessel phenotype and leucocyte influx associated with chronic inflammatory airway disease.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Exaggerated levels of VEGF (vascular endothelial growth factor) are present in persons with asthma, but the role(s) of VEGF in normal and asthmatic lungs has not been defined. We generated lung-targeted VEGF165 transgenic mice and evaluated the role of VEGF in T-helper type 2 cell (TH2)-mediated ...
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature America, Inc.
    Nature biotechnology 17 (1999), S. 14-14 
    ISSN: 1546-1696
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: [Auszug] Dr. McDonald is a Professor of Anatomy and Investigator of the Cardiovascular Research Institute at the University of California, San Francisco. He received his M.D. and Ph.D. degrees from UCSF. Dr. McDonald's research focuses on endothelial cell biology in health and disease with an ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature medicine 9 (2003), S. 713-725 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Advances in imaging are transforming our understanding of angiogenesis and the evaluation of drugs that stimulate or inhibit angiogenesis in preclinical models and human disease. Vascular imaging makes it possible to quantify the number and spacing of blood vessels, measure blood flow and vascular ...
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Pathological increases in vascular leakage lead to edema and swelling, causing serious problems in brain tumors, in diabetic retinopathy, after strokes, during sepsis and also in inflammatory conditions such as rheumatoid arthritis and asthma. Although many agents and disease processes increase ...
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0568
    Keywords: Mast cells ; Globule leukocytes ; Rats ; Trachea ; Compound 48/80 ; Dexamethasone ; Histochemistry ; Naphthol AS-D esterase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Globule leukocytes in the epithelium of the rat trachea may be counterparts of mucosal mast cells that are located in the gastrointestinal tract. If they are indeed similar to mucosal mast cells, globule leukocytes would be expected to decrease in number in rats treated with dexamethasone but not in rats treated with compound 48/80, an agent which causes non-antigenic degranulation of connective tissue mast cells. In this study, we determined the number and compared the distribution of globule leukocytes and connective tissue mast cells in the tracheas of pathogen-free rats. We then determined whether the number of these two types of cells changes in rats treated for 5 days with compound 48/80, dexamethasone, a combination of compound 48/80 and dexamethasone, or saline. We identified globule leukocytes and mast cells in whole mounts and histological sections of rat tracheas by using a histochemical reaction that demonstrates the chymotrypsin-like protease (chloroacetate esterase) present in mast cell granules. Using this method, we found that aproximately 225000 globule leukocytes were present in the epithelium of the trachea. These cells were most abundant in the rostral trachea. Rats treated with dexamethasone had a 91% reduction in the number of globule leukocytes with protease-containing granules, but rats treated with compound 48/80 had a normal number of these cells. We found some 55000 connective tissue mast cells in the same tracheas. Mast cells were most abundant in the posterior membrane of the caudal trachea and in the lamina propria between cartilaginous rings. Rats treated with compound 48/80 had a 96% reduction in mast cells with protease-containing granules, but rats treated with dexamethasone had a normal complement of mast cells. We conclude that globule leukocytes are abundant in the tracheas of healthy rats, are similar in morphology and pharmacological responses to mucosal mast cells located in other organs of rats, and are more numerous than and have a different distribution than connective tissue mast cells. Globule leukocytes in the tracheal epithelium may have a role in respiratory defenses similar to that of mucosal mast cells in other organs.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0568
    Keywords: Capsaicin ; Mucous cells ; Mycoplasmas ; Neurogenic inflammation ; Serous cells ; Trachea ; Vascular permeability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In rats respiratory tract infections due to Sendai virus and coronavirus usually are transient, but they can have long-lasting consequences when accompanied by Mycoplasma pulmonis infections. Morphological alterations in the tracheal epithelium and a potentiation of the inflammatory response evoked by sensory nerve stimulation (“neurogenic inflammation”) are evident nine weeks after the infections begin, but the extent to which these changes are present at earlier times is not known. In the present study we characterized these abnormalities in the epithelium and determined the extent to which they are present 3 and 6 weeks after the infections begin. We also determined the magnitude of the potentiation of neurogenic inflammation at these times, whether the potentiation can be reversed by glucocorticoids, and whether a proliferation of blood vessels contributes to the abnormally large amount of plasma extravasation associated with this potentiation. To this end, we studied Long-Evans rats that acquired these viral and mycoplasmal infections from other rats. We found that the tracheal epithelium of the infected rats had ten times as many Alcian blue-PAS positive mucous cells as did that of pathogen-free rats; but it contained none of the serous cells typical of pathogen-free rats, so the total number of secretory cells was not increased. In addition, the epithelium of the infected rats had three times the number of ciliated cells and had only a third of the number of globule leukocytes. In response to an injection of capsaicin (150 μg/kg i.v.), the tracheas of the infected rats developed an abnormally large amount of extravasation of two tracers Evans blue dye and Monastral blue pigment, and had an abnormally large number of Monastral blue-labeled venules, particularly in regions of mucosa overlying the cartilaginous rings. This abnormally large amount of extravasation was blocked by dexamethasone (1 mg/day i.p. for 5 days). We conclude that M. pulmonis infections, exacerbated at the outset by viral infections, result within three weeks in the transformation of epithelial serous cells into mucous cells, the proliferation of ciliated cells, and the depletion of globule leukocytes. They also cause a proliferation of mediator-sensitive blood vessels in the airway mucosa, which is likely to contribute to the potentiation of neurogenic inflammation that accompanies these infections.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-119X
    Keywords: Connexin ; Endothelial cell ; Cardiac valve ; Shear stress ; Size
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: AbstractEndothelial expression of the gap junction proteins, connexin (Cx) 37, Cx40, and Cx43, varies within the vascular network. While previous studies suggest that shear stress may upregulate Cx43, it is not well understood if shear stress affects the expression of all endothelial connexins and to what extent. Endothelial cells on the upstream and downstream surfaces of cardiac valves are subjected to considerably different intensities of shear stress. We therefore reasoned that we could determine the extent hemodynamic forces affect the expression of Cx37, Cx40, and Cx43 by comparing their immunohistochemical distribution on the upstream and downstream surfaces of rat cardiac valves. We found 70- to 200-fold greater expression of Cx43 in the endothelial cells on the upstream than on the downstream surfaces. However, Cx37 was expressed almost equally in the endothelial cells on upstream and downstream surfaces, and Cx40, a major connexin in most vascular endothelial cells, was not detected on either surface. In addition to the heterogeneity in Cx43 expression, endothelial cells on the upstream surface were 35% to 65% smaller than those on the corresponding downstream surface. These results suggest that shear stress may affect endothelial cell size and Cx43 expression but not Cx37 expression.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study addresses the question of whether increased vascular permeability, which is a prominent feature of neurogenic inflammation in the respiratory tract, is mediated by sensory axons that end near venules in the airway mucosa. In these experiments, neurogenic inflammation was produced in the tracheal and bronchial mucosa of atropine-treated Long-Evans rats by electrical stimulation of the left or right superior laryngeal nerve and/or cervical vagus nerve. The particulate tracer Monastral blue was injected intravenously to localize the sites of increased vascular permeability, and microspectrophotometry was used to measure the amount of extravasated Monastral blue in the trachea and thereby quantify the increase in vascular permeability. In some rats, selective denervations were made to locate the cell bodies of neurons that mediate the increase in vascular permeability; in others, fluorescence immunohistochemistry and quantitative electron microscopic methods were used to determine which structures in the tracheal mucosa are innervated by these neurons. The study revealed that the vagally mediated increase in vascular permeability was sudden, transient (half-life=2.4 min) and restricted to venules. Stimulation of the left or right superior laryngeal nerve increased the permeability of venules in the extrathoracic trachea, whereas stimulation of either vagus nerve increased vascular permeability in the intrathoracic trachea and bronchi. All nerves had bilateral effects in the trachea, but the vagus nerves had largely unilateral effects in the bronchi. Neurons that mediated the increase in venular permeability had their cell bodies in the jugular (superior sensory) ganglion of the vagus nerve or rostral portion of the nodose (inferior sensory) ganglion. Preganglionic autonomic vagal neurons in the brain stem were not essential for this increase in venular permeability. Few nerves identifiable by substance P-immunohistochemistry or electron microscopy were located near the affected venules, and no nerves were within 1 μm of the walls of venules. However, the epithelium and arterioles of the airway mucosa were densely innervated. All intraepithelial nerves were within 0.1 μm of epithelial cells, and at least two-thirds of nerves near arterioles were within 1 μm of the vessel walls. We conclude that the increase in venular permeability associated with neurogenic inflammation in the trachea and bronchi of rats is mediated by sensory axons that travel in the vagus nerves and superior laryngeal nerves. We question whether tachykinins from the sensory nerves mediate the increase in vascular permeability through a direct action on venules, and raise the possibility that these nerves evoke the release from epithelial cells of mediators that contribute to the increase in vascular permeability.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurocytology 12 (1983), S. 117-153 
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The morphology of blood vessels supplying the carotid body and carotid sinus was analysed in 41 rats by using a combination of light microscopic, transmission electron microscopic and scanning electron microscopic methods. We found that a large sphincter-like intimai cushion was located at the orifice of thecarotid body artery, where the vessel arose from the external carotid or occipital artery. The sphincter contained circumferential smooth muscle and constricted the diameter of the orifice to less than half. After reaching the carotid body, the carotid body artery typically divided into three or four first-order and five or more second-order branches. Usually three or foursecond-order branches supplied the carotid body, but all other branches continued on to such structures as the superior cervical ganglion, nodose ganglion, vagus nerve and carotid sinus.Third andfourth-order branches gave rise toterminal arterioles that supplied the glomus tissue. Vessels resemblingprecapillary sphincters were located at the junction of terminal arterioles and capillaries. Precapillary sphincters had a wall comprised of protruding endothelial cells surrounded by smooth muscle cells or pericytes. Most terminal arterioles gave rise to two types of capillaries.Type I capillaries penetrated a glomus cell cluster and had an intimate association with glomus cells of that cluster had a luminal diameter ranging from about 8 to over 20 μm, but varied in calibre along their length. These vessels followed a winding course, made one or more U-shaped turns, and usually had multiple connections with venules. Type I capillaries had a thin fenestrated endothelium, an incomplete covering of pericytes, and a thin basal lamina. By contrast,type II capillaries did not penetrate glomus cell clusters, had a uniform diameter of about 7 μm, and had both straight and curved regions. Both types of capillaries were bypassed byarteriovenous anastomoses formed by terminal arterioles that joined small venules directly.Venules of the carotid body were interconnected with one another and joined major veins of the neck via several routes. Arterioles derived from the carotid body artery also supplied an extensive network of vasa vasorum in the adventitia of the carotid sinus. Short capillaries and larger shunt vessels connected arterioles with the numerous venules in the sinus wall; and the venules in turn were connected to the venous plexus at the surface of the carotid body. We conclude that the arterial branching pattern, intimai cushions and precapillary sphincters participate in the control of carotid body blood flow and also may influence plasma skimming. However, the existence of arteriovenous anastomoses in addition to at least two types of capillaries indicates that blood flow to the chemoreceptive tissue can be regulated independently of total blood flow. Furthermore, the redundancy of venous connections may be related to the sensitivity of carotid body chemoreceptors to changes in venous pressure.
    Type of Medium: Electronic Resource
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