Vascular Injury Due to Topical Application of Cardiovascular Contrast Medium in the Hamster Cheek Pouch

Radiology ◽  
1967 ◽  
Vol 89 (1) ◽  
pp. 20-23 ◽  
Author(s):  
John F. O'Connor ◽  
Steven B. Sitzman ◽  
James B. Dealy
2006 ◽  
Vol 10 (3) ◽  
pp. 211-215 ◽  
Author(s):  
Fernanda Gonçalves Salum ◽  
Karen Cherubini ◽  
Maria Antonia Zancanaro de Figueiredo ◽  
Milton de Oliveira Amado ◽  
Eloni Terezinha Rodrigues ◽  
...  

Oral Oncology ◽  
2010 ◽  
Vol 46 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Giovanni Nicolao Berta ◽  
Paolina Salamone ◽  
Andrea Elio Sprio ◽  
Federica Di Scipio ◽  
Lucy Marcela Marinos ◽  
...  

1998 ◽  
Vol 79 (1) ◽  
pp. 54-58 ◽  
Author(s):  
F Ghezzo ◽  
G N Berta ◽  
B Bussolati ◽  
A Bosio ◽  
G Corvetti ◽  
...  

2000 ◽  
Vol 191 (11) ◽  
pp. 1829-1840 ◽  
Author(s):  
Narinder Gautam ◽  
Heiko Herwald ◽  
Per Hedqvist ◽  
Lennart Lindbom

Activation of polymorphonuclear leukocytes (PMNs) and adhesion to the endothelial lining is a major cause of edema formation. Although known to be dependent on the function of β2 integrins (CD11/CD18), the precise mechanisms by which adherent PMNs may impair endothelial barrier capacity remain unclear. Here, the role of transmembrane signaling by β2 integrins in PMN-induced alterations in tight junctional permeability of cultured endothelial cell (EC) monolayers was investigated. PMN activation, in the absence of proinflammatory stimuli, was accomplished through antibody cross-linking of CD11b/CD18, mimicking adhesion-dependent receptor engagement. CD18 cross-linking in PMNs added to the EC monolayer provoked a prompt increase in EC permeability that coincided with a rise in EC cytosolic free Ca2+ and rearrangement of actin filaments, events similar to those evoked by chemoattractant PMN activation. Cell-free supernatant obtained after CD18 cross-linking in suspended PMNs triggered an EC response indistinguishable from that induced by direct PMN activation, and caused clear-cut venular plasma leakage when added to the hamster cheek pouch in vivo preparation. The PMN-evoked EC response was specific to β2 integrin engagement inasmuch as antibody cross-linking of l-selectin or CD44 was without effect on EC function. Our data demonstrate a causal link between outside-in signaling by β2 integrins and the capacity of PMNs to induce alterations in vascular permeability, and suggest a paracrine mechanism that involves PMN-derived cationic protein(s) in the cellular crosstalk between PMNs and ECs.


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