1997
DOI: 10.1097/00024382-199707000-00004
|View full text |Cite
|
Sign up to set email alerts
|

Ischemia/Reperfusion-Induced Leukocyte-Endothelial Interactions in Postcapillary Venules

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2

Citation Types

3
66
0
3

Year Published

1999
1999
2024
2024

Publication Types

Select...
7

Relationship

0
7

Authors

Journals

citations
Cited by 112 publications
(72 citation statements)
references
References 0 publications
3
66
0
3
Order By: Relevance
“…When Fe 2+ or other transition metals are present and CAT activity is decreased (as in this study), H 2 O 2 is reduced to a very highly oxidizing OH radical. The OH radical cannot be enzymatically detached from cells, but a free radical scavenger may detoxify it (7)(8)(9)(10). Additionally in our study, CAT activity was significantly increased with administration of vitamins C and E.…”
Section: Discussionsupporting
confidence: 53%
See 2 more Smart Citations
“…When Fe 2+ or other transition metals are present and CAT activity is decreased (as in this study), H 2 O 2 is reduced to a very highly oxidizing OH radical. The OH radical cannot be enzymatically detached from cells, but a free radical scavenger may detoxify it (7)(8)(9)(10). Additionally in our study, CAT activity was significantly increased with administration of vitamins C and E.…”
Section: Discussionsupporting
confidence: 53%
“…I/R is the main cause of posttraumatic organ deficiency in these disciplines (7). Holding of white blood cells to the surrounding capillary endothelium is a critical pathophysiologic stage, regardless of the type of the I/R injury (8,9). As a result of adherence to endothelial cells, the neutrophils release proteases and oxygen radicals (10), which damages the endothelial layer.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…9,10,[12][13][14][15][16][19][20][21][32][33][34][35] Infiltrating neutrophils have been implicated as key mediators of I-R injury associated with numerous organs, including the intestine, heart, brain, skeletal muscle, and liver. 21,[36][37][38][39] The neutrophil is thought to have a central role, given the evidence that neutrophil elimination with vinblastin or blocking of neutrophil activity with mAb appears to be cytoprotective in the setting of I-R. 20,21 Our central hypothesis therefore was that RES dysfunction after I-R also was neutrophil dependent, at least to some degree.…”
Section: Discussionmentioning
confidence: 99%
“…A major component of I-R injury is caused by the generation of reactive oxygen intermediates (ROIs) and consequent neutrophil accumulation and activation, which induces secondary endothelial cell injury. [9][10][11] Studies have shown that leukocyte accumulation is a critical determinant of hepatic I-R injury, [12][13][14][15][16] and P-selectin has an important role in leukocyte adhesion after hepatic I-R. 15,16 The leukocyte-endothelial cell interaction that occurs after I-R injury has been shown to be a causative factor in the development of microvascular dysfunction and release of such cytotoxic mediators as ROIs and a variety of proteases. 10,[17][18][19] The importance of neutrophils in this pathophysiologic process is emphasized by the observation that neutropenia (induced with vinblastin and/or an antineutrophil monoclonal antibody [mAb]) results in markedly decreased hepatic cell damage after I-R. 20,21 Alterations in hepatic RES function have been variably modulated under conditions of cold or warm I-R. Caldwell-Kenkel et al 22 reported increased KC activity after cold I-R. 23 Rao et al 23 suggested that the reperfusion injury to the liver that occurs after cold ischemic preservation damages endothelial cells and activates KCs, which, in turn, initate a self-perpetuating injury pathway).…”
mentioning
confidence: 99%