2005
DOI: 10.1167/iovs.04-1102
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Thrombin Inhibitor Reduces Leukocyte–Endothelial Cell Interactions and Vascular Leakage after Scatter Laser Photocoagulation

Abstract: Argatroban suppressed leukocyte-endothelial cell interactions and blood-retinal barrier breakdown after scatter laser photocoagulation, suggesting that argatroban prevents postlaser macular edema.

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Cited by 21 publications
(13 citation statements)
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“…In addition, the vitreous levels of sICAM-1 and VEGF showed no significant correlation with the timing of retinal photocoagulation in the 11 treated eyes. Musashi et al [51] report that leukocyte behavior such as rolling and infiltration showed an increase from 12 h after laser photocoagulation in pigmented male rats, but returned to baseline by 48 h, and that retinal ICAM-1 mRNA expression was also upregulated. Therefore, transient upregulation of ICAM-1 mRNA may occur from about 12 to 48 h after photocoagulation.…”
Section: Discussionmentioning
confidence: 99%
“…In addition, the vitreous levels of sICAM-1 and VEGF showed no significant correlation with the timing of retinal photocoagulation in the 11 treated eyes. Musashi et al [51] report that leukocyte behavior such as rolling and infiltration showed an increase from 12 h after laser photocoagulation in pigmented male rats, but returned to baseline by 48 h, and that retinal ICAM-1 mRNA expression was also upregulated. Therefore, transient upregulation of ICAM-1 mRNA may occur from about 12 to 48 h after photocoagulation.…”
Section: Discussionmentioning
confidence: 99%
“…Scatter laser photocoagulation caused significant inflammatory leukocyte-endothelial interactions not only in the photocoagulated but also in the untreated retina. In the nonphotocoagulated retina, the number of leukocytes rolling along the major retinal veins increased after photocoagulation and peaked at 12 h. Leukocyte accumulation in the untreated half of the retina increased and peaked at 24 h. In addition, the expressions of P-selectin and ICAM-1 genes were significantly upregulated [99]. These leukocyte-endothelial interactions were attenuated with posterior sub-tenon administration of triamcinolone acetonide [100] or systemic administration of thrombin inhibitor [99].…”
Section: Leukocyte-endothelial Interactions In Pathological Conditionsmentioning
confidence: 99%
“…In the nonphotocoagulated retina, the number of leukocytes rolling along the major retinal veins increased after photocoagulation and peaked at 12 h. Leukocyte accumulation in the untreated half of the retina increased and peaked at 24 h. In addition, the expressions of P-selectin and ICAM-1 genes were significantly upregulated [99]. These leukocyte-endothelial interactions were attenuated with posterior sub-tenon administration of triamcinolone acetonide [100] or systemic administration of thrombin inhibitor [99]. The inhibitory effect of triamcinolone acetonide on the macular edema after photocoagulation is consistent with clinical observations [101].…”
Section: Leukocyte-endothelial Interactions In Pathological Conditionsmentioning
confidence: 99%
“…During the transendothelial migration of leukocytes known as extravasation, endothelial permeability and leukocyte adhesion to endothelial cells are affected by chemokines, their receptors, adhesion molecules, and cytoskeletal components [31,38,51,59]. Recently, evidence has accumulated suggesting that leukocyte extravasation is also associated with the pathological mechanisms of retinal diseases accompanied by persistent visual disturbance, such as age-related macular degeneration [2,48,60] and macular edema [42,55]. These studies show that animal models of ischemic reperfusion are powerful tools for investigating the pathological processes of retinal neuronal cell death and leukocyte extravasation.…”
Section: Introductionmentioning
confidence: 99%