Argatroban Attenuates Leukocyte– and Platelet–Endothelial Cell Interactions After Transient Retinal Ischemia

DOI Web Site 被引用文献1件
  • Shinsuke Miyahara
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Junichi Kiryu
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Akitaka Tsujikawa
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Hideto Katsuta
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Kazuaki Nishijima
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Kazuaki Miyamoto
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Kenji Yamashiro
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Atsushi Nonaka
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Yoshihito Honda
    From the Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.

抄録

<jats:p> <jats:bold> <jats:italic>Background and Purpose—</jats:italic> </jats:bold> Argatroban, a direct thrombin inhibitor, has been shown to reduce neural injury after transient cerebral ischemia. It has also been reported that this neuroprotective effect results from an anticoagulant function. This study was designed to evaluate quantitatively the inhibitory effects of argatroban on leukocyte– and platelet–endothelial cell interactions after transient retinal ischemia. </jats:p> <jats:p> <jats:bold> <jats:italic>Methods—</jats:italic> </jats:bold> Retinal ischemia was induced for 60 minutes in male Long-Evans rats by temporary ligation of the optic sheath (n=342). Argatroban was administered just after induction of ischemia. Leukocyte and platelet behavior in the retinal microcirculation was then evaluated in vivo with scanning laser ophthalmoscopy. The expression of P-selectin and intracellular adhesion molecule-1 (ICAM-1) was evaluated by reverse transcription–polymerase chain reaction. After 10 days of reperfusion, ischemia-induced retinal damage was evaluated histologically. </jats:p> <jats:p> <jats:bold> <jats:italic>Results—</jats:italic> </jats:bold> Treatment with argatroban suppressed leukocyte–endothelial cell interactions; the maximum numbers of rolling and accumulated leukocytes were reduced by 90.1% ( <jats:italic>P</jats:italic> <0.05) and 58.7% ( <jats:italic>P</jats:italic> <0.05), respectively, at 12 hours after reperfusion. Treatment with argatroban also suppressed platelet–endothelial cell interactions; the maximum numbers of rolling and adhering platelets were reduced by 91.8% ( <jats:italic>P</jats:italic> <0.01) and 78.9% ( <jats:italic>P</jats:italic> <0.01), respectively, at 12 hours after reperfusion. The expression of P-selectin and ICAM-1 mRNA was suppressed significantly in the argatroban-treated retinas ( <jats:italic>P</jats:italic> <0.01). Histologic examination demonstrated the protective effect of argatroban on ischemia-induced retinal damage ( <jats:italic>P</jats:italic> <0.01). </jats:p> <jats:p> <jats:bold> <jats:italic>Conclusions—</jats:italic> </jats:bold> Argatroban treatment suppressed leukocyte– and platelet–endothelial cell interactions after transient retinal ischemia. This inhibitory effect on postischemic blood cell–endothelial cell interactions might partially contribute to its neuroprotective effects. </jats:p>

収録刊行物

  • Stroke

    Stroke 34 (8), 2043-2049, 2003-08

    Ovid Technologies (Wolters Kluwer Health)

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