Pulmonary vascular injury induced by hemorrhagic shock is mediated by P-selectin in rats

Shigeki Kushimoto, Kenji Okajima, Mitsuhiro Uchiba, Kazunori Murakami, Hiroaki Okabe, Kiyoshi Takatsuki

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21 Citations (Scopus)

Abstract

To investigate whether the P-selectin-mediated leukocyte adhesion to the endothelial cells is involved in pulmonary vascular injury after hemorrhagic shock, we examined the effect of an anti-P-selectin monoclonal antibody (MAb PB1.3) on the pulmonary accumulation of leukocytes and the subsequent pulmonary vascular injury observed after hemorrhagic shock in rats. Two hours after hemorrhagic shock, pulmonary accumulation of leukocytes, as evaluated by measuring myeloperoxidase activity, began to increase and peaked after 6 hours. Pulmonary vascular injury, as evaluated by the extravascular leakage of 125I-albumin, was significantly increased 6 hours after hemorrhagic shock. MAb PB1.3 significantly prevented both the pulmonary accumulation of leukocytes and subsequent pulmonary vascular injury. MAb PNB1.6, an anti-P-selectin monoclonal antibody incapable of inhibiting P-selectin-mediated leukocyte adhesion, did not prevent either of these effects. These observations strongly suggest that the pulmonary sequestration of leukocytes and the subsequent pulmonary vascular injury after hemorrhagic shocks are mediated by P-selectin.

Original languageEnglish
Pages (from-to)97-106
Number of pages10
JournalThrombosis Research
Volume82
Issue number1
DOIs
Publication statusPublished - 1996 Apr 1

Keywords

  • activated leukocytes
  • adult respiratory distress syndrome
  • hemorrhagic shock
  • myeloperoxidase
  • P-selectin
  • pulmonary vascular injury

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