Thrombin increases permeability only in venules exposed to inflammatory conditions

F. E. Curry, M. Zeng, R. H. Adamson

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Thrombin is widely used to stimulate a variety of responses in cultured endothelial cell monolayers as a model of acute vascular endothelial reponse to inflammatory mediators. However, preliminary results indicated that rat mesenteric venules did not respond acutely to thrombin. We tested the hypothesis that rat venules would respond to thrombin 24 h after prior injury by microperfusion. Vessel responsiveness was measured as hydraulic conductivity (Lp). When venules were exposed to rat thrombin (10 U/ml) within 2 h of initial perfusion with vehicle control, there was no increase in L p of any vessel from a mean baseline of 1.2 ± 0.2 × 10-7 cm·s-1·cmH2O-1. In contrast, when perfused with thrombin at 25-27 h after initial perfusion, every venule responded to thrombin with a transient increase in Lp. The mean peak Lp on day 2 in response to thrombin was 24 ± 4. 2 × 10-7 cm·s-1·cmH2O -1. Our results suggest that prior endothelial injury modifies the endothelial cell phenotype and alters the response of endothelial cells to thrombin after 24 h. Phenotypic plasticity of endothelial cells may play a key role in the regulation of permeability of some endothelial cells in culture and in intact venules, where localized leaky sites may form where there had been a previous inflammatory response.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume285
Issue number6 54-6
StatePublished - Dec 2003

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Venules
Thrombin
Permeability
Endothelial Cells
Perfusion
Wounds and Injuries
Blood Vessels
Cultured Cells
Cell Culture Techniques
Phenotype

Keywords

  • Endothelium
  • Inflammation
  • Kinase
  • Mesentery
  • Platelet activating factor
  • Rat

ASJC Scopus subject areas

  • Physiology

Cite this

Thrombin increases permeability only in venules exposed to inflammatory conditions. / Curry, F. E.; Zeng, M.; Adamson, R. H.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 285, No. 6 54-6, 12.2003.

Research output: Contribution to journalArticle

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