Activation of Endothelial Cells in Conduit Veins of Dogs With Heart Failure and Veins of Normal Dogs After Vascular Stretch by Acute Volume Loading

Paolo C. Colombo, Sharad Rastogi, Duygu Onat, Valerio Zacà, Ramesh C. Gupta, Ulrich P. Jorde, Hani N. Sabbah

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Background: The venous endothelium is a key regulator of central blood volume, organ perfusion, and hemostasis in heart failure (HF). We previously reported activation of the inflammatory/oxidative program in venous endothelial cells collected from decompensated HF patients. The underlying causes are unknown. We tested the hypothesis that the pro-inflammatory state of HF and vascular strain associated with congestion can activate the endothelial inflammatory/oxidative and hemostatic programs. Methods and Results: We studied 6 normal (NL) dogs (left ventricular ejection fraction [LVEF] >50%, central venous pressure [CVP] = 8 ± 2 mm Hg) and 6 dogs with HF (LVEF ∼30%, CVP 8 ± 2 mm Hg) produced by intracoronary microembolizations. Normal dogs were studied at baseline and 1 hour after fluid load to a target CVP ≥20 mm Hg. Endothelial cells were scraped from jugular veins; mRNA expression was analyzed by reverse transcription polymerase chain reaction. The endothelial inflammatory/oxidative and hemostatic programs were significantly activated in HF dogs compared with NL. In NL dogs, fluid load significantly activated the endothelial inflammatory/oxidative and hemostatic programs, and, concurrently, caused a significant increase in plasma neurohumoral indices to levels that approached those of HF dogs. Conclusions: The pro-inflammatory state of HF and vascular strain associated with congestion can both activate venous endothelial cells in dogs in a manner consistent with that seen in HF patients.

Original languageEnglish (US)
Pages (from-to)457-463
Number of pages7
JournalJournal of Cardiac Failure
Volume15
Issue number5
DOIs
StatePublished - Jun 1 2009
Externally publishedYes

Keywords

  • Heart failure
  • endothelium
  • inflammation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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