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 language | English (US) |
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Pages (from-to) | 457-463 |
Number of pages | 7 |
Journal | Journal of Cardiac Failure |
Volume | 15 |
Issue number | 5 |
DOIs | |
State | Published - Jun 2009 |
Externally published | Yes |
Keywords
- Heart failure
- endothelium
- inflammation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine