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October 1, 1991Cardiovascular Research

Release of endothelium derived nitric oxide in relation to pressure and flow

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Population

Porcine macrovascular endothelial cells cultured on microcarrier beads

Comparison

Perfusion at different flow rates and perfusion… vs Different levels of flow and pressure

Design

Preclinical

Authors

Malte KelmMalte KelmInterventional / Structural CardiologyMFMartin FeelischGeneral / Preventive / LipidsADAndreas DeußenUniversity Hospital Carl Gustav Carus

Discussion

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Implication

Flow modulates endothelial NO release independently of pressure in this model; leaves open relevance to intact human vessels.

Key Points

  • To investigate how the rate of endothelium-derived nitric oxide (NO) release is modulated by two primary determinants of vascular conductance: perfusion pressure and flow rate.
  • Perfused packed columns of porcine macrovascular endothelial cells cultured on microcarrier beads at varied flow rates (2, 10, and 20 ml·min⁻¹) and perfusion pressures (6 to 200 mm Hg).
  • Continuously quantified NO release rates under basal and ATP-stimulated (10⁻⁴ M) conditions using a difference spectrophotometric assay.
  • Increasing flow rate from 2 to 20 ml·min⁻¹ increased basal NO release 5-fold and increased ATP-stimulated NO release 5.8-fold (>180 pmol·min⁻¹·mg⁻¹ endothelial cell protein).
  • ATP stimulation augmented endothelial NO release more than 10-fold at every flow level tested.
  • Varying perfusion pressure between 6 and 200 mm Hg produced no change in the rate of basal NO release.

Structured PICO

P
Population
Porcine macrovascular endothelial cells cultured on microcarrier beads
I
Intervention
Perfusion at different flow rates (2, 10, 20 ml.min-1) and perfusion pressures (ranging from 6 to 200 mm Hg), under basal and ATP (10(-4) M) stimulated conditions
C
Comparator
Different levels of flow and pressure
O
Outcome
Rate of endothelium derived nitric oxide (NO) releasesurrogate

Endothelial nitric oxide release is highly responsive to changes in flow but not to changes in perfusion pressure.

Cite This Study

Kelm et al. (1991) studied this question.

synapsesocial.com/papers/6a82120860b4a58d31d243cfhttps://doi.org/10.1093/cvr/25.10.831
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Flow-Dependent Regulation of Nitric Oxide Formation in the IsolatedCanine Mesenteric Arterial Bed.1997 · 5 citations
  2. 2Flow-Dependent Regulation of Nitric Oxide Formation in the Isolated Canine Mesenteric Arterial Bed1997 · 1 citations
  3. 3Flow-mediated NO release from endothelial cells is independent of K+ channel activation or intracellular Ca2+1995 · 81 citations
  4. 4Pulsatile flow enhances endothelium-derived nitric oxide release in the peripheral vasculature2000 · 108 citations
  5. 5Role of calcium and calmodulin in flow-induced nitric oxide production in endothelial cells1994 · 521 citations