September 1, 1990AJP Heart and Circulatory Physiology
Flow stimulates endothelial cells to release a nitrovasodilator that is potentiated by reduced thiol
Key result
Flow induces the release of a diffusible, short-lived nitrovasodilator from endothelial cells, causing endothelium-dependent relaxation that is augmented by the reduced thiol N-acetyl-L-cysteine.
Why the study?
Does flow stimulate endothelial cells to release a nitrovasodilator that is potentiated by reduced thiol?
Population
Vascular rings of rabbit thoracic aorta and bovine endothelial cells on microcarrier beads
Comparison
Vortical flow and addition of N-acetyl-L-cysteine vs Absence of flow, or presence of inhibitors
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Supports flow-mediated endothelial relaxation in models; leaves open clinical translation of thiol augmentation.
Structured PICO
Does flow stimulate endothelial cells to release a nitrovasodilator that is potentiated by reduced thiol?
P
Population
Vascular rings of rabbit thoracic aorta and bovine endothelial cells on microcarrier beads
I
Intervention
Vortical flow (induced by a magnetic stirrer) and addition of N-acetyl-L-cysteine
C
Comparator
Absence of flow, or presence of inhibitors (methylene blue, bovine hemoglobin, N-monomethyl-L-arginine)
O
Outcome
Endothelium-dependent relaxation of vascular ringssurrogate
Flow stimulates endothelial cells to release a short-lived nitrovasodilator, whose action and half-life are augmented by the reduced thiol N-acetyl-L-cysteine.
Cite This Study
Cooke et al. (1990) studied Flow-mediated endothelium-dependent vasodilation. Flow and N-acetyl-L-cysteine vs. Absence of flow was evaluated on Endothelium-dependent relaxation of vascular rings. Flow induces the release of a diffusible, short-lived nitrovasodilator from endothelial cells, causing endothelium-dependent relaxation that is augmented by the reduced thiol N-acetyl-L-cysteine.