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08:42
Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
Published on: October 22, 2014
PAF attenuates endothelium-dependent coronary arteriolar vasodilation
D V DeFily1, L Kuo, W M Chilian
1Department of Medical Physiology, Texas A & M University Health Science Center, College Station 77843-1114, USA.
The American Journal of Physiology
|June 1, 1996
Summary
Platelet-activating factor (PAF) causes coronary microvascular dysfunction by impairing endothelium-dependent dilation. This dysfunction occurs independently of activated neutrophils, affecting coronary resistance vessels.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Microcirculation Research
Background:
- Platelet-activating factor (PAF) is implicated in neutrophil activation and vascular dysfunction.
- Its specific role in coronary resistance vessels and independence from neutrophils remains unclear.
Purpose of the Study:
- To investigate if PAF induces coronary arteriolar endothelial dysfunction in vivo.
- To determine if this dysfunction is independent of activated neutrophils.
Main Methods:
- Intravital videomicroscopy in canine hearts to measure coronary microvascular diameters.
- Intracoronary infusion of PAF and subsequent assessment of responses to dilators (acetylcholine, serotonin, papaverine).
- In vitro studies on isolated coronary arterioles treated with PAF.
Main Results:
- PAF significantly attenuated endothelium-dependent dilation to acetylcholine and serotonin in vivo.
- PAF impaired endothelium-dependent relaxation to serotonin in isolated arterioles but not nitroprusside-induced relaxation.
- Endothelium-independent relaxation to papaverine (in vivo) and nitroprusside (in vitro) remained unchanged.
Conclusions:
- PAF directly causes coronary microvascular endothelial dysfunction.
- Activated neutrophils are not required for PAF-induced coronary arteriolar dysfunction.
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