In conclusion, these data demonstrate that a decreased ability to synthesize and release NO may occur in polymorphonuclear cells of a selected group of young patients with unstable angina pectoris. Further evidence is required to assess whether this could account for a more generalized deficiency in the mechanisms, maintaining vascular endothelium into an antiadhesive and vasodilating state, that involve NO release. However, detection of NO generation in circulating cells, such as polymorphonuclear cells, may represent a novel and potentially useful approach in evaluating the possible role of the L-arginine-NO pathway in the pathophysiology of severe coronary artery disease.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine