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Home > Journals > Minerva Cardioangiologica > Past Issues > Minerva Cardioangiologica 2000 November;48(11) > Minerva Cardioangiologica 2000 November;48(11):379-86



A Journal on Heart and Vascular Diseases

Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752

Frequency: Bi-Monthly

ISSN 0026-4725

Online ISSN 1827-1618


Minerva Cardioangiologica 2000 November;48(11):379-86


Cardiovascular diseases and nitric oxide in humans

Ferlito S.

The production of nitric oxide is impaired in patients with clinical and instrumental signs of arteriosclerosis (chronic coronary heart disease, stable and unstable angina, myocardial infarction); the NO deficiency is assessed through the vascular response to the infusion of stimulating (acetycholine) or inhibiting (N-mono-methylarginine) substances upon NO synthesis. Also in hypertensive subjects a weak endothelium-dependent vascular relaxation was documented, but this phenomenon is not constant and is still to be confirmed. In hypercholesterolemic patients a hyporesponsive endothelium-dependent vasodilation has been well documented, lipid lowering agents (drugs, apheresis) improve endothelium function. In heart failure low NO levels are found proportionally to the severity of disease: the expression of NO is depressed, but citokine mediated i NOS expression is enhanced, causing exaggerated amounts of NO and producing myocyte damage or death. Interesting findings indicated NO inhalation as a useful tool for reducing pulmonary hypertension and congestive heart failure.

language: English


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