Abstract

We have studied the role of endothelium in control of forearm blood flow in patients with heart failure as well as in normal subjects. First, endothelium-dependent forearm vasodilation in response to acetylcholine (ACh), substance P, and endothelium-independent forearm vasodilation to sodium nitroprusside (SNP) were examined in patients with heart failure and in normal subjects. Endothelium-dependent forearm vasodilation in response to ACh but not to substance P was impaired in patients with heart failure. Endothelium-independent forearm vasodilation to SNP was also preserved in patients with heart failure. Second, the role of nitric oxide (NO) in reactive hyperemia and exercise-induced vasodilation were examined using N G-monomethyl-l-arginine (l-NMMA), a blocker of NO synthesis, in normal subjects. Results suggested that NO plays a minimal role in reactive hyperemia and exercise-induced vasodilation in normal human forearm vessels. Finally, we determined if l-arginine, a precursor of NO, improves impaired endothelium-dependent vasodilation to ACh and reactive hyperemia in patients with heart failure. l-Arginine augmented impaired ACh-induced vasodilation as well as reactive hyperemia in patients with heart failure. Our results suggested that defective endothelial function may contribute to abnormal control of regional blood flow in patients with heart failure.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call