Aac 2010 avec petit supplément spécial amcox

AMERICAN COLLEGE OF CARDIO 2


Auj. à 10:48
1274-351 Nitric Oxide Donation From The Cinod Naproxcinod
Counteracts Cyclooxygenase Inhibition-dependent
Contraction In Human Mammary Arteries
Manlio Bolla, Alessandra Poggi, Barbara Vergani, Guido Gelpi, Julio
Padron, Daniela Miglietta, NicOx Research, Milan, Italy, NicOx SA,
Sophia Antipolis, France


Learning Objective: Understand the role of NO donation from
naproxcinod in the control of vascular
Conclusions: NO donation from naproxcinod is able to counteract
the contracting effects of COX-2 inhibition from NSAIDs in arteries...

Merci Vinsse !
Bon WE

merci bien vinsse voilà la présentation complète , la conclusion me plait bien

Nitric Oxide Donation From The Cinod Naproxcinod Counteracts
Cyclooxygenase Inhibition-dependent Contraction In Human Mammary
Arteries
Presentation Time: Tuesday, Mar 16, 2010, 9:30 AM -10:30 AM

Author Block: Manlio Bolla, Alessandra Poggi, Barbara Vergani, Guido
Gelpi, Julio Padron, Daniela Miglietta, NicOx Research, Milan, Italy,
NicOx SA, Sophia Antipolis, France

Learning Objective 1: Understand the role of NO donation from
naproxcinod in the control of vascular tone in arteries with endothelial
dysfunction
Abstract: Background: Hypertension and osteoarthritis (OA) show
frequent co-morbidity. Current treatment of OA with traditional NSAIDs
and COX-2 inhibitors may predispose to increased risk of cardiovascular
events and blood pressure destabilization. Hypertension is frequently
associated with endothelial dysfunction, characterized by a defect in
vascular biosynthesis and activity of nitric oxide (NO).
Naproxcinod is the first-in-class cyclooxygenase inhibiting nitric oxide
donator (CINOD) designed to provide anti-inflammatory efficacy in OA
from its metabolite naproxen while donating NO, which is intended to
mitigate the NSAID-dependent side effects at vascular level.
The aim of this study was to evaluate the effect of NO donation by
naproxcinod in the presence of cyclooxygenase (COX) inhibition in human
isolated mammary arteries (hIMA).
Methods: Artery specimens were obtained from patients undergoing
coronary artery bypass grafting and prepared as rings for isometric tone
recording. Morphology was assessed by electron transmission microscopy.
Results: In pre-contracted hIMA, endothelium-dependent vasorelaxation
(acetylcholine) was reduced in comparison to the endothelium-independent
(sodium nitroprusside) response. Accordingly, electron microscopy
showed cellular abnormalities such as intima hyperplasia and endothelial
cell degeneration. Naproxcinod (10 nM - 100 μM) caused a
NO-mediated concentration-dependent relaxation (Emax= -52.4±6.9%,
p<0.05, n=6). Conversely, naproxen caused a slight but significant
vasoconstriction (Emax=8±4%, p<0.05, n=6). In non-precontracted hIMA,
naproxcinod and the selective COX-1 inhibitor SC-560 showed no effect
on vascular tone, while naproxen (Emax=17±2.7%, n=12), ibuprofen
(Emax=8.8±2.3%, n=4) and rofecoxib (Emax=6.8±1.7%, n=4) caused a mild
but significant vasoconstriction (p<0.05).
Conclusions: NO donation from naproxcinod is able to counteract the
contracting effects of COX-2 inhibition from NSAIDs in arteries from
patients with endothelial dysfunction. These data provide mechanistic
support to clinical studies showing a differentiated blood pressure
profile for naproxcinod as compared to naproxen in OA
patients.

bravo pour ta trouvaille
j'ai bien moins de mérite que toi puisque je dispose d'accès illimités à beaucoup de revues électroniques....beaucoup sont sous embargo et copyright et exigent une certaine confidentialité ce qui explique ma prudence

Merci à vous deux et bon dimanche.