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Articles in PresS, published online ahead of print December 5, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00168.2002
Submitted on February 27, 2002
Accepted on November 27, 2002
1 Whitaker Institute of Biomedical Engineering, University of California, San Diego, La Jolla, CA, USA
* To whom correspondence should be addressed. E-mail: jomens{at}ucsd.edu.
Alteration of hemodynamic loading induces remodeling that includes changes in myocardial properties and extracellular matrix structure. We investigated the hypothesis that cardiac hypertrophy due to volume overload produces changes in myocardial diastolic mechanics and stiffness that are in part due to alterations in advanced glycation endproduct (AGE) collagen crosslinking. Rats developed volume overload due to arteriovenous fistula (AVF). To assess the dependence of AGE crosslinking on mechanics, we prevented AGE formation by administering the drug aminoguanidine to one group of AVF rats (AG+AVF). Volume overload did not modify collagen concentration. Right ventricular (RV) AGE crosslinks were modestly elevated in AVF hearts, but were significantly reduced by aminoguanidine. AVF rats exhibited significantly increased septal AGE crosslinks that were inhibited in the AG+AVF group. AVF-induced increases in LV longitudinal stiffness and septal circumferential stiffness were prevented in AG+AVF hearts. Volume overload appears to regionally modify AGE collagen crosslinking and stiffness, and aminoguanidine treatment prevented these increases, demonstrating that AGE crosslinking plays a role in mediating diastolic compliance in volume overload hypertrophy.
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