Harpreet S Sood

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The hypothesis is that chronic increases in left ventricular (LV) load induce oxidative stress and latent matrix metalloproteinase (MMP) is activated, allowing the heart to dilate in the absence of endothelial nitric oxide (NO) and thereby reduce filling pressure. To create volume overload, an arteriovenous (A-V) fistula was placed in male Sprague-Dawley(More)
The hypothesis is that homocysteine decreases endothelial nitric oxide (NO) availability by generating nitrotyrosine. In the absence of NO, and in an attempt to reduce endocardial load by dilatation, the matrix metalloproteinase (MMP) is activated. To address this hypothesis, homocysteine (0.67 mg/ml) was administered in drinking water of Sprague-Dawley(More)
To test the hypothesis that endothelial dysfunction in hyperhomocysteinemia was due to increased levels of nitrotyrosine and matrix metalloproteinase (MMP) activity in response to antagonism of peroxisome proliferator-activated receptor-alpha (PPAR-alpha), cystathionine beta-synthase (CBS) -/+ mice were bred, tail tissue was analyzed for genotype by PCR,(More)
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