Apoptosis in the left ventricle of chronic volume overload causes endocardial endothelial dysfunction in rats.

@article{Cox2002ApoptosisIT,
  title={Apoptosis in the left ventricle of chronic volume overload causes endocardial endothelial dysfunction in rats.},
  author={Michael J Cox and H. Sood and M. Hunt and D. Chandler and J. Henegar and G. Aru and S. Tyagi},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2002},
  volume={282 4},
  pages={
          H1197-205
        }
}
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 rats. To decrease oxidative stress and apoptosis, 0.08 mg/ml nicotinamide (Nic) was administered in drinking water 2 days before surgery. The… Expand
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