eja, sildenafil not only protected against necrosis, accidental cell death occurring due to oxygen deprivation, but also against apoptosis, cell death following DNA fragmentation. Furthermore, the researchers found the presence of phosphodiesterase-5 (PDE-5), an enzyme responsible for the destruction of the cGMP molecule, in the heart cells. The cGMP is an intracellular messenger molecule that plays an important role in the dilation of arteries in the body. Sildenafil is able to preserve cGMP, and therefore dilation of the arteries by inhibiting PDE-5.

"These observations have far-reaching implications for the treatment of patients with heart failure where loss of cells is primarily due to apoptosis," he said.

Kukreja and his colleagues began studying sildenafil in 2002 as part of an on-going research program into "preconditioning," which is a way to protect the heart muscle from serious damage in the future by depriving it for very brief periods of blood flow and, therefore, oxygen. In papers published in the September 2002 issue of the American Journal of Physiology, and the March 2003 issue of Circulation Research, Kukreja and his colleagues observed a powerful, protective effect of sildenafil in the heart during experimental heart attack in animal models.

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Contact: Sathya Achia-Abraham
sbachia@vcu.edu
804-828-1231
Virginia Commonwealth University
31-Jan-2005

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