"Once we add the enzymes, however, we can make the gel degrade away within a few hours, and we also showed that the level of enzyme correlates very nicely with how fast the gel degrades away and releases the inhibitor," Burdick said.
The researchers demonstrated this responsiveness in a petri dish, but also showed its potential for clinical effectiveness in an animal model. They used pigs, due to the anatomical similarity between porcine and human hearts.
"We used a microdialysis technique," Purcell said, "to show that, after a heart attack, local enzyme levels go way up, but when the inhibitor molecules are delivered via the gel, we see the activity level of this enzyme go down. Over the next 28 days, we also used imaging techniques to show thicker cardiac walls and less expansion and dilation of the ventricle. And, as a result, we see better performance in the heart using clinical measurements like ejection fraction, the amount of the blood the heart is pumping."
The study is part of an ongoing collaborative research effort between the Gorman Cardiovascular Research Group and the Burdick Biomaterials Laboratory, developing therapies intended to improve the heart's long-term response to a heart attack.
"While most groups working in this field are attempting to develop myocardial regenerative therapies, our team is focused on the biomechanical stabilization of the heart after heart attack," Robert Gorman said. "Most researchers working towards regenerative therapies often overlook an important fact, namely, that the overwhelming majority of patients who suffer heart attack initially have adequate heart function. We strongly be
|Contact: Evan Lerner|
University of Pennsylvania