Trying to understand and stop the collateral lung damage that can occur in babies with congenital heart disease is the focus of a new study.
When a babys heart defect results in too much blood in the lungs, more blood vessels are made, apparently to handle the increased volume, then new blood vessel growth is abruptly halted.
You get this burst in the first month of life of blood vessel activity, then we think the system gets shut down and the lungs dont get any bigger, says Dr. Stephen M. Black, cell and molecular physiologist at the Medical College of Georgia Vascular Biology Center. What we are trying to work out is what are the mechanisms.
Dr. Black and his colleague, Dr. Jeffrey Fineman, a whole-animal physiologist and physician at the University of California, San Francisco, are using sheep whose four-chambered hearts are essentially identical to human hearts as a model to identify events that trigger blood vessel production, called angiogenesis, and the abrupt halt.
Their hope is the findings will lead to improved treatment for children born with heart defects.
The most common of the defects, ventricular septal defect, causes oxygen-rich blood that should be pumped out to the body by the left ventricle, to mix with oxygen-poor blood in the adjacent right ventricle. The blood then re-circulates to the lungs, resulting in too much volume in the lungs and too little in the body. The overworked heart, trying to take care of the body, can fail; the lungs, overwhelmed with blood, become congested.
Theres about three times as much blood flow going to the lungs as to the systemic circulation, says Dr. Black. Their heart rates go up to compensate. Over time, the heart muscle gets oversized from too much work.
And there is more going on. The blood volume in the lungs puts high pressure on blood vessels that, before birth, were idle because the mother provides the fetus with essentials such as
|Contact: Toni Baker|
Medical College of Georgia