In a five-year laboratory study, UC surgeon-scientist Karyn Butler, MD, found that when the heart experiences short periods of stress, either from reduced blood flow or high blood pressure, it activates a protective molecular pathway — known as JAK-STAT — that protects the heart muscle. The pathway, which is normally dormant in the heart, was originally identified in disease-fighting white blood cells as a mediator of infection and has recently been targeted for its role in heart health.
Butler says when the JAK-STAT pathway is active and functioning, it can help precondition and protect the heart from damage caused when blood flow is restored after a period of decreased flow, as occurs after a heart attack.
“These mini stress tests appear to push the heart muscle into an adaptive state where it gets used to how long-term stress feels,” Butler explains. “This preconditioning helps the heart muscle better tolerate longer episodes of compromised blood flow.”
Butler wanted to determine how she could help patients with heart disease from high blood pressure tolerate cardiac ischemia. To study the heart’s response to restored blood flow after cardiac ischemia and in the presence of hypertension, Butler developed a hypertrophied (enlarged) animal heart model to mimic the conditions of heart enlargement and congestive heart failure in humans.
The enlarged heart model was then subjected to preconditioning — a series of short periods of blood flow blockage — to simulate what happens in humans with serious heart disease. Butler found that these mini stress tests activated the dormant JAK-STAT pathway, and helped protect the muscle from injury when blood flowed back into the heart.
MEDICA.de; Source: University of Cincinnati