January 7, 2008 - Ischemia experienced in brief episodes could protect the heart by preparing it for a heart attack, according to early findings from an animal study by researchers at the University of Cincinnati, which was published in the January issue of the American Journal of Physiology: Heart and Circulatory Physiology.
Rat hearts transfused with blood preconditioned by mini “stress tests” from reduced blood flow had significantly better reperfusion after heart attack-like ischemia than those that received a transfusion from donors that were not subjected to stress beforehand (P
Preconditioning activated a protective pathway called Janus kinase (JAK) to signal transducers and activators of transcription (STAT). The JAK-STAT pathway could offer a therapy against the damage of a heart attack.
A transfer of protection suggested that the effect was mediated by a soluble molecule released during brief periods of stress. Researchers indicated that this molecular mediator likely activates the JAK-STAT pathway.
Hearts that received effluent from preconditioned hearts but were treated with the JAK 2 inhibitor AG-490 recovered less than any other group.
Increased STAT-3 activation, reduced STAT-1 activation, and decreased expression of the pro-apoptotic protein Bax were associated with the protective effect.
Researchers do not yet know how long the cardioprotective effect lasts after a brief period of ischemia. However, "translating this phenomenon into a clinically useful tool may protect the myocardium from potential injury in a variety of settings," she said, "including acute myocardial infarction, cardiac revascularization surgery, supply/demand imbalance in congestive heart failure, and ischemia/reperfusion challenge following shock."
For more information: ajpheart.physiology.org