From Washington, D.C., at the Experimental Biology 2004 meeting
Though heart tissue starved of oxygen in a heart attack for more than a few minutes typically begins to die, it doesn't always succumb—especially if the tissue has recently sustained a few short bouts of oxygen deprivation. Such a situation might ensue if an artery to the area had temporarily shut down, as often occurs just before a bona fide heart attack. Something about the deprivation episodes elicits chemical changes that cause cells "to autoprotect," explains Steven Jones of the Johns Hopkins Medical Institutions in Baltimore.
Physicians refer to this process as ischemic preconditioning.
Jones now reports evidence from mice indicating that the brief periods of oxygen deprivation induce the body to tack a sugar molecule onto heart-muscle proteins. His group's experiments indicate that this sugar appendage, which goes by the unwieldy name of O-linked N-acetyl glucosamine (O-GlcNAc), protects the muscle from a subsequent heart attack and the related oxygen damage that can occur in the moments just after a flow of blood is restored.
Ordinarily, enzymes remove the added sugar after a few hours. However, the Johns Hopkins researchers gave the mice a drug that blocks the activity of those enzymes. When the animals then underwent simulated heart attacks, they were protected from serious injury, Jones told Science News. The protection of heart tissue was roughly equivalent to the effect of preconditioning the tissue with short bouts of oxygen deprivation, he adds.
Steven P. Jones
Institute of Molecular Cardiobiology
Department of Medicine - Division of Cardiology
Johns Hopkins University School of Medicine
720 Rutland Avenue - ROSS 844
Baltimore, MD 21205