Many different types of brain cells are essential for normal breathing, but only a small subset of these is required for gasping or autoresuscitation. If normal breathing should stop, this backup system is activated to induce gasping. This restores oxygen supplies and kick-starts the heartbeat so that normal breathing can resume.

A failure to gasp has long been proposed as the basis for SIDS. "Our studies resolve a 15-year long controversy by showing that pacemaker cells in the brain appear responsible for gasping but not normal breathing," said Professor Julian Paton who heads up the University of Bristol research team that made the finding. "Importantly, cot death has been proposed to result from a failure of autoresuscitation and gasping," he added.

Backup System When Breathing Stops

Using a unique experimental set-up developed in Bristol, Paton combined forces with two other world leaders in respiration -- Dr. Jeffrey Smith of the US National Institutes of Health and Professor Walter St.-John of Dartmouth -- to discover how gasping works. They found that many different types of brain cells are essential for normal breathing, but only a small subset of these is required for gasping or autoresuscitation.

If normal breathing should stop, this backup system is activated to induce gasping. This restores oxygen supplies and kick-starts the heart beat so that normal breathing can resume.

"A very important aspect of this work is that we have discovered a mechanism within the brain that allows autoresuscitation of both breathing and the heartbeat to come about when oxygen levels are critically low," said Dr. Smith.

Unique Protein

Paton and colleagues found that these pacemaking cells were dependent upon a unique protein that forms a tiny hole or pore within the membrane of the cells. When oxygen levels are low, this pore opens wider to allow the passage of sodium ions into the cell and provides a way in which gasping can occur automatically.

The team showed that when this pore was blocked it eliminated pacemaking and the ability to gasp. Consequently, the heart would fail and death would be inevitable. This raises the intriguing possibility that a genetic defect in this special protein found in pacemaking cells could prevent gasping.

"Our findings are exciting," St.-John commented. "They demonstrate that emergency breathing, or gasping, is regulated by different mechanisms than those for normal breathing. This result explains why gasping is such a powerful mechanism for autoresuscitation.."