When a heart attack strikes, blood stops flowing to parts of the heart, starving the tissue of oxygen and killing cardiac cells. Scientists have long speculated that if they could provide those cells with an emergency supply of oxygen until surgeons restored blood flow with a coronary bypass, some permanent damage to cardiac tissue could be prevented, thereby preserving heart function. A new study with rats suggests an innovative way to do that: infecting the heart with photosynthesizing bacteria that naturally produce oxygen when exposed to light.

The technique was effective at preserving cardiac function in the rodents, yet experts note there are significant obstacles to implementing it as a human therapy. “This is a fascinating, radical idea, and I’m glad it’s being tested,” says Hina Chaudhry, a cardiologist at Mount Sinai Hospital in New York City, “but it’s a long road from small animals to humans. If I were a betting person, I’d bet it’s not going to translate.”

The bacterium used was Synechococcus elongatus, which, like plants, photosynthesizes light for energy and converts carbon dioxide and water into oxygen. It’s well known among bioengineers, some of whom study it as a tool to enhance biofuel production or as a model organism to investigate circadian rhythms.

Wondering whether these microbes could provide oxygen on demand to a tissue, researchers at Stanford University in Palo Alto, California, infected the heart muscles of rats with the bacteria, then induced a heart attack by opening the chest and blocking the organ’s main blood-supplying artery. They left the heart exposed to the laboratory’s natural light and the bacteria went to work, resulting in a 25-fold increase in the tissue’s oxygen levels 10 minutes after the heart attack. Forty-five minutes after the heart attack, the hearts of the bacteria-laced rats pumped about 60% more blood than did rats that also had heart attacks but were not given the bacteria, and 30% more blood than rats that were infected with the bacteria but left in the dark.

In humans, preserving that much heart function following a heart attack “would have profound clinical implications, likely representing the difference between a healthy patient and one suffering from heart failure,” the researchers report today in Science Advances. Based on blood samples taken from the rats during the first week of their recovery, the team found no evidence that the bacteria had spread or caused any toxic effects, and it’s not known to be a human pathogen.

But there are major hurdles in the way of the technique working in people, Chaudhry says. For one thing, she says, humans have thicker cardiac muscles than rats, making it unlikely that light could penetrate deeply enough to reach the bacteria. She also is unconvinced the bacterium is as harmless as the researchers report, claiming their investigation into the rodent immune response to it was “superficial and cursory.”