Photosynthetic Bacteria Prevent Cardiac Arrests in Rats

A network of blood vessels known as coronary arteries surrounds the heart muscle and supply it with blood that is rich in oxygen. The heart muscle needs this oxygen to function. A heart attack occurs when a coronary artery becomes suddenly blocked, stopping the flow of blood to the heart muscle and damaging it. All or part of the heart muscle becomes cut off from its oxygen supply. Left without oxygen, the heart muscle is injured. If it is possible to provide these tissues with an emergency supply of oxygen until surgeons restored blood flow with a coronary bypass, permanent damage to cardiac tissue could be prevented to some extent, in this manner protecting heart function. A new experiment conducted on rat models suggests a pioneering technique to do that: Infecting the heart with photosynthesizing bacteria so that oxygen can be produced naturally on exposure to light.

The method is proved to be effective at preserving cardiac function in the rodents; however researchers explain that there are significant obstacles in implementing it as a human therapy. Hina Chaudhry, a cardiologist at Mount Sinai Hospital in New York City said that it was a fascinating, radical idea and was glad that

it was being tested, but she also expressed the concern that it was a long road from testing it on small animals to humans.

Synechococcus elongates was the bacteria that was used to infect the tissues, which, like plants, photosynthesizes light to produce energy and converts carbon dioxide and water into oxygen. It’s well known among bioengineers, who use it as a tool to improve biofuel production or as a model organism to examine circadian rhythms.

To verify 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, and then induced a heart attack by opening the chest and blocking the organ’s main blood-supplying artery. The heart was exposed to the laboratory’s natural light and the bacteria were allowed to react, which consequently increased the levels of oxygen to 25 times the normal levels within the tissues 10 minutes after the heart attack. 45 minutes after the heart attack, the hearts of the infected rats pumped around 60% more blood than the rats that also were not infected, but had a heart attack, and 30% more blood than rats that were infected with the bacteria but left in the dark.

Researchers reported in Science Advances that 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. Based on blood samples taken from the rats during the first week of their recovery, the squad found no proof that the bacteria had spread or caused any lethal effects, and it’s not known to be a human pathogen.

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