The compound, named MitoSNO, could also potentially deliver the same benefits after a stroke or major surgery, according to the research, published yesterday in the prestigious international journal Nature Medicine.
The potential new drug was developed by a team led by former Otago University biochemist Dr Mike Murphy in collaboration with Prof Smith.
The pair specialise in creating new molecules that can enter cells and act inside mitochondria, which generate energy for cells.
Prof Smith (69) formally retired last year but is continuing some university research.
Yesterday's research publication was ''a highlight'' of his more than 40-year career.
He had helped develop MitoSNO four or five years ago, at the time not seeking to create a new medical therapy - ''it was pure science''.
''If we help the human condition, I would feel very, very good,'' he added.
He had earlier been helping develop man-made compounds which can enter mitochondria.
In this case, he had also been investigating whether a small molecule, nitric oxide, could be released within mitochondria.
Some ''hard yards'' and ''hard days'' had been put in over the years to develop the compound.
Clinicians linked to the project were impressed by the ''great activity'' achieved, but considerable further testing would be required before human clinical trials could be considered.
The new study was led by Dr Murphy, who is now based at the United Kingdom Medical Research Council's Mitochondrial Biology Unit, and University of Cambridge colleagues.
The authors, including Prof Smith, have published findings that MitoSNO helps protect heart muscle from reperfusion injury when tested in mice.
Reperfusion injury occurs when the blood supply is suddenly restored to tissue that has undergone prolonged oxygen starvation.
Returning blood triggers overproduction of devastating free radical molecules inside mitochondria, killing the cells.
The initial oxygen starvation in a heart attack itself damages tissue, but most cell death occurs through reperfusion injury after medical intervention has unblocked major blood vessels supplying the heart.
Prof Smith said MitoSNO worked by briefly ''switching off'' mitochondria in the first few minutes after blood flow is returned, preventing the build-up of free radicals.
There were no established treatments that could be given at this crucial time.
