Cyclosporin A is a potent immunosuppressant used to prevent graft rejection. The cellular target of cyclosporin A in T lymphocytes is believed to be cyclophilin, a ubiquitous protein with peptidyl prolyl cis trans isomerase activity located in both the cytosol and mitochondria. Recently, cyclosporin A-inhibition of mitochondrial cyclophilin has been implicated in the prevention of mitochondrial dysfunction induced in vitro by Ca2+ overload and other factors potentially relevant to ischaemic cell injury. This study investigates the effect of cyclosporin A on injury to cardiomyocytes induced by substrate-free anoxia. It is shown that cyclosporin A retards progression of the injury, most probably at a late step in the injury process.