The effects of supercooling chemicals on myocardial ultrastructure: a transmission electron microscopy case study.

Extended ischemia results in organ infarction which limits the availability of donor hearts. Hypothermic storage extends heart preservation by effectively stopping cellular metabolism, thereby preventing toxic accumulations of metabolic wastes and depletion of energy stores. However, cell swelling as a result of ion concentration changes and cell laceration due to ice crystal growth are consequences of hypothermic ischemia. Supercooling successfully preserves hearts for an extended time without associated myocardial necrosis. The efficacies of four supercooling preservative solutions, containing hypertonic glucose, polyethylene glycol, and or winter flounder antifreeze protein, are assessed using the Langendorff isolated organ perfusion apparatus and transmission electron microscopy. Polyethylene glycol seems the most effective in preventing myocardial necrosis possibly by dehydrating, minimizing cellular ice formation, protecting against cell swelling, and functioning as an antioxidant. Hypertonic glucose seems the most effective in reducing cell swelling; it may also depress solution freezing points, bind water, adjust both intra- and extracellular osmolarities, stabilize proteins, and assist in adenosine triphosphate (ATP) production. Antifreeze protein seems to bind effectively to ice and inhibit its growth; it may also reduce membrane permeabilities to Ca2+ and K+ ions.