The ability of heat stress and metabolic preconditioning to protect primary rat cardiac myocytes

1435-1803

Heat stress ; ischaemia ; hsp70 ; cardiac myocytes

Springer Online Journal Archives 1860-2000

Medicine

Abstract Primary rat cardiocytes were subjected to either thermal “preconditioning” for 30 min at 43°C or 20 min metabolic “preconditioning” (10 mM deoxyglucose, 20 mM lactate, pH 6.5). Eighteen hours later cells were analysed either for hsp 70i expression or subjected to a subsequent lethal heat stress or simulated ischaemia (10 mM deoxyglucose, 20 mM lactate, 0.75 mM sodium dithionite, 12 mM potassium chloride, pH 6.5) for 2 hours and assessed for survival by trypan blue exclusion. Hsp 70i was induced over 100 fold by thermal “preconditioning” and 30 fold by metabolic “preconditioning” (p〈0.001, p〈0.05), hsp 90 was induced 2.71 fold and 2.24 fold (p〈0.001, p〈0.001) by thermal and metabolic “preconditioning” respectively, while hsp 60 was not induced by either treatment. Preconditioned cultures had improved survival against subsequent lethal heat stress or simulated ischaemia: Thermal “preconditioning” reduced death from 69.22% to 52.46% upon subsequent “lethal” heat stress and from 49.13% to 36.66% upon subsequent “lethal” simulated ischaemia. Metabolic “preconditioning” reduced cell death from 51.29% to 33.8% against subsequent “lethal” heat stress, and from 69.09% to 55.61% upon subsequent “lethal” simulated ischaemia. A second marker of cell death, the release of lactate dehydrogenase activity into the culture media, was reduced to 65% and 60% of control values for thermally preconditioned cells subjected to “lethal” heat or “lethal” simulated ischaemia respectively. Metabolically “preconditioned” cells demonstrated lactate dehydrogenase activity of 59% and 51% that of control values, when subjected to “lethal” heat or “lethal” simulated “ischaemia” respectively.

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