Contractile and morphological properties of hamster retractor muscle following 16 h of cold preservation

• Published in: Cryobiology 2009-12, Vol.59 (3), p.308-316
• Main Authors: de With, Miriam C.J., van der Heijden, E.P.A. Brigitte, van Oosterhout, Matthijs F., Kon, M., Kroese, Alfons B.A.
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Calcium homeostasis; Chromans - pharmacology; Cold Temperature; Composite tissue allograft; Cricetinae; Hamster; Hibernation; Ischemia; Male; Mesocricetus; Muscle Contraction - drug effects; Muscle, Skeletal - anatomy & histology; Muscle, Skeletal - physiology; Organ Preservation; Organ Preservation Solutions - pharmacology; Preservation; Pyridones - pharmacology; Rats; Reactive oxygen species; Reoxygenation; Skeletal muscle
• ISSN: 0011-2240; 1090-2392
• DOI: 10.1016/j.cryobiol.2009.08.008

Cold hypoxia is a common factor in cold tissue preservation and mammalian hibernation. The purpose of this study was to determine the effects of cold preservation on the function of the retractor (RET) muscle of the hamster in the non-hibernating state and compare these with previously published data (van der Heijden et al., 2000) [52] on the rat cutaneus trunci (CT) muscle. After cold storage (16h at 4°C), muscles were stimulated electrically to measure maximum tetanus tension (P0) and histologically analyzed. The protective effects of addition of the antioxidants trolox and deferiprone and the calcium release inhibitor BDM to the storage fluid were determined. After storage, the twitch threshold current was increased (from 60 to 500μA) and P0 was decreased to 27% of control. RET morphology remained unaffected. RET muscle function was protected by trolox and deferiprone (P0, resp., 43% and 59% of control). Addition of BDM had no effect on the RET. The observed effects of cold preservation and of trolox and deferiprone on the RET were comparable to those on CT muscle function, as reported in a previously published study (van der Heijden et al., 2000) [52]. Both hamster RET and rat CT muscles show considerable functional damage due to actions of reactive oxygen species. In contrast to the CT, in the RET cold preservation-induced functional injury could not be prevented by BDM and was not accompanied by morphological damage such as necrosis and edema. This suggests that the RET myocytes possess a specific adaptation to withstand the Ca2+ overload induced by cold ischemia.