Abstract
The effect of dimethylsulfoxide (DMSO) on the morphologic features of cells and cellular enzyme release was studied in Langendorf-perfused rat hearts at 37 C. Ten percent DMSO greatly reduced the magnitude of oxygen-induced creatine kinase release (O2-CK) after a 60-minute period of hypoxic perfusion. DMSO also protected cells from development of severe contracture with formation of contraction bands. A linear correlation was found between the magnitude of O2-CK release and the percentage of cells in hearts containing contraction bands. Hypertonic mannitol did not protect hearts from CK release due to the calcium paradox, although DMSO was effective in this regard. DMSO reduced contractile force of hearts and tensions caused by hypoxic contracture as measured by an intraventricular balloon. This study suggests that DMSO affords protection from O2-CK release by actions on cells other than its osmotic effects. DMSO may alter the response of injured cells to the effects of calcium ions.
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