Figure 1.

Proposed mechanisms of action of LE. LE may repartition drug (A): lipophilic substances are drawn into ‘lipid sink’; a concentration gradient develops between tissue and blood, and the toxic drug moves from tissue into aqueous phase into lipid phase. LE may affect sodium channel function (B), or calcium channel function or flux (C), with an increase in intracellular calcium and inotropy (D). Alternatively, LE may revert the cell to fatty acid metabolism or provide FA substrate (E), which may increase inotropy or reverse vasodilatation. LE may provide cytoprotection or stimulate repair after ischaemic injury (F).