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Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac contractile dysfunction as well as myocardial injury. These deleterious effects are due in large part to endothelial dysfunction leading to an upregulation of cell adhesion molecules and subsequent neutrophil-induced cardiac injury. At physiologically relevant concentrations, N,N,N-trimethylsphingosine (TMS), a synthetic N-methylated sphingosine derivative, has been shown to attenuate leukocyte-endothelial cell interactions. We wanted to test the effects of TMS on neutrophil-mediated cardiac dysfunction in ischemia/reperfusion.

Beneficial effects of N,N,N-trimethylsphingosine following ischemia and reperfusion in the isolated perfused rat heart