A Sphingosine Kinase Form 2 Knockout Sensitizes Mouse Myocardium to Ischemia/Reoxygenation Injury and Diminishes Responsiveness to Ischemic Preconditioning
Figure 4
Hemodynamic function and infarct sizes in wild-type and SphK2 KO (SK2KO) hearts in ischemia-reoxygenation injury and ischemic preconditioning. Equilibrated ex vivo hearts were exposed to 40 min of ischemia followed by 40 min of reoxygenation either in the absence of any preconditioning (−IPC) or with ischemic preconditioning (+IPC) or with pharmacologic preconditioning using 0.4 μM S1P (+S1P). Data are expressed as . versus −IPC. /group. (a) Maximum left ventricular developed pressure (LVDP) achieved during 40 min of reperfusion expressed as % recovery relative to the preischemic value. LVDP is shown for wild-type (WT) and SphK2 knockout (SK2KO) mouse hearts. (b) Infarct size expressed as percent of the area at risk (which is the total heart area in this global ischemia model) determined at the end of 40 min of reperfusion in wild-type (WT) and SphK2 knockout (SK2KO) hearts.
