ESRA19-0604 Rescue of LPS-induced left ventricular dysfunction by intralipid is mediated by phosphorylation of stat3

Background and aims Intralipid (ILP) has been demonstrated in animal models and humans to mitigate the cardio-depressant effects of local anesthetics and I/R injury, possibly via restoration of metabolic dysfunction, activation of cardio-protective signaling and augmentation of contractility. Methods 8 adult female SD rats received a single intraperitoneal injection of LPS (20 mg/kg). Echocardiography was performed on the rats at baseline prior to injection of LPS, and then at 6h post-LPS, in order to assess LV ejection fraction. Rats were randomly divided to receive either 20% ILP (n=4) or phosphate buffered saline (PBS; n=4) as a 5 ml/kg bolus followed by a 0.5 ml/kg/min infusion over 10 min and echocardiography was conducted at 1, 5 and 10 min to reassess LVEF. At 10 min, LV tissue was collected and Western blots were performed to assess for GSK and STAT3 phosphorylation. Values are expressed as mean±SEM. P Results Baseline LVEF in PBS and ILP before LPS were 75.7±1.1% and 74.2±1.2%, respectively. 6 h after LPS, LVEF was decreased (LVEF= 54.3±4.8% in PBS, and 46.0±2.5% in ILP; both p Conclusions Administration of ILP significantly improves LVF likely mediated via STAT3 phosphorylation.