Abstract 17446: Intra-arrest Hypothermia Protection Requires Endothelial Nitric Oxide Synthase

TL;DRAbstract

Introduction: Intra-arrest hypothermia (IH), cooling the body to 30 - 32°C during cardiac arrest, has previously been shown as protective in a mouse model of cardiac arrest. Hypothermia has also been shown to protect cultured cardiomyocytes exposed to simulated ischemia/reperfusion (I/R) in a nitric oxide synthase-dependent manner. However, the effect of IH on NOS signaling in whole animal models of cardiac arrest has not been studied. We hypothesized that mice deficient in endothelial NOS (NOS3) would not be protected by IH following cardiac arrest. Furthermore, we hypothesized that IH would alter NOS3 signaling in WT mouse hearts. METHODS: Adult NOS3 -/- (B6.129P2-Nos3tm1Unc/J, n = 30) and WT (C57Bl/6J, n = 24) mice underwent 8 min of cardiac arrest. At 6 min, mice were randomized to normothermia (NT, 37°C) or IH (30°C) followed by re-warming to 37°C at 60 min post-ROSC. Animals were hemodynamically monitored for 2 h and then neurologically scored at regular intervals up to 48 h. In

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