Abstract 197: Whole Body Periodic Acceleration Induces Tissue Nitric Oxide Production
Introduction: Whole body periodic acceleration (pGz) increases expression of eNOS, phospho-eNOS and nNOS and has been demonstrated to improve cardiac function after cardiac arrest and reduce brain infarction after experimental stroke. Nitrite production results from the oxidation of nitric oxide (NO) and has been demonstrated to sensitively reflect NO synthase (NOS) activity and endothelial function.
Hypothesis: We hypothesized that pGz results in early increases in NO production through NO synthase activation permitting subsequent cytoprotection through NO and S-nitrosothiol (SNO) based signaling.
Methods: Adult Sprague-Dawley rats (n=4 per group) were anesthetized and subjected to 1 hour of pGz or control (no motion). Blood was obtained for whole blood and plasma nitrite quantification 1 minute before and after pGz (or control) and forebrain, heart and liver were isolated 5 minutes after pGz (or control) for quantification of tissue nitrite and SNO. Nitrite and SNO quantification were performed by tri-iodide based reductive ozone chemiluminescence and tissue values normalized to total protein measured by Bradford assay.
Results: One hour of pGz resulted in significant (mean±SD [pmol/mg protein], p<0.05) increases in heart (78.2±24.5) and forebrain (60.1±5.4) nitrite levels and heart SNO (33.0±3.1) compared to control heart nitrite (42.8±7.1; p=0.013), forebrain nitrite (48.6±5.6; p=0.026) and heart SNO (8.2±1.7; p<0.001). Whole blood, plasma and liver nitrite levels did not differ significantly between pGz and control animals. Control values were similar to levels in naïve (no experiment) animals.
Conclusions: pGZ results in increases in tissue nitrite and SNO indicative of increased NOS activity. The selective increases in heart and brain where pGz protection against ischemia-reperfusion injury has been documented and eNOS is localized suggest a mechanism of signaling.
- © 2010 by American Heart Association, Inc.