Browsing by Author "Serkova, Natalie"
Now showing 1 - 2 of 2
Results Per Page
Sort Options
Item Open Access Early propranolol treatment induces lung heme-oxygenase-1, attenuates metabolic dysfunction, and improves survival following experimental sepsis.(Crit Care, 2013-09-10) Wilson, Joel; Higgins, David; Hutting, Haley; Serkova, Natalie; Baird, Christine; Khailova, Ludmila; Queensland, Kelly; Vu Tran, Zung; Weitzel, Lindsay; Wischmeyer, Paul EINTRODUCTION: Pharmacological agents that block beta-adrenergic receptors have been associated with improved outcome in burn injury. It has been hypothesized that injuries leading to a hypermetabolic state, such as septic shock, may also benefit from beta-blockade; however, outcome data in experimental models have been contradictory. Thus, we investigated the effect of beta-blockade with propranolol on survival, hemodynamics, lung heat shock protein (HSP) expression, metabolism and inflammatory markers in a rat cecal ligation and puncture (CLP) model of sepsis. METHODS: Sprague-Dawley rats receiving either repeated doses (30 minutes pre-CLP and every 8 hours for 24 hours postoperatively) of propranolol or control (normal saline), underwent CLP and were monitored for survival. Additionally, lung and blood samples were collected at 6 and 24 hours for analysis. Animals also underwent monitoring to evaluate global hemodynamics. RESULTS: Seven days following CLP, propranolol improved survival versus control (P < 0.01). Heart rates in the propranolol-treated rats were approximately 23% lower than control rats (P < 0.05) over the first 24 hours, but the mean arterial blood pressure was not different between groups. Metabolic analysis of lung tissue demonstrated an increase in lung ATP/ADP ratio and NAD+ content and a decreased ratio of polyunsaturated fatty acids to monounsaturated fatty acids (PUFA/MUFA). Cytokine analysis of the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) demonstrated decreased expression of TNF-alpha in both lung and plasma at 24 hours post CLP induced sepsis. Finally, propranolol led to a significant increase in lung hemeoxygenase-1 expression, a key cellular protective heat shock protein (HSP) in the lung. Other lung HSP expression was unchanged. CONCLUSIONS: These results suggest that propranolol treatment may decrease mortality during sepsis potentially via a combination of improving metabolism, suppressing aspects of the inflammatory response and enhancing tissue protection.Item Open Access Recommendations towards standards for quantitative MRI (qMRI) and outstanding needs.(Journal of magnetic resonance imaging : JMRI, 2019-01-24) Keenan, Kathryn E; Biller, Joshua R; Delfino, Jana G; Boss, Michael A; Does, Mark D; Evelhoch, Jeffrey L; Griswold, Mark A; Gunter, Jeffrey L; Hinks, R Scott; Hoffman, Stuart W; Kim, Geena; Lattanzi, Riccardo; Li, Xiaojuan; Marinelli, Luca; Metzger, Gregory J; Mukherjee, Pratik; Nordstrom, Robert J; Peskin, Adele P; Perez, Elena; Russek, Stephen E; Sahiner, Berkman; Serkova, Natalie; Shukla-Dave, Amita; Steckner, Michael; Stupic, Karl F; Wilmes, Lisa J; Wu, Holden H; Zhang, Huiming; Jackson, Edward F; Sullivan, Daniel CLEVEL OF EVIDENCE:5 Technical Efficacy: Stage 5 J. Magn. Reson. Imaging 2019.