Key result
Administration of PEG-SOD to endotoxin-treated rats prevented mitochondrial dysfunction, preserving mitochondrial ATP generation (753 vs 392 nmol/min/mg, p<0.001) and cardiac contractility.
Why the study?
Does PEG-SOD prevent endotoxin-induced cardiac mitochondrial and contractile dysfunction in a rat model of sepsis?
Population
Adult male Sprague-Dawley rats weighing between 250 and 350 g.
Comparison
Polyethylene glycol-adsorbed-superoxide… vs Endotoxin alone, PEG-SOD alone, and…
Design
Preclinical
Follow-up
48 hours
Authors
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Cautions against clinical use of PEG-SOD; leaves open translation of superoxide scavenging to human septic cardiomyopathy.
Does PEG-SOD prevent endotoxin-induced cardiac mitochondrial and contractile dysfunction in a rat model of sepsis?
Absolute Event Rate: 753% vs 392%
p-value: p=<0.001
In a rat model of sepsis, the superoxide scavenger PEG-SOD prevented endotoxin-induced cardiac mitochondrial and contractile dysfunction, suggesting a critical role for superoxide-derived oxidants in sepsis-induced cardiomyopathy.
Supinski et al. (2006) studied Endotoxin-induced cardiac dysfunction (sepsis). Polyethylene glycol-adsorbed-superoxide dismutase (PEG-SOD) vs. Endotoxin alone was evaluated on Mitochondrial ATP generation (nmol/min/mg) (p=<0.001). Administration of PEG-SOD to endotoxin-treated rats prevented mitochondrial dysfunction, preserving mitochondrial ATP generation (753 vs 392 nmol/min/mg, p<0.001) and cardiac contractility.
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